{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T18:27:59Z","timestamp":1793298479638,"version":"4.5.0"},"reference-count":43,"publisher":"American Medical Association (AMA)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA"],"published-print":{"date-parts":[[2023,8,1]]},"abstract":"<jats:sec id=\"ab-joi230078-4\"><jats:title>Importance<\/jats:title><jats:p>Black patients with dilated cardiomyopathy (DCM) have increased familial risk and worse outcomes than White patients, but most DCM genetic data are from White patients.<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-5\"><jats:title>Objective<\/jats:title><jats:p>To compare the rare variant genetic architecture of DCM by genomic ancestry within a diverse population of patients with DCM.<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-6\"><jats:title>Design<\/jats:title><jats:p>Cross-sectional study enrolling patients with DCM who self-identified as non-Hispanic Black, Hispanic, or non-Hispanic White from June 7, 2016, to March 15, 2020, at 25 US advanced heart failure programs. Variants in 36 DCM genes were adjudicated as pathogenic, likely pathogenic, or of uncertain significance.<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-7\"><jats:title>Exposure<\/jats:title><jats:p>Presence of DCM.<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-8\"><jats:title>Main Outcomes and Measures<\/jats:title><jats:p>Variants in DCM genes classified as pathogenic\/likely pathogenic\/uncertain significance and clinically actionable (pathogenic\/likely pathogenic).<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-9\"><jats:title>Results<\/jats:title><jats:p>A total of 505, 667, and 26 patients with DCM of predominantly African, European, or Native American genomic ancestry, respectively, were included. Compared with patients of European ancestry, a lower percentage of patients of African ancestry had clinically actionable variants (8.2% [95% CI, 5.2%-11.1%] vs 25.5% [95% CI, 21.3%-29.6%]), reflecting the lower odds of a clinically actionable variant for those with any pathogenic variant\/likely pathogenic variant\/variant of uncertain significance (odds ratio, 0.25 [95% CI, 0.17-0.37]). On average, patients of African ancestry had fewer clinically actionable variants in <jats:italic>TTN<\/jats:italic> (difference, \u22120.09 [95% CI, \u22120.14 to \u22120.05]) and other genes with predicted loss of function as a disease-causing mechanism (difference, \u22120.06 [95% CI, \u22120.11 to \u22120.02]). However, the number of pathogenic variants\/likely pathogenic variants\/variants of uncertain significance was more comparable between ancestry groups (difference, \u22120.07 [95% CI, \u22120.22 to 0.09]) due to a larger number of non-<jats:italic>TTN<\/jats:italic> non\u2013predicted loss of function variants of uncertain significance, mostly missense, in patients of African ancestry (difference, 0.15 [95% CI, 0.00-0.30]). Published clinical case-based evidence supporting pathogenicity was less available for variants found only in patients of African ancestry (<jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u2009.001).<\/jats:p><\/jats:sec><jats:sec id=\"ab-joi230078-10\"><jats:title>Conclusion and Relevance<\/jats:title><jats:p>Patients of African ancestry with DCM were less likely to have clinically actionable variants in DCM genes than those of European ancestry due to differences in genetic architecture and a lack of representation of African ancestry in clinical data sets.<\/jats:p><\/jats:sec>","DOI":"10.1001\/jama.2023.11970","type":"journal-article","created":{"date-parts":[[2023,8,1]],"date-time":"2023-08-01T11:01:23Z","timestamp":1690887683000},"page":"432","source":"Crossref","is-referenced-by-count":53,"title":["Genetic Architecture of Dilated Cardiomyopathy in Individuals of African and European Ancestry"],"prefix":"10.1001","volume":"330","author":[{"given":"Elizabeth","family":"Jordan","sequence":"first","affiliation":[{"name":"Division of Human Genetics, Department of Internal Medicine, The Ohio State University, Columbus"},{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel D.","family":"Kinnamon","sequence":"additional","affiliation":[{"name":"Division of Human Genetics, Department of Internal Medicine, The Ohio State University, Columbus"},{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Garrie J.","family":"Haas","sequence":"additional","affiliation":[{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus"},{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University, Columbus"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Hofmeyer","sequence":"additional","affiliation":[{"name":"MedStar Health Research Institute, MedStar Washington Hospital Center, Washington, DC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evan","family":"Kransdorf","sequence":"additional","affiliation":[{"name":"Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory A.","family":"Ewald","sequence":"additional","affiliation":[{"name":"Washington University, St Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alanna A.","family":"Morris","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine, Atlanta, Georgia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anjali","family":"Owens","sequence":"additional","affiliation":[{"name":"Center for Inherited Cardiovascular Disease, Division of Cardiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Lowes","sequence":"additional","affiliation":[{"name":"University of Nebraska Medical Center, Omaha"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas","family":"Stoller","sequence":"additional","affiliation":[{"name":"University of Nebraska Medical Center, Omaha"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. 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