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1385 lines
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||
<!--
|
||
UID=445
|
||
ConceptID=C0004238
|
||
-->
|
||
<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Atrial fibrillation</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>445</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0004238</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome; Finding</dd></dl></div></div><table class="medgenTable"><tbody><tr><td>Synonyms:</td>
|
||
<td>Atrial Fibrillation; Atrial Fibrillations; Auricular Fibrillation; Auricular Fibrillations; Fibrillation, Atrial; Fibrillation, Auricular; Fibrillations, Atrial; Fibrillations, Auricular</td></tr>
|
||
<tr><td><span class="bold">SNOMED CT: </span></td>
|
||
<td>AF - Atrial fibrillation (49436004); Atrial fibrillation (49436004)</td></tr>
|
||
<tr><td colspan="2" class="small"> </td></tr><tr><td><a class="help" data-jig="ncbipopper" href="#target-gene-related">Related genes:<img src="//static.pubmed.gov/portal/portal3rc.fcgi/4223267/img/4204968" /></a><div id="target-gene-related" class="display-none">
|
||
Gene(s) associated with related conditions. For conditions<br />
|
||
in a hierarchy, the parent condition will list the genes<br />
|
||
associated with the children conditions.</div></td>
|
||
<td><a target="_blank" href="/gene/10060">ABCC9</a>, <a target="_blank" href="/gene/9992">KCNE2</a>, <a target="_blank" href="/gene/3784">KCNQ1</a>, <a target="_blank" href="/gene/3759">KCNJ2</a>, <a target="_blank" href="/gene/3741">KCNA5</a>, <a target="_blank" href="/gene/2702">GJA5</a></td></tr><tr><td colspan="2" class="small"> </td></tr><tr><td>HPO:</td>
|
||
<td><a target="_blank" title="Human Phenotype Ontology" href="https://hpo.jax.org/app/browse/term/HP:0005110">HP:0005110</a></td></tr>
|
||
<tr><td>Monarch Initiative:</td>
|
||
<td><a href="https://monarchinitiative.org/disease/MONDO:0004981" target="_blank">MONDO:0004981</a></td></tr>
|
||
</tbody></table></div><div class="rprt-body jig-ncbiinpagenav" data-jigconfig="smoothScroll: false, gotoTopLink: true, gotoTopLinkText: '', gotoTopLinkAttrs: {'title': 'Go to the top of the page'},allHeadingLevels: ['h1'], topOfPageTOC: true, tocId: 'my-toc'"><div id="rprt-tabs-1" class="rprt-tab"><div id="tb-termsProp-1"><div class="leftCol mgCol"><div>
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<div class="portlet mgSection" id="ID_100">
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||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Definition">Definition</h1><a sid="100" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln">An atrial arrhythmia characterized by disorganized atrial activity without discrete P waves on the surface EKG, but instead by an undulating baseline or more sharply circumscribed atrial deflections of varying amplitude an frequency ranging from 350 to 600 per minute. [from <a title="Human Phenotype Ontology" href="http://www.human-phenotype-ontology.org" class="defSource" target="_blank">HPO</a>]</div>
|
||
</div>
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||
|
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<div class="portlet mgSection" id="ID_118">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Term_Hierarchy">Term Hierarchy</h1><a sid="118" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln HierarchyGTR"><div class="jig-ncbitabs"><ul><li><a href="#tabGTR">GTR</a></li><li><a href="#tabMGEN">MeSH</a></li></ul><div id="tabGTR"><div class="search_result"><div class="rprts"><div class="chiclet_legend"><span class="chiclet_list" style="position:static;"><span title="Clinical test" class="chiclet Ccolor round">C</span><span>Clinical test, </span><span title="Research test" class="chiclet Rcolor round">R</span><span>Research test, </span><span title="OMIM" class="chiclet Ocolor ">O</span><span>OMIM, </span><span title="GeneReview" class="chiclet Gcolor">G</span><span><em>GeneReviews</em>, </span><span title="ClinVar" class="chiclet Vcolor">V</span><span>ClinVar </span></span></div><div id="hierarchy" class="margin_t1"><div class="ds_tree"><ul><li class="matched_ds"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C0004238[DISCUI]&test_type=Clinical" ref="ncbi_uid=445">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet unavailable" title="OMIM">O</span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=445" ref="ncbi_uid=445">V</a></span></span><span class="TLline">Atrial fibrillation</span><ul><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C1837014[DISCUI]&test_type=Clinical" ref="ncbi_uid=373232">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=373232" target="_blank" href="/omim/607542">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=373232" ref="ncbi_uid=373232">V</a></span></span><span class="TLline"><a href="/medgen/373232" ref="tree=GTR&ncbi_uid=373232&link_uid=373232" title="View MedGen record for 'Atrial fibrillation, familial, 3'">Atrial fibrillation, familial, 3</a></span></li><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C1862394[DISCUI]&test_type=Clinical" ref="ncbi_uid=400041">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=400041" target="_blank" href="/omim/603796">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=400041" ref="ncbi_uid=400041">V</a></span></span><span class="TLline"><a href="/medgen/400041" ref="tree=GTR&ncbi_uid=400041&link_uid=400041" title="View MedGen record for 'Atrial fibrillation, familial, 4'">Atrial fibrillation, familial, 4</a></span></li><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C2677106[DISCUI]&test_type=Clinical" ref="ncbi_uid=393658">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=393658" target="_blank" href="/omim/176267">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=393658" ref="ncbi_uid=393658">V</a></span></span><span class="TLline"><a href="/medgen/393658" ref="tree=GTR&ncbi_uid=393658&link_uid=393658" title="View MedGen record for 'Atrial fibrillation, familial, 7'">Atrial fibrillation, familial, 7</a></span></li><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C3151431[DISCUI]&test_type=Clinical" ref="ncbi_uid=462781">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=462781" target="_blank" href="/omim/600681">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=462781" ref="ncbi_uid=462781">V</a></span></span><span class="TLline"><a href="/medgen/462781" ref="tree=GTR&ncbi_uid=462781&link_uid=462781" title="View MedGen record for 'Atrial fibrillation, familial, 9'">Atrial fibrillation, familial, 9</a></span></li><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C3279693[DISCUI]&test_type=Clinical" ref="ncbi_uid=481323">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=481323" target="_blank" href="/omim/121013">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=481323" ref="ncbi_uid=481323">V</a></span></span><span class="TLline"><a href="/medgen/481323" ref="tree=GTR&ncbi_uid=481323&link_uid=481323" title="View MedGen record for 'Atrial fibrillation, familial, 11'">Atrial fibrillation, familial, 11</a></span></li><li class="TLclosed"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C3279695[DISCUI]&test_type=Clinical" ref="ncbi_uid=481325">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet Ocolor" title="OMIM"><a ref="ncbi_uid=481325" target="_blank" href="/omim/601439">O</a></span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=481325" ref="ncbi_uid=481325">V</a></span></span><span class="TLline"><a href="/medgen/481325" ref="tree=GTR&ncbi_uid=481325&link_uid=481325" title="View MedGen record for 'Atrial fibrillation, familial, 12'">Atrial fibrillation, familial, 12</a></span></li></ul></li></ul></div></div></div></div></div><div id="tabMGEN"><div class="ds_tree"><ul><li><span class="TLline"><a href="/medgen/116727" ref="tree=MeSH" title="MedGen record for Abnormality of the cardiovascular system">Abnormality of the cardiovascular system</a></span><ul><li><span class="TLline"><a href="/medgen/869166" ref="tree=MeSH" title="MedGen record for Abnormal cardiovascular system physiology">Abnormal cardiovascular system physiology</a></span><ul><li><span class="TLline"><a href="/medgen/1393551" ref="tree=MeSH" title="MedGen record for Abnormality of cardiovascular system electrophysiology">Abnormality of cardiovascular system electrophysiology</a></span><ul><li><span class="TLline"><a href="/medgen/2039" ref="tree=MeSH" title="MedGen record for Cardiac arrhythmia">Cardiac arrhythmia</a></span><ul><li><span class="TLline"><a href="/medgen/96544" ref="tree=MeSH" title="MedGen record for Supraventricular arrhythmia">Supraventricular arrhythmia</a></span><ul><li><span class="TLline"><a href="/medgen/39317" ref="tree=MeSH" title="MedGen record for Atrial arrhythmia">Atrial arrhythmia</a></span><ul><li><span class="matched_ds">Atrial fibrillation</span><ul><li><span class="TLline"><a href="/medgen/373232" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 3">Atrial fibrillation, familial, 3</a></span></li><li><span class="TLline"><a href="/medgen/400041" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 4">Atrial fibrillation, familial, 4</a></span></li><li><span class="TLline"><a href="/medgen/393658" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 7">Atrial fibrillation, familial, 7</a></span></li><li><span class="TLline"><a href="/medgen/462781" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 9">Atrial fibrillation, familial, 9</a></span></li><li><span class="TLline"><a href="/medgen/481323" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 11">Atrial fibrillation, familial, 11</a></span></li><li><span class="TLline"><a href="/medgen/481325" ref="tree=MeSH" title="MedGen record for Atrial fibrillation, familial, 12">Atrial fibrillation, familial, 12</a></span></li><li><span class="TLline"><a href="/medgen/151957" ref="tree=MeSH" title="MedGen record for Chronic atrial fibrillation">Chronic atrial fibrillation</a></span></li><li><span class="TLline"><a href="/medgen/115990" ref="tree=MeSH" title="MedGen record for Paroxysmal atrial fibrillation">Paroxysmal atrial fibrillation</a></span></li><li><span class="TLline"><a href="/medgen/750308" ref="tree=MeSH" title="MedGen record for Permanent atrial fibrillation">Permanent atrial fibrillation</a></span></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></div></div></div></div>
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Conditions_with_this_feature">Conditions with this feature</h1><a sid="112" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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<div class="portlet_content ln clinfeat">
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<div class="divPopper rprt" id="rdis_4435"><div><strong>Ebstein anomaly</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>4435</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0013481</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Congenital Abnormality</dd></dl></div></div></div>
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<div class="spaceAbove">Ebstein anomaly is characterized by downward displacement of variable severity of the tricuspid valve into the right ventricle. The valve leaflets may be dysplastic, and a variable portion of the proximal part of the right ventricle is in continuity with the right atrium ('atrialized'), because of the abnormally positioned tricuspid valve. The severity of this defect includes a spectrum ranging from severe disturbance in fetal and neonatal life to virtually asymptomatic survival to adult life. Associated extracardiac anomalies in the setting of chromosomal or mendelian disorders occur in about 20% of patients with Ebstein anomaly. Nonsyndromic Ebstein anomaly can occur as a sporadic or a familial defect (summary by Digilio et al., 2011).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/4435">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_140765"><div><strong>McLeod neuroacanthocytosis syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>140765</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0398568</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">McLeod neuroacanthocytosis syndrome (designated as MLS throughout this review) is a multisystem disorder with central nervous system (CNS), neuromuscular, cardiovascular, and hematologic manifestations in males: CNS manifestations are a neurodegenerative basal ganglia disease including movement disorders, cognitive alterations, and psychiatric symptoms. Neuromuscular manifestations include a (mostly subclinical) sensorimotor axonopathy and muscle weakness or atrophy of different degrees. Cardiac manifestations include dilated cardiomyopathy, atrial fibrillation, and tachyarrhythmia. Hematologically, MLS is defined as a specific blood group phenotype (named after the first proband, Hugh McLeod) that results from absent expression of the Kx erythrocyte antigen and weakened expression of Kell blood group antigens. The hematologic manifestations are red blood cell acanthocytosis and compensated hemolysis. Alloantibodies in the Kell and Kx blood group system can cause strong reactions to transfusions of incompatible blood and severe anemia in affected male newborns of Kell-negative mothers. Females heterozygous for XK pathogenic variants have mosaicism for the Kell and Kx blood group antigens. Although they usually lack CNS and neuromuscular manifestations, some heterozygous females may develop clinical manifestations including chorea or late-onset cognitive decline.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/140765">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_96073"><div><strong>Familial cutaneous collagenoma</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>96073</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0406817</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Neoplastic Process</dd></dl></div></div></div>
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<div class="spaceAbove">Familial cutaneous collagenoma is a connective tissue nevus characterized by multiple, flesh-colored asymptomatic nodules distributed symmetrically on the trunk and upper arms (mainly on the upper two-thirds of the back), manifesting around adolescence. The skin biopsy reveals an accumulation of collagen fibers with reduction in the number of elastic fibers. Cardiac anomalies may be observed. Familial cutaneous collagenoma follows an autosomal dominant mode of transmission.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/96073">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_258500"><div><strong>Dilated cardiomyopathy 1A</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>258500</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1449563</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">LMNA-related dilated cardiomyopathy (DCM) is characterized by left ventricular enlargement and/or reduced systolic function preceded (sometimes by many years) by or accompanied by conduction system disease and/or arrhythmias. LMNA-related DCM usually presents in early to mid-adulthood with symptomatic conduction system disease or arrhythmias, or with symptomatic DCM including heart failure or embolus from a left ventricular mural thrombus. Sudden cardiac death can occur, and in some instances is the presenting manifestation; sudden cardiac death may occur with minimal or no systolic dysfunction.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/258500">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_354526"><div><strong>Familial partial lipodystrophy, Dunnigan type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>354526</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1720860</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Familial partial lipodystrophy (FPLD) is a metabolic disorder characterized by abnormal subcutaneous adipose tissue distribution beginning in late childhood or early adult life. Affected individuals gradually lose fat from the upper and lower extremities and the gluteal and truncal regions, resulting in a muscular appearance with prominent superficial veins. In some patients, adipose tissue accumulates on the face and neck, causing a double chin, fat neck, or cushingoid appearance. Metabolic abnormalities include insulin-resistant diabetes mellitus with acanthosis nigricans and hypertriglyceridemia; hirsutism and menstrual abnormalities occur infrequently. Familial partial lipodystrophy may also be referred to as lipoatrophic diabetes mellitus, but the essential feature is loss of subcutaneous fat (review by Garg, 2004). The disorder may be misdiagnosed as Cushing disease (see 219080) (Kobberling and Dunnigan, 1986; Garg, 2004). Genetic Heterogeneity of Familial Partial Lipodystrophy Familial partial lipodystrophy is a clinically and genetically heterogeneous disorder. Types 1 and 2 were originally described as clinical subtypes: type 1 (FPLD1; 608600), characterized by loss of subcutaneous fat confined to the limbs (Kobberling et al., 1975), and FPLD2, characterized by loss of subcutaneous fat from the limbs and trunk (Dunnigan et al., 1974; Kobberling and Dunnigan, 1986). No genetic basis for FPLD1 has yet been delineated. FPLD3 (604367) is caused by mutation in the PPARG gene (601487) on chromosome 3p25; FPLD4 (613877) is caused by mutation in the PLIN1 gene (170290) on chromosome 15q26; FPLD5 (615238) is caused by mutation in the CIDEC gene (612120) on chromosome 3p25; FPLD6 (615980) is caused by mutation in the LIPE gene (151750) on chromosome 19q13; FPLD7 (606721) is caused by mutation in the CAV1 gene (601047) on chromosome 7q31; FPLD8 (620679), caused by mutation in the ADRA2A gene (104210) on chromosome 10q25; and FPLD9 (620683), caused by mutation in the PLAAT3 gene (613867) on chromosome 11q12.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/354526">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_316943"><div><strong>Dilated cardiomyopathy 1D</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>316943</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1832243</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Left ventricular noncompaction is a heart (cardiac) muscle disorder that occurs when the lower left chamber of the heart (left ventricle), which helps the heart pump blood, does not develop correctly. Instead of the muscle being smooth and firm, the cardiac muscle in the left ventricle is thick and appears spongy. The abnormal cardiac muscle is weak and has an impaired ability to pump blood because it either cannot completely contract or it cannot completely relax. For the heart to pump blood normally, cardiac muscle must contract and relax fully.\n\nSome individuals with left ventricular noncompaction experience no symptoms at all; others have heart problems that can include sudden cardiac death. Additional signs and symptoms include abnormal blood clots, irregular heart rhythm (arrhythmia), a sensation of fluttering or pounding in the chest (palpitations), extreme fatigue during exercise (exercise intolerance), shortness of breath (dyspnea), fainting (syncope), swelling of the legs (lymphedema), and trouble laying down flat. Some affected individuals have features of other heart defects. Left ventricular noncompaction can be diagnosed at any age, from birth to late adulthood. Approximately two-thirds of individuals with left ventricular noncompaction develop heart failure.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/316943">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_331341"><div><strong>Dilated cardiomyopathy 1E</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>331341</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1832680</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the SCN5A gene.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/331341">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_331466"><div><strong>Hypertrophic cardiomyopathy 6</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>331466</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1833236</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Mutations in the PRKAG2 gene (602743) give rise to a moderate, essentially heart-specific, nonlysosomal glycogenosis with clinical onset typically in late adolescence or in the third decade of life, ventricular pre-excitation predisposing to supraventricular arrhythmias, mild to severe cardiac hypertrophy, enhanced risk of sudden cardiac death in midlife, and autosomal dominant inheritance with full penetrance (summary by Burwinkel et al., 2005).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/331466">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_320273"><div><strong>Sick sinus syndrome 2, autosomal dominant</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>320273</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1834144</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Sick sinus syndrome (also known as sinus node dysfunction) is a group of related heart conditions that can affect how the heart beats. "Sick sinus" refers to the sino-atrial (SA) node, which is an area of specialized cells in the heart that functions as a natural pacemaker. The SA node generates electrical impulses that start each heartbeat. These signals travel from the SA node to the rest of the heart, signaling the heart (cardiac) muscle to contract and pump blood. In people with sick sinus syndrome, the SA node does not function normally. In some cases, it does not produce the right signals to trigger a regular heartbeat. In others, abnormalities disrupt the electrical impulses and prevent them from reaching the rest of the heart.\n\nSick sinus syndrome occurs most commonly in older adults, although it can be diagnosed in people of any age. The condition increases the risk of several life-threatening problems involving the heart and blood vessels. These include a heart rhythm abnormality called atrial fibrillation, heart failure, cardiac arrest, and stroke.\n\nSick sinus syndrome tends to cause the heartbeat to be too slow (bradycardia), although occasionally the heartbeat is too fast (tachycardia). In some cases, the heartbeat rapidly switches from being too fast to being too slow, a condition known as tachycardia-bradycardia syndrome. Symptoms related to abnormal heartbeats can include dizziness, light-headedness, fainting (syncope), a sensation of fluttering or pounding in the chest (palpitations), and confusion or memory problems. During exercise, many affected individuals experience chest pain, difficulty breathing, or excessive tiredness (fatigue). Once symptoms of sick sinus syndrome appear, they usually worsen with time. However, some people with the condition never experience any related health problems.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/320273">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_373232"><div><strong>Atrial fibrillation, familial, 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>373232</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1837014</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/373232">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_324886"><div><strong>Atrial fibrillation, familial, 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>324886</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1837812</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/324886">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_334469"><div><strong>Atrial fibrillation, familial, 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>334469</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1843687</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). Genetic Heterogeneity of Familial Atrial Fibrillation ATFB1 shows linkage to chromosome 10q22-q24. ATFB2 (608988) maps to chromosome 6q. ATFB3 (607554) is caused by mutation in the KCNQ1 gene (607542) on chromosome 11. ATFB4 (611493) is caused by mutation in the KCNE2 gene (603796) on chromosome 21. Variants in a region of chromosome 4q25 are associated with ATFB5 (611494). ATFB6 (612201) is caused by mutation in the NPPA gene (108780) on chromosome 1p36. ATFB7 (612240) is caused by mutation in the KCNA5 gene (176267) on chromosome 12p13. ATFB8 (613055) maps to chromosome 16q22. ATFB9 (613980) is caused by mutation in the KCNJ2 gene (600681) on chromosome 17q24.3. ATFB10 (614022) is caused by mutation in the SCN5A gene (600163) on chromosome 3p21. ATFB11 (614049) is caused by mutation in the GJA5 (121013) gene on chromosome 1q21.1. ATFB12 (614050) is caused by mutation in the ABCC9 gene (601439) on chromosome 12p12.1. ATFB13 (615377) is caused by mutation in the SCN1B gene (600235) on chromosome 19q13. ATFB14 (615378) is caused by mutation in the SCN2B gene (601327) on chromosome 11q23. ATFB15 (615770) is caused by mutation in the NUP155 gene (606694) on chromosome 5p13. ATFB16 (see 613120) is caused by mutation in the SCN3B gene (608214) on chromosome 11q24. ATFB17 (see 611819) is caused by mutation in the SCN4B gene (608256) on chromosome 11q23. ATFB18 (617280) is caused by mutation in the MYL4 gene (160770) on chromosome 17q21. Olesen et al. (2014) analyzed 192 Danish Caucasian patients with onset of lone atrial fibrillation before the age of 40 years for the presence of rare variants in 14 AF-associated genes and found that 29 (7.6%) alleles harbored a very rare variant (minor allele frequency less than 1%), a significantly higher percentage than that found in 6,503 individuals in the NHLBI Exome Variant Server database (4.1%; p = 0.0012). Twenty-four of the 29 rare variants found in the lone AF patient cohort had previously been studied, with 23 (96%) showing abnormal ion channel function by patch-clamp analysis. Olesen et al. (2014) suggested that rare variants in AF susceptibility genes may play a role in the pathophysiology of AF.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/334469">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_349005"><div><strong>Left ventricular noncompaction 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>349005</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1858725</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Left ventricular noncompaction (LVNC) is characterized by numerous prominent trabeculations and deep intertrabecular recesses in hypertrophied and hypokinetic segments of the left ventricle (Sasse-Klaassen et al., 2004). The mechanistic basis is thought to be an intrauterine arrest of myocardial development with lack of compaction of the loose myocardial meshwork. LVNC may occur in isolation or in association with congenital heart disease. Distinctive morphologic features can be recognized on 2-dimensional echocardiography (Kurosaki et al., 1999). Noncompaction of the ventricular myocardium is sometimes referred to as spongy myocardium. Stollberger et al. (2002) commented that the term 'isolated LVNC,' meaning LVNC without coexisting cardiac abnormalities, is misleading, because additional cardiac abnormalities are found in nearly all patients with LVNC. Genetic Heterogeneity of Left Ventricular Noncompaction A locus for autosomal dominant left ventricular noncompaction has been identified on chromosome 11p15 (LVNC2; 609470). LVNC3 (see 605906) is caused by mutation in the LDB3 gene (605906) on chromosome 10q23. LVNC4 (see 613424) is caused by mutation in the ACTC1 gene (102540) on chromosome 15q14. LVNC5 (see 613426) is caused by mutation in the MYH7 gene (160760) on chromosome 14q12. LVNC6 (see 601494) is caused by mutation in the TNNT2 gene (191045) on chromosome 1q32. LVNC7 (615092) is caused by mutation in the MIB1 gene (608677) on chromosome 18q11. LVNC8 (615373) is caused by mutation in the PRDM16 gene (605557) on chromosome 1p36. LVNC9 (see 611878) is caused by mutation in the TPM1 gene (191010) on chromosome 15q22. LVNC10 (615396) is caused by mutation in the MYBPC3 gene (600958) on chromosome 11p11. LVNC can also occur as part of an X-linked disorder, Barth syndrome (302060), caused by mutation in the TAZ gene (300394) on chromosome Xq28.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/349005">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_347714"><div><strong>Dilated cardiomyopathy 1G</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>347714</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1858763</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Dilated cardiomyopathy-1G (CMD1G) is an autosomal dominant disorder characterized by ventricular dilatation and systolic contractile dysfunction (Siu et al., 1999). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy (CMD), see CMD1A (115200).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/347714">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_348695"><div><strong>Hypertrophic cardiomyopathy 7</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>348695</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1860752</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. \n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/348695">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_349383"><div><strong>Hypertrophic cardiomyopathy 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>349383</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1861864</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. \n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/349383">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_400041"><div><strong>Atrial fibrillation, familial, 4</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>400041</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1862394</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/400041">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_355890"><div><strong>Short QT syndrome type 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>355890</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1865019</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Short QT syndrome is a cardiac channelopathy associated with a predisposition to atrial fibrillation and sudden cardiac death. Patients have a structurally normal heart, but electrocardiography (ECG) exhibits abbreviated QTc (Bazett's corrected QT) intervals of less than 360 ms (summary by Moreno et al., 2015). For a discussion of genetic heterogeneity of short QT syndrome, see SQT1 (609620).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/355890">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_369411"><div><strong>Atrial fibrillation, familial, 5</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>369411</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1969099</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/369411">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_370181"><div><strong>Cardiac arrhythmia, ankyrin-B-related</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>370181</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1970119</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Loss-of-function mutations in ANK2 can result in a broad spectrum of clinical cardiac phenotypes. Carriers of some mutations (e.g., E1425G, 106410.0001) display QT interval prolongation, stress- and/or exercise-induced polymorphic ventricular arrhythmia, syncope, and sudden cardiac death. Patients with other variants show clinical phenotypes, sometimes mild, extending beyond LQTS, leading to the label 'ankyrin-B syndrome.' These phenotypes include bradycardia, sinus arrhythmia, delayed conduction/conduction block, idiopathic ventricular fibrillation, and catecholaminergic polymorphic ventricular tachycardia (Mohler et al., 2007).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/370181">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_394252"><div><strong>Atrial fibrillation, familial, 6</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>394252</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2677294</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/394252">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_393713"><div><strong>Dilated cardiomyopathy 1AA</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>393713</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2677338</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the ACTN2 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/393713">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_437215"><div><strong>Dilated cardiomyopathy 1Y</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>437215</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2678476</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Dilated cardiomyopathy-1Y (CMD1Y) is characterized by severe progressive cardiac failure, resulting in death in the third to sixth decades of life in some patients. Electron microscopy shows an abnormal sarcomere structure (Olson et al., 2001). In left ventricular noncompaction-9 (LVNC9), patients may present with cardiac failure or may be asymptomatic. Echocardiography shows noncompaction of the apex and midventricular wall of the left ventricle (Probst et al., 2011). Some patients also exhibit Ebstein anomaly of the tricuspid valve (Kelle et al., 2016) and some have mitral valve insufficiency (Nijak et al., 2018).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/437215">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_395632"><div><strong>Brugada syndrome 4</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>395632</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2678477</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/395632">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_395633"><div><strong>Brugada syndrome 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>395633</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2678478</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/395633">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_394836"><div><strong>Long QT syndrome 10</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>394836</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2678484</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any long QT syndrome in which the cause of the disease is a mutation in the SCN4B gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/394836">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_412871"><div><strong>Congenital generalized lipodystrophy type 4</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>412871</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2750069</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Berardinelli-Seip congenital lipodystrophy (BSCL) is usually diagnosed at birth or soon thereafter. Because of the absence of functional adipocytes, lipid is stored in other tissues, including muscle and liver. Affected individuals develop insulin resistance and approximately 25%-35% develop diabetes mellitus between ages 15 and 20 years. Hepatomegaly secondary to hepatic steatosis and skeletal muscle hypertrophy occur in all affected individuals. Hypertrophic cardiomyopathy is reported in 20%-25% of affected individuals and is a significant cause of morbidity from cardiac failure and early mortality.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/412871">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_442487"><div><strong>Hypertrophic cardiomyopathy 13</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>442487</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2750472</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the TNNC1 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/442487">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_414348"><div><strong>Atrial septal defect 6</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>414348</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2751315</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Congenital Abnormality</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any atrial heart septal defect in which the cause of the disease is a mutation in the TLL1 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/414348">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_414420"><div><strong>Atrial fibrillation, familial, 8</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>414420</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2751607</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/414420">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462308"><div><strong>Dilated cardiomyopathy 1V</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462308</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3150958</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the PSEN2 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462308">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462437"><div><strong>Aneurysm-osteoarthritis syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462437</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3151087</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, and cervical spine malformation and/or instability), craniofacial features (hypertelorism, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462437">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462554"><div><strong>Hypertrophic cardiomyopathy 16</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462554</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3151204</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the MYOZ2 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462554">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462614"><div><strong>Hypertrophic cardiomyopathy 17</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462614</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3151264</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">An autosomal dominant subtype of familial hypertrophic cardiomyopathy caused by mutation(s) in the JPH2 gene, encoding junctophilin-2.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462614">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462615"><div><strong>Hypertrophic cardiomyopathy 18</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462615</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3151265</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the PLN gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462615">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462617"><div><strong>Hypertrophic cardiomyopathy 20</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462617</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3151267</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the NEXN gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/462617">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_886881"><div><strong>Steinert myotonic dystrophy syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>886881</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3250443</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Myotonic dystrophy type 1 (DM1) is a multisystem disorder that affects skeletal and smooth muscle as well as the eye, heart, endocrine system, and central nervous system. The clinical findings, which span a continuum from mild to severe, have been categorized into three somewhat overlapping phenotypes: mild, classic, and congenital. Mild DM1 is characterized by cataract and mild myotonia (sustained muscle contraction); life span is normal. Classic DM1 is characterized by muscle weakness and wasting, myotonia, cataract, and often cardiac conduction abnormalities; adults may become physically disabled and may have a shortened life span. Congenital DM1 is characterized by hypotonia and severe generalized weakness at birth, often with respiratory insufficiency and early death; intellectual disability is common.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/886881">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_477726"><div><strong>Atrial septal defect 7</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>477726</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3276096</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">An extremely rare genetic congenital heart disease characterized by the presence of atrial septal defect, mostly of the ostium secundum type, associated with conduction anomalies like atrioventricular block, atrial fibrillation or right bundle branch block.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/477726">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_481323"><div><strong>Atrial fibrillation, familial, 11</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>481323</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3279693</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of familial atrial fibrillation, see ATFB1 (608583).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/481323">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_765974"><div><strong>Emery-Dreifuss muscular dystrophy 7, autosomal dominant</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>765974</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3553060</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Emery-Dreifuss muscular dystrophy is a genetically heterogeneous muscular disease that presents with muscular dystrophy, joint contractures, and cardiomyopathy with conduction defects (summary by Liang et al., 2011). For a discussion of genetic heterogeneity of EDMD, see 310300.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/765974">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_766323"><div><strong>Dilated cardiomyopathy 2B</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>766323</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3553409</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the GATAD1 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/766323">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_766356"><div><strong>Hypertrophic cardiomyopathy 21</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>766356</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3553442</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hypertrophic cardiomyopathy (CMH) is characterized by unexplained cardiac hypertrophy: thickening of the myocardial wall in the absence of any other identifiable cause for left ventricular hypertrophy such as systemic hypertension or valvular heart disease. Myocyte hypertrophy, disarray, and fibrosis are the histopathologic hallmarks of this disorder. Clinical features are diverse and include arrhythmias, sudden cardiac death, and heart failure. With an estimated prevalence of 1 in 500, CMH is the most common cardiovascular genetic disease and the most common cause of sudden death in competitive athletes in the United States (summary by Song et al., 2006). For a discussion of genetic heterogeneity of familial hypertrophic cardiomyopathy, see CMH1 (192600).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/766356">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_767108"><div><strong>Congenital heart defects, multiple types, 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>767108</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3554194</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Multiple types of congenital heart defects-3 (CHTD3) is an autosomal dominant condition characterized by various types of congenital heart defects and low atrial rhythm (van de Meerakker et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of multiple types of congenital heart defects, see 306955.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/767108">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_767193"><div><strong>Congenital heart defects, multiple types, 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>767193</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3554279</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Multiple types of congenital heart defects-2 (CHTD2) is characterized by variable congenital heart defects, primarily involving the valves, but also including septal defects or aneurysms, and complex defects such as tetralogy of Fallot. Dilated cardiomyopathy and myocardial noncompaction have been reported in some patients. In addition, some affected individuals exhibit facial dysmorphism and features of connective tissue disease (Thienpont et al., 2010; Ackerman et al., 2016; Ritelli et al., 2018). For a discussion of genetic heterogeneity of CHTD, see 306955.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/767193">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_811544"><div><strong>Dilated cardiomyopathy 1KK</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>811544</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3714995</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any dilated cardiomyopathy in which the cause of the disease is a mutation in the MYPN gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/811544">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_862706"><div><strong>Atrial fibrillation, familial, 15</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>862706</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4014269</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. It is the most common sustained cardiac rhythm disturbance, and its prevalence increases as the population ages. An estimated 70,000 strokes each year are caused by atrial fibrillation (summary by Oberti et al., 2004). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/862706">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863722"><div><strong>Atrial conduction disease</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863722</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4015285</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">A rare genetic cardiac disease characterized by variably expressed atrial tachyarrhythmia (such as atrial flutter, paroxysmal or chronic atrial fibrillation, ectopic atrial tachycardia, or multifocal atrial tachycardia), infra-Hisian conduction system disease, and vulnerability to dilated cardiomyopathy. Age of onset ranges between childhood and adulthood.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863722">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863805"><div><strong>Aortic aneurysm, familial thoracic 9</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863805</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4015368</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any familial thoracic aortic aneurysm and aortic dissection in which the cause of the disease is a mutation in the MFAP5 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863805">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863911"><div><strong>Chronic atrial and intestinal dysrhythmia</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863911</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4015474</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Syndrome with characteristics of sick sinus syndrome and intestinal pseudo-obstruction. The heart and digestive issues develop at the same time, usually by age 20. The syndrome is caused by mutations in the SGO1 gene. This gene provides instructions for making part of a protein complex cohesin. This protein complex helps control the placement of chromosomes during cell division. Research suggests that SGO1 gene mutations may result in a cohesin complex that is less able to hold sister chromatids together, resulting in decreased chromosomal stability during cell division. This instability is thought to cause senescence of cells in the intestinal muscle and in the sinoatrial node, resulting in problems maintaining proper rhythmic movements of the heart and intestines.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863911">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_934716"><div><strong>Hypertrophic cardiomyopathy 26</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>934716</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4310749</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial cardiomyopathy caused by mutation in the FLNC gene has been described as hypertrophic, restrictive, dilated, or arrhythmogenic right ventricular cardiomyopathy. Affected individuals, especially those with dilated cardiomyopathy, are at risk for arrhythmias and sudden death. Arrhythmias without cardiomyopathy, and left ventricular noncompaction, have also been reported (Ortiz-Genga et al., 2016; Verdonschot et al., 2020).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/934716">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1646402"><div><strong>Brugada syndrome 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1646402</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4551804</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1646402">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1636547"><div><strong>Congenital heart defects, multiple types, 5</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1636547</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4693563</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1636547">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1648402"><div><strong>Orthostatic hypotension 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1648402</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4746777</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Dopamine beta-hydroxylase (DBH) deficiency is characterized by lack of sympathetic noradrenergic function resulting in profound deficits in autonomic regulation of cardiovascular function (orthostatic hypotension) and other autonomic dysfunction (ptosis, nasal stuffiness, sleep difficulties, and impaired ejaculation in males). Although DBH deficiency is present from birth, the diagnosis is often not generally recognized until late childhood. In the perinatal period, DBH deficiency has been complicated by vomiting, dehydration, hypotension, hypothermia, and hypoglycemia requiring repeated hospitalization, and the diagnosis may be identified fortuitously in the neonatal period with investigation of hypoglycemia. Children may report reduced exercise capacity. By early adulthood, individuals have profound orthostatic hypotension, greatly reduced exercise tolerance, ptosis, and nasal stuffiness. Presyncopal symptoms include dizziness, blurred vision, dyspnea, nuchal discomfort, and chest pain; symptoms may worsen in hot environments or after heavy meals or alcohol ingestion. Some individuals have abnormal kidney function, joint laxity, hypotonia, high-arched palate, anemia, and/or hypoglycemia.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1648402">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1779612"><div><strong>Cardiomyopathy, familial hypertrophic, 28</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1779612</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5543616</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial hypertrophic cardiomyopathy-28 (CMH28) is characterized by asymmetric septal hypertrophy, atrial fibrillation and nonsustained ventricular tachycardia, and risk of sudden death. Dyspnea is the most common symptom, but more than half of affected individuals are asymptomatic. Hypertrabeculation of the left ventricle with noncompaction has been observed in some patients (Ochoa et al., 2018). For a general phenotypic description and discussion of genetic heterogeneity of familial hypertrophic cardiomyopathy, see CMH1 (192600).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1779612">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1858408"><div><strong>Cardiomyopathy, familial hypertrophic, 30, atrial</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1858408</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5935586</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial atrial hypertrophic cardiomyopathy-30 (CMH30) is characterized by atrial arrhythmias, including flutter and fibrillation, atrial structural abnormalities with hypertrophic cardiomyopathy and fibrosis, and hypertension (Baris Feldman et al., 2023).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1858408">Condition Record</a></div></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462437" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Aneurysm-osteoarthritis syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_863805" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Aortic aneurysm, familial thoracic 9</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_863722" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial conduction disease</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_334469" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_481323" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 11</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (55)', lessText: 'Show less', nodeBefore: 0"><span id="clinMore">
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_862706" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 15</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_324886" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 2</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_373232" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_400041" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 4</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_369411" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 5</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_394252" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 6</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_414420" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial fibrillation, familial, 8</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_414348" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial septal defect 6</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_477726" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Atrial septal defect 7</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1646402" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Brugada syndrome 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_395633" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Brugada syndrome 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_395632" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Brugada syndrome 4</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_370181" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Cardiac arrhythmia, ankyrin-B-related</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1779612" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Cardiomyopathy, familial hypertrophic, 28</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1858408" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Cardiomyopathy, familial hypertrophic, 30, atrial</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_863911" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Chronic atrial and intestinal dysrhythmia</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_412871" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital generalized lipodystrophy type 4</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_767193" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital heart defects, multiple types, 2</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_767108" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital heart defects, multiple types, 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1636547" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital heart defects, multiple types, 5</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_258500" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1A</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_393713" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1AA</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_316943" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1D</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_331341" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1E</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_347714" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1G</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_811544" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1KK</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462308" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1V</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_437215" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 1Y</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_766323" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dilated cardiomyopathy 2B</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_4435" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Ebstein anomaly</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_765974" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Emery-Dreifuss muscular dystrophy 7, autosomal dominant</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_96073" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial cutaneous collagenoma</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_354526" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial partial lipodystrophy, Dunnigan type</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_442487" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 13</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462554" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 16</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462614" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 17</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462615" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 18</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_349383" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 2</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462617" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 20</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_766356" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 21</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_934716" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 26</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_331466" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 6</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_348695" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypertrophic cardiomyopathy 7</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_349005" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Left ventricular noncompaction 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_394836" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Long QT syndrome 10</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_140765" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">McLeod neuroacanthocytosis syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1648402" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Orthostatic hypotension 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_355890" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Short QT syndrome type 2</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_320273" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Sick sinus syndrome 2, autosomal dominant</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_886881" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Steinert myotonic dystrophy syndrome</a></div></span></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_105">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Professional_guidelines">Professional guidelines</h1><a sid="105" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">PubMed<a class="help jig-ncbi-popper" data-jig="ncbipopper" href="#guidelinesHelpPM"><img class="pulldown" src="//static.pubmed.gov/portal/portal3rc.fcgi/4223267/img/4204968" /></a></h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38033089">2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Joglar JA,
|
||
Chung MK,
|
||
Armbruster AL,
|
||
Benjamin EJ,
|
||
Chyou JY,
|
||
Cronin EM,
|
||
Deswal A,
|
||
Eckhardt LL,
|
||
Goldberger ZD,
|
||
Gopinathannair R,
|
||
Gorenek B,
|
||
Hess PL,
|
||
Hlatky M,
|
||
Hogan G,
|
||
Ibeh C,
|
||
Indik JH,
|
||
Kido K,
|
||
Kusumoto F,
|
||
Link MS,
|
||
Linta KT,
|
||
Marcus GM,
|
||
McCarthy PM,
|
||
Patel N,
|
||
Patton KK,
|
||
Perez MV,
|
||
Piccini JP,
|
||
Russo AM,
|
||
Sanders P,
|
||
Streur MM,
|
||
Thomas KL,
|
||
Times S,
|
||
Tisdale JE,
|
||
Valente AM,
|
||
Van Wagoner DR;
|
||
Peer Review Committee Members</span><br />
|
||
<span class="medgenPMjournal">Circulation</span>
|
||
2024 Jan 2;149(1):e1-e156.
|
||
Epub 2023 Nov 30
|
||
doi: 10.1161/CIR.0000000000001193.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38033089" target="_blank">38033089</a><a href="/pmc/articles/PMC11095842" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35363499">2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Heidenreich PA,
|
||
Bozkurt B,
|
||
Aguilar D,
|
||
Allen LA,
|
||
Byun JJ,
|
||
Colvin MM,
|
||
Deswal A,
|
||
Drazner MH,
|
||
Dunlay SM,
|
||
Evers LR,
|
||
Fang JC,
|
||
Fedson SE,
|
||
Fonarow GC,
|
||
Hayek SS,
|
||
Hernandez AF,
|
||
Khazanie P,
|
||
Kittleson MM,
|
||
Lee CS,
|
||
Link MS,
|
||
Milano CA,
|
||
Nnacheta LC,
|
||
Sandhu AT,
|
||
Stevenson LW,
|
||
Vardeny O,
|
||
Vest AR,
|
||
Yancy CW;
|
||
ACC/AHA Joint Committee Members</span><br />
|
||
<span class="medgenPMjournal">Circulation</span>
|
||
2022 May 3;145(18):e895-e1032.
|
||
Epub 2022 Apr 1
|
||
doi: 10.1161/CIR.0000000000001063.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35363499" target="_blank">35363499</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30879355">2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Arnett DK,
|
||
Blumenthal RS,
|
||
Albert MA,
|
||
Buroker AB,
|
||
Goldberger ZD,
|
||
Hahn EJ,
|
||
Himmelfarb CD,
|
||
Khera A,
|
||
Lloyd-Jones D,
|
||
McEvoy JW,
|
||
Michos ED,
|
||
Miedema MD,
|
||
Muñoz D,
|
||
Smith SC Jr,
|
||
Virani SS,
|
||
Williams KA Sr,
|
||
Yeboah J,
|
||
Ziaeian B</span><br />
|
||
<span class="medgenPMjournal">Circulation</span>
|
||
2019 Sep 10;140(11):e596-e646.
|
||
Epub 2019 Mar 17
|
||
doi: 10.1161/CIR.0000000000000678.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30879355" target="_blank">30879355</a><a href="/pmc/articles/PMC7734661" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22atrial%20fibrillation%22%5Btiab%3A~0%5D)%20AND%20(%22english%20and%20humans%22%5BFilter%5D)%20AND%20(%20(%22practice%20guideline%22%5BFilter%5D)%20OR%20(practice*%5Btitl%5D%20AND%20(guideline%5Btitl%5D%20OR%20parameter%5Btitl%5D%20OR%20resource%5Btitl%5D%20OR%20bulletin%5Btitl%5D%20OR%20best%5Btitl%5D))%20OR%20(genetic*%5Btitl%5D%20AND%20(evaluation%5Btitl%5D%20OR%20counseling%5Btitl%5D%20OR%20screening%5Btitl%5D%20OR%20test*%5Btitl%5D))%20OR%20(clinical%5Btitl%5D%20AND%20((expert%5Btitl%5D%20AND%20consensus%5Btitl%5D)%20OR%20utility%5Btitl%5D%20OR%20guideline*%5Btitl%5D))%20OR%20(management%5Btitl%5D%20AND%20(clinical%5Btitl%5D%20OR%20diagnos*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20pain%5Btitl%5D%20OR%20surveillance%5Btitl%5D%20OR%20emergency%5Btitl%5D%20OR%20guideline*%5Btitl%5D%20OR%20therap*))%20OR%20(treatment%5Btitl%5D%20AND%20((evaluation%5Btitl%5D%20AND%20diagnosis%5Btitl%5D)%20OR%20(assessment%5Btitl%5D%20AND%20prevention%5Btitl%5D)%20OR%20therap*))%20OR%20(Diagnos*%5Btitl%5D%20AND%20(prenatal%5Btitl%5D%20OR%20treatment%5Btitl%5D%20OR%20follow-up%5Btitl%5D%20OR%20statement%5Btitl%5D%20OR%20criteria%5Btitl%5D%20OR%20newborn%5Btitl%5D%20OR%20differential%5Btitl%5D%20OR%20neonatal%5Btitl%5D%20OR%20neonate%5Btitl%5D))%20OR%20(guideline*%5Btitl%5D%20AND%20(pharmacogenetic*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20evidence-based%5Btitl%5D%20OR%20consensus%5Btitl%5D%20OR%20(technical%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20(molecular%5Btitl%5D%20AND%20testing%5Btitl%5D)))%20OR%20(risk%5Btitl%5D%20AND%20assessment%5Btitl%5D)%20OR%20(recommendation*%5Btitl%5D%20AND%20(statement%5Btitl%5D%20OR%20Evidence-based%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(care%20AND%20((Patient%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20primary%5Btitl%5D%20OR%20psychosocial%5Btitl%5D))%20OR%20(Health%5Btitl%5D%20AND%20supervision%5Btitl%5D)%20OR%20(statement%5Btitl%5D%20AND%20(policy%5Btitl%5D%20OR%20position%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(pharmacogenetics%5Btitl%5D%20AND%20(Dosing%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20genotype*%5Btitl%5D%20OR%20drug*%5Btitl%5D))%20OR%20(Chemotherapy%5Btitl%5D%20AND%20decision*%5Btitl%5D)%20OR%20(screening%5Btitl%5D%20AND%20(newborn%5Btitl%5D%20OR%20neonat*%5Btitl%5D%20OR%20detection%5Btitl%5D%20OR%20diagnos*%5Btitl%5D))%20OR%20(criteria%5Btitl%5D%20OR%20genotype*%5Btitl%5D)%20)%20NOT%20(%22Case%20reports%22%5BPublication%20type%5D%20OR%20%22clinical%20study%22%5BPublication%20Type%5D%20OR%20%22randomized%20controlled%20trial%22%5BPublication%20Type%5D)" title="PubMed search">See all (4751)</a></div><h3 class="subhead">Curated<a class="help jig-ncbi-popper" data-jig="ncbipopper" href="#guidelinesHelpCurated"><img class="pulldown" src="//static.pubmed.gov/portal/portal3rc.fcgi/4223267/img/4204968" /></a></h3><h3 class="nl vspace"><a href="https://www.nice.org.uk/guidance/ng196" target="_blank">UK NICE Guideline NG196, Atrial fibrillation: diagnosis and management, 2021</a></h3>
|
||
<h3 class="nl vspace"><a href="https://www.nice.org.uk/guidance/dg41" target="_blank">UK NICE Diagnostics Guidance DG41, Implantable cardiac monitors to detect atrial fibrillation after cryptogenic stroke, 2020</a></h3>
|
||
</div>
|
||
</div>
|
||
<div class="display-none help-popup" id="guidelinesHelpPM">These guidelines are articles in PubMed that match specific search criteria developed by MedGen to capture the most relevant practice guidelines. This list may not be comprehensive and may include broader topics as well. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div><div class="display-none help-popup" id="guidelinesHelpCurated">These guidelines are manually curated by the MedGen team
|
||
to supplement articles available in PubMed. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div>
|
||
<div class="portlet mgSection" id="ID_103">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Recent_clinical_studies">Recent clinical studies</h1><a sid="103" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">Etiology</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/36514212">Omega-3 fatty acids and atrial fibrillation.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Huh JH,
|
||
Jo SH</span><br />
|
||
<span class="medgenPMjournal">Korean J Intern Med</span>
|
||
2023 May;38(3):282-289.
|
||
Epub 2022 Dec 14
|
||
doi: 10.3904/kjim.2022.266.
|
||
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|
||
<span class="bold">PMID: </span><a href="/pubmed/31378392" target="_blank">31378392</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Atrial%20fibrillation%22%20AND%20Clinical%20prediction%20guides%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (30908)</a></div></div>
|
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</div>
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|
||
<div class="portlet mgSection" id="ID_104">
|
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Recent_systematic_reviews">Recent systematic reviews</h1><a sid="104" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln">
|
||
<div class="nl"><a target="_blank" href="/pubmed/35659945">Frailty prevalence and impact on outcomes in patients with atrial fibrillation: A systematic review and meta-analysis of 1,187,000 patients.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Proietti M,
|
||
Romiti GF,
|
||
Raparelli V,
|
||
Diemberger I,
|
||
Boriani G,
|
||
Dalla Vecchia LA,
|
||
Bellelli G,
|
||
Marzetti E,
|
||
Lip GY,
|
||
Cesari M</span><br />
|
||
<span class="medgenPMjournal">Ageing Res Rev</span>
|
||
2022 Aug;79:101652.
|
||
Epub 2022 May 31
|
||
doi: 10.1016/j.arr.2022.101652.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35659945" target="_blank">35659945</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35093388">Beta-blockers for the treatment of arrhythmias: Bisoprolol - a systematic review.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Muresan L,
|
||
Cismaru G,
|
||
Muresan C,
|
||
Rosu R,
|
||
Gusetu G,
|
||
Puiu M,
|
||
Mada RO,
|
||
Martins RP</span><br />
|
||
<span class="medgenPMjournal">Ann Pharm Fr</span>
|
||
2022 Sep;80(5):617-634.
|
||
Epub 2022 Jan 31
|
||
doi: 10.1016/j.pharma.2022.01.007.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35093388" target="_blank">35093388</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34274577">Diltiazem versus metoprolol for the management of atrial fibrillation: A systematic review and meta-analysis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Jafri SH,
|
||
Xu J,
|
||
Warsi I,
|
||
Cerecedo-Lopez CD</span><br />
|
||
<span class="medgenPMjournal">Am J Emerg Med</span>
|
||
2021 Oct;48:323-327.
|
||
Epub 2021 Jun 30
|
||
doi: 10.1016/j.ajem.2021.06.053.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34274577" target="_blank">34274577</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34162502">Intravenous magnesium in the management of rapid atrial fibrillation: A systematic review and meta-analysis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Ramesh T,
|
||
Lee PYK,
|
||
Mitta M,
|
||
Allencherril J</span><br />
|
||
<span class="medgenPMjournal">J Cardiol</span>
|
||
2021 Nov;78(5):375-381.
|
||
Epub 2021 Jun 20
|
||
doi: 10.1016/j.jjcc.2021.06.001.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34162502" target="_blank">34162502</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/32921618">Diagnostic accuracy of smart gadgets/wearable devices in detecting atrial fibrillation: A systematic review and meta-analysis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Prasitlumkum N,
|
||
Cheungpasitporn W,
|
||
Chokesuwattanaskul A,
|
||
Thangjui S,
|
||
Thongprayoon C,
|
||
Bathini T,
|
||
Vallabhajosyula S,
|
||
Kanitsoraphan C,
|
||
Leesutipornchai T,
|
||
Chokesuwattanaskul R</span><br />
|
||
<span class="medgenPMjournal">Arch Cardiovasc Dis</span>
|
||
2021 Jan;114(1):4-16.
|
||
Epub 2020 Sep 10
|
||
doi: 10.1016/j.acvd.2020.05.015.
|
||
<span class="bold">PMID: </span><a href="/pubmed/32921618" target="_blank">32921618</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Atrial%20fibrillation%22%20AND%20systematic%5Bsb%5D%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (2298)</a></div></div>
|
||
</div>
|
||
</div></div></div></div></div></div></div>
|
||
<div id="messagearea_bottom">
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||
|
||
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||
<div class=" bottom">
|
||
|
||
</div>
|
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|
||
</div>
|
||
</div>
|
||
<div class="supplemental col three_col last">
|
||
<h2 class="offscreen_noflow">Supplemental Content</h2>
|
||
|
||
<div>
|
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|
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<div class="portlet mgSection" id="ID_113">
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Table_of_contents">Table of contents</h1><a sid="113" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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<div class="portlet_content ln"><ul id="my-toc"></ul></div>
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Genetic_Testing_Registry">Genetic Testing Registry</h1><a sid="106" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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||
<div class="portlet_content ln"><ul><li><a href="/gtr/tests?term=C0004238%5bDISCUI%5d&filter=method%3A2%5F8" target="_blank">Deletion/duplication analysis (19)</a></li>
|
||
<li><a href="/gtr/tests?term=C0004238%5bDISCUI%5d&filter=method%3A2%5F9" target="_blank">Sequence analysis of select exons (1)</a></li>
|
||
<li><a href="/gtr/tests?term=C0004238%5bDISCUI%5d&filter=method%3A2%5F7" target="_blank">Sequence analysis of the entire coding region (21)</a></li>
|
||
<li><a href="/gtr/tests?term=C0004238%5bDISCUI%5d&filter=method%3A2%5F19" target="_blank">Targeted variant analysis (4)</a></li>
|
||
<li class="portletSeeAll portletSeeAllPad"><total><a href="/gtr/tests?term=C0004238%5bDISCUI%5d" target="_blank">See all (24)</a></total></li>
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Clinical_resources">Clinical resources</h1><a sid="119" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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<div class="portlet_content ln"><ul><li><a href="https://clinicaltrials.gov/search?cond=Atrial%20fibrillation" target="_blank">ClinicalTrials.gov</a></li></ul></div>
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||
</div>
|
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Practice_guidelines">Practice guidelines</h1><a sid="121" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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<div class="portlet_content ln"><ul class="a_poppers"><li><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22atrial%20fibrillation%22%5Btiab%3A~0%5D)%20AND%20(%22english%20and%20humans%22%5BFilter%5D)%20AND%20(%20(%22practice%20guideline%22%5BFilter%5D)%20OR%20(practice*%5Btitl%5D%20AND%20(guideline%5Btitl%5D%20OR%20parameter%5Btitl%5D%20OR%20resource%5Btitl%5D%20OR%20bulletin%5Btitl%5D%20OR%20best%5Btitl%5D))%20OR%20(genetic*%5Btitl%5D%20AND%20(evaluation%5Btitl%5D%20OR%20counseling%5Btitl%5D%20OR%20screening%5Btitl%5D%20OR%20test*%5Btitl%5D))%20OR%20(clinical%5Btitl%5D%20AND%20((expert%5Btitl%5D%20AND%20consensus%5Btitl%5D)%20OR%20utility%5Btitl%5D%20OR%20guideline*%5Btitl%5D))%20OR%20(management%5Btitl%5D%20AND%20(clinical%5Btitl%5D%20OR%20diagnos*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20pain%5Btitl%5D%20OR%20surveillance%5Btitl%5D%20OR%20emergency%5Btitl%5D%20OR%20guideline*%5Btitl%5D%20OR%20therap*))%20OR%20(treatment%5Btitl%5D%20AND%20((evaluation%5Btitl%5D%20AND%20diagnosis%5Btitl%5D)%20OR%20(assessment%5Btitl%5D%20AND%20prevention%5Btitl%5D)%20OR%20therap*))%20OR%20(Diagnos*%5Btitl%5D%20AND%20(prenatal%5Btitl%5D%20OR%20treatment%5Btitl%5D%20OR%20follow-up%5Btitl%5D%20OR%20statement%5Btitl%5D%20OR%20criteria%5Btitl%5D%20OR%20newborn%5Btitl%5D%20OR%20differential%5Btitl%5D%20OR%20neonatal%5Btitl%5D%20OR%20neonate%5Btitl%5D))%20OR%20(guideline*%5Btitl%5D%20AND%20(pharmacogenetic*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20evidence-based%5Btitl%5D%20OR%20consensus%5Btitl%5D%20OR%20(technical%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20(molecular%5Btitl%5D%20AND%20testing%5Btitl%5D)))%20OR%20(risk%5Btitl%5D%20AND%20assessment%5Btitl%5D)%20OR%20(recommendation*%5Btitl%5D%20AND%20(statement%5Btitl%5D%20OR%20Evidence-based%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(care%20AND%20((Patient%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20primary%5Btitl%5D%20OR%20psychosocial%5Btitl%5D))%20OR%20(Health%5Btitl%5D%20AND%20supervision%5Btitl%5D)%20OR%20(statement%5Btitl%5D%20AND%20(policy%5Btitl%5D%20OR%20position%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(pharmacogenetics%5Btitl%5D%20AND%20(Dosing%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20genotype*%5Btitl%5D%20OR%20drug*%5Btitl%5D))%20OR%20(Chemotherapy%5Btitl%5D%20AND%20decision*%5Btitl%5D)%20OR%20(screening%5Btitl%5D%20AND%20(newborn%5Btitl%5D%20OR%20neonat*%5Btitl%5D%20OR%20detection%5Btitl%5D%20OR%20diagnos*%5Btitl%5D))%20OR%20(criteria%5Btitl%5D%20OR%20genotype*%5Btitl%5D)%20)%20NOT%20(%22Case%20reports%22%5BPublication%20type%5D%20OR%20%22clinical%20study%22%5BPublication%20Type%5D%20OR%20%22randomized%20controlled%20trial%22%5BPublication%20Type%5D)" title="PubMed search">PubMed</a><div class="help-popup">See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div></li><li><a target="_blank" href="/books/?term=((%22clinical%20guidelines%22%5BResource%20Type%5D)%20OR%20%22practice%20guideline%22%5BPublication%20Type%5D)%20AND%20(%22Atrial%20fibrillation%22)">Bookshelf</a><div class="help-popup">See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div></li></ul><h3 class="subhead">Curated</h3><ul class="a_poppers"><li><a target="_blank" href="https://www.nice.org.uk/guidance/ng196">NICE, 2021</a><div>UK NICE Guideline NG196, Atrial fibrillation: diagnosis and management, 2021</div></li><li><a target="_blank" href="https://www.nice.org.uk/guidance/dg41">NICE, 2020</a><div>UK NICE Diagnostics Guidance DG41, Implantable cardiac monitors to detect atrial fibrillation after cryptogenic stroke, 2020</div></li></ul></div>
|
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<div class="portlet_content ln"><ul><li><a href="https://vsearch.nlm.nih.gov/vivisimo/cgi-bin/query-meta?v:project=medlineplus&query=Atrial%20fibrillation" target="_blank">MedlinePlus</a></li></ul></div>
|
||
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|
||
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|
||
<div class="portlet brieflink">
|
||
<div class="portlet_head">
|
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<h3>Reviews</h3>
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<a href="/pubmed/clinical?term=Atrial%20fibrillation" ref="ncbi_uid=&discoId=gtr_reviews&linkpos=1&linkpostotal=2" target="_blank">PubMed Clinical Queries</a>
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||
<a href="/pubmed?term=Atrial%20fibrillation%20AND%20humans[mesh]%20AND%20review[publication%20type]" ref="ncbi_uid=&discoId=gtr_reviews&linkpos=2&linkpostotal=2" target="_blank">Reviews in PubMed</a>
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||
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|
||
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|
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||
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||
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<h3>Related information</h3>
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||
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||
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||
<a class="brieflinkpopperctrl" href="/clinvar?LinkName=medgen_clinvar&from_uid=445" ref="log$=recordlinks">ClinVar</a>
|
||
<div class="brieflinkpop offscreen_noflow">Related medical variations</div>
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||
</li>
|
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<li class="brieflinkpopper">
|
||
<a class="brieflinkpopperctrl" href="/gtr/tests?term=C0004238[DISCUI]" ref="log$=recordlinks">GTR</a>
|
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<div class="brieflinkpop offscreen_noflow">Related information in GTR</div>
|
||
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|
||
<li class="brieflinkpopper">
|
||
<a class="brieflinkpopperctrl" href="/gtr/tests?term=C0004238[DISCUI]&test_type=Clinical" ref="log$=recordlinks">GTR(Clinical)</a>
|
||
<div class="brieflinkpop offscreen_noflow">Clinical tests in GTR</div>
|
||
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|
||
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||
<a class="brieflinkpopperctrl" href="/mesh?LinkName=medgen_mesh&from_uid=445" ref="log$=recordlinks">MeSH</a>
|
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<div class="brieflinkpop offscreen_noflow">Related Medical Subject Headings</div>
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<a class="brieflinkpopperctrl" href="/pmc?LinkName=medgen_pmc&from_uid=445" ref="log$=recordlinks">PMC Articles</a>
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<a class="brieflinkpopperctrl" href="/pubmed?LinkName=medgen_pubmed&from_uid=445" ref="log$=recordlinks">PubMed</a>
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|
||
|
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||
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<h3>Recent activity</h3>
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<a name="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory" sid="1" realname="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory" cmd="ClearHT" href="?cmd=ClearHT&" onclick="return false;" id="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory">
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Clear
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<a name="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle" sid="1" realname="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle" class="HTOn" cmd="HTOff" href="?cmd=HTOff&" onclick="return false;" id="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle">
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Turn On
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<ul id="activity">
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||
<li class="ra_rcd ralinkpopper two_line">
|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=1" href="/portal/utils/pageresolver.fcgi?recordid=67d48acb67c23b31e083e807">Atrial fibrillation</a>
|
||
<div class="ralinkpop offscreen_noflow">Atrial fibrillation<div class="brieflinkpopdesc"></div></div>
|
||
<div class="tertiary">MedGen</div>
|
||
</li>
|
||
<li class="ra_rcd ralinkpopper two_line">
|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=2" href="/portal/utils/pageresolver.fcgi?recordid=67d48abf84f3725e59075806">LMNA-Related Dilated Cardiomyopathy - GeneReviews®</a>
|
||
<div class="ralinkpop offscreen_noflow">LMNA-Related Dilated Cardiomyopathy - GeneReviews®<div class="brieflinkpopdesc"></div></div>
|
||
<div class="tertiary"></div>
|
||
</li>
|
||
<li class="ra_rcd ralinkpopper two_line">
|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=3" href="/portal/utils/pageresolver.fcgi?recordid=67d48abe84f3725e590755d1">Table B. [OMIM Entries for LMNA-Related Dilated Cardiomyopathy (View All in OMIM...</a>
|
||
<div class="ralinkpop offscreen_noflow">Table B. [OMIM Entries for LMNA-Related Dilated Cardiomyopathy (View All in OMIM)]. - GeneReviews®<div class="brieflinkpopdesc"></div></div>
|
||
<div class="tertiary"></div>
|
||
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|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=4" href="/portal/utils/pageresolver.fcgi?recordid=67d48abd84f3725e590753e2">Table A. [LMNA-Related Dilated Cardiomyopathy: Genes and Databases]. - GeneRevie...</a>
|
||
<div class="ralinkpop offscreen_noflow">Table A. [LMNA-Related Dilated Cardiomyopathy: Genes and Databases]. - GeneReviews®<div class="brieflinkpopdesc"></div></div>
|
||
<div class="tertiary"></div>
|
||
</li>
|
||
<li class="ra_rcd ralinkpopper two_line">
|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=5" href="/portal/utils/pageresolver.fcgi?recordid=67d48abc84f3725e59075082">Table 4. [Treatment of Manifestations in Individuals with LMNA-related DCM]. - G...</a>
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