Prevalence and Cumulative Risk of Familial Idiopathic Dilated Cardiomyopathy
Idiopathic dilated cardiomyopathy (DCM) aggregates in families, and early detection in at-risk family members can provide opportunity to initiate treatment prior to late-phase disease. Most studies have included only White patients, yet Black patients with DCM have higher risk of heart failure-relat...
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| Published in: | JAMA : the journal of the American Medical Association Vol. 327; no. 5; p. 454 |
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| Format: | Journal Article |
| Language: | English |
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01.02.2022
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| ISSN: | 1538-3598, 1538-3598 |
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| Abstract | Idiopathic dilated cardiomyopathy (DCM) aggregates in families, and early detection in at-risk family members can provide opportunity to initiate treatment prior to late-phase disease. Most studies have included only White patients, yet Black patients with DCM have higher risk of heart failure-related hospitalization and death.
To estimate the prevalence of familial DCM among DCM probands and the age-specific cumulative risk of DCM in first-degree relatives across race and ethnicity groups.
A family-based, cross-sectional study conducted by a multisite consortium of 25 US heart failure programs. Participants included patients with DCM (probands), defined as left ventricular systolic dysfunction and left ventricular enlargement after excluding usual clinical causes, and their first-degree relatives. Enrollment commenced June 7, 2016; proband and family member enrollment concluded March 15, 2020, and April 1, 2021, respectively.
The presence of DCM in a proband.
Familial DCM defined by DCM in at least 1 first-degree relative; expanded familial DCM defined by the presence of DCM or either left ventricular enlargement or left ventricular systolic dysfunction without known cause in at least 1 first-degree relative.
The study enrolled 1220 probands (median age, 52.8 years [IQR, 42.4-61.8]; 43.8% female; 43.1% Black and 8.3% Hispanic) and screened 1693 first-degree relatives for DCM. A median of 28% (IQR, 0%-60%) of living first-degree relatives were screened per family. The crude prevalence of familial DCM among probands was 11.6% overall. The model-based estimate of the prevalence of familial DCM among probands at a typical US advanced heart failure program if all living first-degree relatives were screened was 29.7% (95% CI, 23.5% to 36.0%) overall. The estimated prevalence of familial DCM was higher in Black probands than in White probands (difference, 11.3% [95% CI, 1.9% to 20.8%]) but did not differ significantly between Hispanic probands and non-Hispanic probands (difference, -1.4% [95% CI, -15.9% to 13.1%]). The estimated prevalence of expanded familial DCM was 56.9% (95% CI, 50.8% to 63.0%) overall. Based on age-specific disease status at enrollment, estimated cumulative risks in first-degree relatives at a typical US advanced heart failure program reached 19% (95% CI, 13% to 24%) by age 80 years for DCM and 33% (95% CI, 27% to 40%) for expanded DCM inclusive of partial phenotypes. The DCM hazard was higher in first-degree relatives of non-Hispanic Black probands than non-Hispanic White probands (hazard ratio, 1.89 [95% CI, 1.26 to 2.83]).
In a US cross-sectional study, there was substantial estimated prevalence of familial DCM among probands and modeled cumulative risk of DCM among their first-degree relatives.
ClinicalTrials.gov Identifier: NCT03037632. |
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| AbstractList | Idiopathic dilated cardiomyopathy (DCM) aggregates in families, and early detection in at-risk family members can provide opportunity to initiate treatment prior to late-phase disease. Most studies have included only White patients, yet Black patients with DCM have higher risk of heart failure-related hospitalization and death.ImportanceIdiopathic dilated cardiomyopathy (DCM) aggregates in families, and early detection in at-risk family members can provide opportunity to initiate treatment prior to late-phase disease. Most studies have included only White patients, yet Black patients with DCM have higher risk of heart failure-related hospitalization and death.To estimate the prevalence of familial DCM among DCM probands and the age-specific cumulative risk of DCM in first-degree relatives across race and ethnicity groups.ObjectiveTo estimate the prevalence of familial DCM among DCM probands and the age-specific cumulative risk of DCM in first-degree relatives across race and ethnicity groups.A family-based, cross-sectional study conducted by a multisite consortium of 25 US heart failure programs. Participants included patients with DCM (probands), defined as left ventricular systolic dysfunction and left ventricular enlargement after excluding usual clinical causes, and their first-degree relatives. Enrollment commenced June 7, 2016; proband and family member enrollment concluded March 15, 2020, and April 1, 2021, respectively.Design, Setting, and ParticipantsA family-based, cross-sectional study conducted by a multisite consortium of 25 US heart failure programs. Participants included patients with DCM (probands), defined as left ventricular systolic dysfunction and left ventricular enlargement after excluding usual clinical causes, and their first-degree relatives. Enrollment commenced June 7, 2016; proband and family member enrollment concluded March 15, 2020, and April 1, 2021, respectively.The presence of DCM in a proband.ExposuresThe presence of DCM in a proband.Familial DCM defined by DCM in at least 1 first-degree relative; expanded familial DCM defined by the presence of DCM or either left ventricular enlargement or left ventricular systolic dysfunction without known cause in at least 1 first-degree relative.Main Outcomes and MeasuresFamilial DCM defined by DCM in at least 1 first-degree relative; expanded familial DCM defined by the presence of DCM or either left ventricular enlargement or left ventricular systolic dysfunction without known cause in at least 1 first-degree relative.The study enrolled 1220 probands (median age, 52.8 years [IQR, 42.4-61.8]; 43.8% female; 43.1% Black and 8.3% Hispanic) and screened 1693 first-degree relatives for DCM. A median of 28% (IQR, 0%-60%) of living first-degree relatives were screened per family. The crude prevalence of familial DCM among probands was 11.6% overall. The model-based estimate of the prevalence of familial DCM among probands at a typical US advanced heart failure program if all living first-degree relatives were screened was 29.7% (95% CI, 23.5% to 36.0%) overall. The estimated prevalence of familial DCM was higher in Black probands than in White probands (difference, 11.3% [95% CI, 1.9% to 20.8%]) but did not differ significantly between Hispanic probands and non-Hispanic probands (difference, -1.4% [95% CI, -15.9% to 13.1%]). The estimated prevalence of expanded familial DCM was 56.9% (95% CI, 50.8% to 63.0%) overall. Based on age-specific disease status at enrollment, estimated cumulative risks in first-degree relatives at a typical US advanced heart failure program reached 19% (95% CI, 13% to 24%) by age 80 years for DCM and 33% (95% CI, 27% to 40%) for expanded DCM inclusive of partial phenotypes. The DCM hazard was higher in first-degree relatives of non-Hispanic Black probands than non-Hispanic White probands (hazard ratio, 1.89 [95% CI, 1.26 to 2.83]).ResultsThe study enrolled 1220 probands (median age, 52.8 years [IQR, 42.4-61.8]; 43.8% female; 43.1% Black and 8.3% Hispanic) and screened 1693 first-degree relatives for DCM. A median of 28% (IQR, 0%-60%) of living first-degree relatives were screened per family. The crude prevalence of familial DCM among probands was 11.6% overall. The model-based estimate of the prevalence of familial DCM among probands at a typical US advanced heart failure program if all living first-degree relatives were screened was 29.7% (95% CI, 23.5% to 36.0%) overall. The estimated prevalence of familial DCM was higher in Black probands than in White probands (difference, 11.3% [95% CI, 1.9% to 20.8%]) but did not differ significantly between Hispanic probands and non-Hispanic probands (difference, -1.4% [95% CI, -15.9% to 13.1%]). The estimated prevalence of expanded familial DCM was 56.9% (95% CI, 50.8% to 63.0%) overall. Based on age-specific disease status at enrollment, estimated cumulative risks in first-degree relatives at a typical US advanced heart failure program reached 19% (95% CI, 13% to 24%) by age 80 years for DCM and 33% (95% CI, 27% to 40%) for expanded DCM inclusive of partial phenotypes. The DCM hazard was higher in first-degree relatives of non-Hispanic Black probands than non-Hispanic White probands (hazard ratio, 1.89 [95% CI, 1.26 to 2.83]).In a US cross-sectional study, there was substantial estimated prevalence of familial DCM among probands and modeled cumulative risk of DCM among their first-degree relatives.Conclusions and RelevanceIn a US cross-sectional study, there was substantial estimated prevalence of familial DCM among probands and modeled cumulative risk of DCM among their first-degree relatives.ClinicalTrials.gov Identifier: NCT03037632.Trial RegistrationClinicalTrials.gov Identifier: NCT03037632. Idiopathic dilated cardiomyopathy (DCM) aggregates in families, and early detection in at-risk family members can provide opportunity to initiate treatment prior to late-phase disease. Most studies have included only White patients, yet Black patients with DCM have higher risk of heart failure-related hospitalization and death. To estimate the prevalence of familial DCM among DCM probands and the age-specific cumulative risk of DCM in first-degree relatives across race and ethnicity groups. A family-based, cross-sectional study conducted by a multisite consortium of 25 US heart failure programs. Participants included patients with DCM (probands), defined as left ventricular systolic dysfunction and left ventricular enlargement after excluding usual clinical causes, and their first-degree relatives. Enrollment commenced June 7, 2016; proband and family member enrollment concluded March 15, 2020, and April 1, 2021, respectively. The presence of DCM in a proband. Familial DCM defined by DCM in at least 1 first-degree relative; expanded familial DCM defined by the presence of DCM or either left ventricular enlargement or left ventricular systolic dysfunction without known cause in at least 1 first-degree relative. The study enrolled 1220 probands (median age, 52.8 years [IQR, 42.4-61.8]; 43.8% female; 43.1% Black and 8.3% Hispanic) and screened 1693 first-degree relatives for DCM. A median of 28% (IQR, 0%-60%) of living first-degree relatives were screened per family. The crude prevalence of familial DCM among probands was 11.6% overall. The model-based estimate of the prevalence of familial DCM among probands at a typical US advanced heart failure program if all living first-degree relatives were screened was 29.7% (95% CI, 23.5% to 36.0%) overall. The estimated prevalence of familial DCM was higher in Black probands than in White probands (difference, 11.3% [95% CI, 1.9% to 20.8%]) but did not differ significantly between Hispanic probands and non-Hispanic probands (difference, -1.4% [95% CI, -15.9% to 13.1%]). The estimated prevalence of expanded familial DCM was 56.9% (95% CI, 50.8% to 63.0%) overall. Based on age-specific disease status at enrollment, estimated cumulative risks in first-degree relatives at a typical US advanced heart failure program reached 19% (95% CI, 13% to 24%) by age 80 years for DCM and 33% (95% CI, 27% to 40%) for expanded DCM inclusive of partial phenotypes. The DCM hazard was higher in first-degree relatives of non-Hispanic Black probands than non-Hispanic White probands (hazard ratio, 1.89 [95% CI, 1.26 to 2.83]). In a US cross-sectional study, there was substantial estimated prevalence of familial DCM among probands and modeled cumulative risk of DCM among their first-degree relatives. ClinicalTrials.gov Identifier: NCT03037632. |
| Author | Garg, Sonia Wilcox, Jane E Kinnamon, Daniel D Ewald, Gregory A Judge, Daniel P Haas, Garrie J Pamboukian, Salpy V Jordan, Elizabeth Morris, Alanna A Stoller, Douglas Jimenez, Javier Aaronson, Keith D Fishbein, Daniel P Moore, Charles K Wheeler, Matthew T Burke, Wylie Hershberger, Ray E Sweitzer, Nancy K Tang, W H Wilson Gottlieb, Stephen S Ni, Hanyu Lowes, Brian Kransdorf, Evan Pan, Stephen Katz, Stuart Mead, Jonathan O Shah, Palak Huggins, Gordon S Hofmeyer, Mark Wang, Jessica Owens, Anjali Trachtenberg, Barry H Smart, Frank |
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Walter Jr. Transplant Center, Houston, Texas – sequence: 15 givenname: Palak surname: Shah fullname: Shah, Palak organization: Inova Heart and Vascular Institute, Falls Church, Virginia – sequence: 16 givenname: Salpy V surname: Pamboukian fullname: Pamboukian, Salpy V organization: University of Alabama, Birmingham – sequence: 17 givenname: Nancy K surname: Sweitzer fullname: Sweitzer, Nancy K organization: Sarver Heart Center, University of Arizona, Tucson – sequence: 18 givenname: Matthew T surname: Wheeler fullname: Wheeler, Matthew T organization: Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California – sequence: 19 givenname: Jane E surname: Wilcox fullname: Wilcox, Jane E organization: Northwestern University Feinberg School of Medicine, Chicago, Illinois – sequence: 20 givenname: Stuart surname: Katz fullname: Katz, Stuart organization: New York University Langone Medical Center, New York – sequence: 21 givenname: Stephen surname: Pan fullname: Pan, Stephen organization: Department of Cardiology, Westchester Medical Center and New York Medical College, Valhalla – sequence: 22 givenname: Javier surname: Jimenez fullname: Jimenez, Javier organization: Miami Cardiac & Vascular Institute, Baptist Health South, Miami, Florida – sequence: 23 givenname: Keith D surname: Aaronson fullname: Aaronson, Keith D organization: University of Michigan Medical Center, Ann Arbor – sequence: 24 givenname: Daniel P surname: Fishbein fullname: Fishbein, Daniel P organization: University of Washington, Seattle – sequence: 25 givenname: Frank surname: Smart fullname: Smart, Frank organization: Louisiana State University Health Sciences Center, New Orleans – sequence: 26 givenname: Jessica surname: Wang fullname: Wang, Jessica organization: University of California Los Angeles Medical Center, Los Angeles – sequence: 27 givenname: Stephen S surname: Gottlieb fullname: Gottlieb, Stephen S organization: University of Maryland School of Medicine, Baltimore – sequence: 28 givenname: Daniel P surname: Judge fullname: Judge, Daniel P organization: Medical University of South Carolina, Charleston – sequence: 29 givenname: Charles K surname: Moore fullname: Moore, Charles K organization: University of Mississippi Medical Center, Jackson – sequence: 30 givenname: Jonathan O surname: Mead fullname: Mead, Jonathan O organization: The Davis Heart and Lung Research Institute, The Ohio State University, Columbus – sequence: 31 givenname: Hanyu surname: Ni fullname: Ni, Hanyu organization: The Davis Heart and Lung Research Institute, The Ohio State University, Columbus – sequence: 32 givenname: Wylie surname: Burke fullname: Burke, Wylie organization: Department of Bioethics and Humanities, University of Washington, Seattle – sequence: 33 givenname: Ray E surname: Hershberger fullname: Hershberger, Ray E organization: Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University, Columbus |
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| SubjectTerms | Adult Age Factors Black or African American Black People - statistics & numerical data Cardiomyopathy, Dilated - diagnosis Cardiomyopathy, Dilated - epidemiology Cardiomyopathy, Dilated - ethnology Confidence Intervals Cross-Sectional Studies Early Diagnosis Family Health - ethnology Family Health - statistics & numerical data Female Hispanic or Latino - statistics & numerical data Humans Hypertrophy, Left Ventricular - diagnosis Hypertrophy, Left Ventricular - epidemiology Hypertrophy, Left Ventricular - ethnology Male Middle Aged Prevalence Racial Groups - ethnology Racial Groups - statistics & numerical data Risk United States - epidemiology Ventricular Dysfunction, Left - diagnosis Ventricular Dysfunction, Left - epidemiology Ventricular Dysfunction, Left - ethnology White People - statistics & numerical data |
| Title | Prevalence and Cumulative Risk of Familial Idiopathic Dilated Cardiomyopathy |
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