Association of African Ancestry with Electrocardiographic Voltage and Concentric Left Ventricular Hypertrophy

The Dallas Heart Study

Aya J. Alame, Sonia Garg, Julia Kozlitina, Colby Ayers, Ronald M Peshock, Susan A Matulevicius, Mark H Drazner

Research output: Contribution to journalArticle

Abstract

Importance: Compared with white individuals, black individuals have increased electrocardiographic voltage and an increased prevalence of concentric left ventricular (LV) hypertrophy. Whether environmental or genetic factors lead to these racial differences is unknown. Objective: To determine whether proportion of genetically determined African ancestry among self-reported black individuals is associated with increased electrocardiographic voltage and concentric LV hypertrophy (LVH). Design, Setting, and Participants: The Dallas Heart Study is a probability-based cohort study of English- or Spanish-speaking Dallas County, Texas, residents, with deliberate oversampling of black individuals. Participants underwent extensive phenotyping, which included electrocardiography (ECG), cardiac magnetic resonance imaging (CMR), and dual-energy radiography absorptiometry (DEXA) at a single center. Participants aged 18 to 65 years who enrolled in the Dallas Heart Study between July 2000 and December 2002, self-identified as black (n = 1251) or white (n = 826), and had ECG, CMR, and DEXA data were included in this analysis. Data were analyzed from June 2017 to September 2018. Exposures: Proportion of African ancestry. Main Outcomes and Measures: Electrocardiographic voltage (12-lead and 9-lead) and markers of concentric LVH as assessed by CMR (LV concentricity0.67 [LV mass/end-diastolic volume0.67], LV wall thickness [LVWT], and prevalent LVH [defined by LV mass/height2.7]). Results: Of the 2077 participants included in the study, 1138 (54.8%) were women, and the mean (SD) age was 45.2 (9.9) years. Black race and African ancestry were individually associated with increased ECG voltage, LV concentricity0.67, LVWT, and prevalent LVH in multivariable analyses adjusting for age, sex, systolic blood pressure, antihypertensive medication use, and body composition. When African ancestry and black race were entered together into multivariable models, African ancestry but not black race remained associated with ECG voltage, LVWT, LV concentricity0.67, and prevalent LVH. Among black participants, African ancestry remained associated with these 4 phenotypes (12-lead voltage: β, 0.05; P =.04; LVWT: β, 0.05; P =.02; LV concentricty0.67: β, 0.05; P =.045; prevalent LVH: odds ratio, 1.2; 95% CI, 1.03-1.4; P =.02). Conclusions and Relevance: Genetically determined African ancestry was associated with electrocardiographic voltage, measures of concentric LV remodeling, and prevalent LVH. These data support a genetic basis related to African ancestry for the increased prevalence of these cardiovascular traits in black individuals.

Original languageEnglish (US)
JournalJAMA Cardiology
DOIs
StateAccepted/In press - Jan 1 2018

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Left Ventricular Hypertrophy
Hypertrophy
Electrocardiography
Magnetic Resonance Imaging
Blood Pressure
Ventricular Remodeling
Body Composition
Radiography
Antihypertensive Agents
Cohort Studies
Odds Ratio
Outcome Assessment (Health Care)
Phenotype
Lead

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

@article{f41311fe60524724bc83a77169958841,
title = "Association of African Ancestry with Electrocardiographic Voltage and Concentric Left Ventricular Hypertrophy: The Dallas Heart Study",
abstract = "Importance: Compared with white individuals, black individuals have increased electrocardiographic voltage and an increased prevalence of concentric left ventricular (LV) hypertrophy. Whether environmental or genetic factors lead to these racial differences is unknown. Objective: To determine whether proportion of genetically determined African ancestry among self-reported black individuals is associated with increased electrocardiographic voltage and concentric LV hypertrophy (LVH). Design, Setting, and Participants: The Dallas Heart Study is a probability-based cohort study of English- or Spanish-speaking Dallas County, Texas, residents, with deliberate oversampling of black individuals. Participants underwent extensive phenotyping, which included electrocardiography (ECG), cardiac magnetic resonance imaging (CMR), and dual-energy radiography absorptiometry (DEXA) at a single center. Participants aged 18 to 65 years who enrolled in the Dallas Heart Study between July 2000 and December 2002, self-identified as black (n = 1251) or white (n = 826), and had ECG, CMR, and DEXA data were included in this analysis. Data were analyzed from June 2017 to September 2018. Exposures: Proportion of African ancestry. Main Outcomes and Measures: Electrocardiographic voltage (12-lead and 9-lead) and markers of concentric LVH as assessed by CMR (LV concentricity0.67 [LV mass/end-diastolic volume0.67], LV wall thickness [LVWT], and prevalent LVH [defined by LV mass/height2.7]). Results: Of the 2077 participants included in the study, 1138 (54.8{\%}) were women, and the mean (SD) age was 45.2 (9.9) years. Black race and African ancestry were individually associated with increased ECG voltage, LV concentricity0.67, LVWT, and prevalent LVH in multivariable analyses adjusting for age, sex, systolic blood pressure, antihypertensive medication use, and body composition. When African ancestry and black race were entered together into multivariable models, African ancestry but not black race remained associated with ECG voltage, LVWT, LV concentricity0.67, and prevalent LVH. Among black participants, African ancestry remained associated with these 4 phenotypes (12-lead voltage: β, 0.05; P =.04; LVWT: β, 0.05; P =.02; LV concentricty0.67: β, 0.05; P =.045; prevalent LVH: odds ratio, 1.2; 95{\%} CI, 1.03-1.4; P =.02). Conclusions and Relevance: Genetically determined African ancestry was associated with electrocardiographic voltage, measures of concentric LV remodeling, and prevalent LVH. These data support a genetic basis related to African ancestry for the increased prevalence of these cardiovascular traits in black individuals.",
author = "Alame, {Aya J.} and Sonia Garg and Julia Kozlitina and Colby Ayers and Peshock, {Ronald M} and Matulevicius, {Susan A} and Drazner, {Mark H}",
year = "2018",
month = "1",
day = "1",
doi = "10.1001/jamacardio.2018.3804",
language = "English (US)",
journal = "JAMA Cardiology",
issn = "2380-6583",
publisher = "American Medical Association",

}

TY - JOUR

T1 - Association of African Ancestry with Electrocardiographic Voltage and Concentric Left Ventricular Hypertrophy

T2 - The Dallas Heart Study

AU - Alame, Aya J.

AU - Garg, Sonia

AU - Kozlitina, Julia

AU - Ayers, Colby

AU - Peshock, Ronald M

AU - Matulevicius, Susan A

AU - Drazner, Mark H

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Importance: Compared with white individuals, black individuals have increased electrocardiographic voltage and an increased prevalence of concentric left ventricular (LV) hypertrophy. Whether environmental or genetic factors lead to these racial differences is unknown. Objective: To determine whether proportion of genetically determined African ancestry among self-reported black individuals is associated with increased electrocardiographic voltage and concentric LV hypertrophy (LVH). Design, Setting, and Participants: The Dallas Heart Study is a probability-based cohort study of English- or Spanish-speaking Dallas County, Texas, residents, with deliberate oversampling of black individuals. Participants underwent extensive phenotyping, which included electrocardiography (ECG), cardiac magnetic resonance imaging (CMR), and dual-energy radiography absorptiometry (DEXA) at a single center. Participants aged 18 to 65 years who enrolled in the Dallas Heart Study between July 2000 and December 2002, self-identified as black (n = 1251) or white (n = 826), and had ECG, CMR, and DEXA data were included in this analysis. Data were analyzed from June 2017 to September 2018. Exposures: Proportion of African ancestry. Main Outcomes and Measures: Electrocardiographic voltage (12-lead and 9-lead) and markers of concentric LVH as assessed by CMR (LV concentricity0.67 [LV mass/end-diastolic volume0.67], LV wall thickness [LVWT], and prevalent LVH [defined by LV mass/height2.7]). Results: Of the 2077 participants included in the study, 1138 (54.8%) were women, and the mean (SD) age was 45.2 (9.9) years. Black race and African ancestry were individually associated with increased ECG voltage, LV concentricity0.67, LVWT, and prevalent LVH in multivariable analyses adjusting for age, sex, systolic blood pressure, antihypertensive medication use, and body composition. When African ancestry and black race were entered together into multivariable models, African ancestry but not black race remained associated with ECG voltage, LVWT, LV concentricity0.67, and prevalent LVH. Among black participants, African ancestry remained associated with these 4 phenotypes (12-lead voltage: β, 0.05; P =.04; LVWT: β, 0.05; P =.02; LV concentricty0.67: β, 0.05; P =.045; prevalent LVH: odds ratio, 1.2; 95% CI, 1.03-1.4; P =.02). Conclusions and Relevance: Genetically determined African ancestry was associated with electrocardiographic voltage, measures of concentric LV remodeling, and prevalent LVH. These data support a genetic basis related to African ancestry for the increased prevalence of these cardiovascular traits in black individuals.

AB - Importance: Compared with white individuals, black individuals have increased electrocardiographic voltage and an increased prevalence of concentric left ventricular (LV) hypertrophy. Whether environmental or genetic factors lead to these racial differences is unknown. Objective: To determine whether proportion of genetically determined African ancestry among self-reported black individuals is associated with increased electrocardiographic voltage and concentric LV hypertrophy (LVH). Design, Setting, and Participants: The Dallas Heart Study is a probability-based cohort study of English- or Spanish-speaking Dallas County, Texas, residents, with deliberate oversampling of black individuals. Participants underwent extensive phenotyping, which included electrocardiography (ECG), cardiac magnetic resonance imaging (CMR), and dual-energy radiography absorptiometry (DEXA) at a single center. Participants aged 18 to 65 years who enrolled in the Dallas Heart Study between July 2000 and December 2002, self-identified as black (n = 1251) or white (n = 826), and had ECG, CMR, and DEXA data were included in this analysis. Data were analyzed from June 2017 to September 2018. Exposures: Proportion of African ancestry. Main Outcomes and Measures: Electrocardiographic voltage (12-lead and 9-lead) and markers of concentric LVH as assessed by CMR (LV concentricity0.67 [LV mass/end-diastolic volume0.67], LV wall thickness [LVWT], and prevalent LVH [defined by LV mass/height2.7]). Results: Of the 2077 participants included in the study, 1138 (54.8%) were women, and the mean (SD) age was 45.2 (9.9) years. Black race and African ancestry were individually associated with increased ECG voltage, LV concentricity0.67, LVWT, and prevalent LVH in multivariable analyses adjusting for age, sex, systolic blood pressure, antihypertensive medication use, and body composition. When African ancestry and black race were entered together into multivariable models, African ancestry but not black race remained associated with ECG voltage, LVWT, LV concentricity0.67, and prevalent LVH. Among black participants, African ancestry remained associated with these 4 phenotypes (12-lead voltage: β, 0.05; P =.04; LVWT: β, 0.05; P =.02; LV concentricty0.67: β, 0.05; P =.045; prevalent LVH: odds ratio, 1.2; 95% CI, 1.03-1.4; P =.02). Conclusions and Relevance: Genetically determined African ancestry was associated with electrocardiographic voltage, measures of concentric LV remodeling, and prevalent LVH. These data support a genetic basis related to African ancestry for the increased prevalence of these cardiovascular traits in black individuals.

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U2 - 10.1001/jamacardio.2018.3804

DO - 10.1001/jamacardio.2018.3804

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JF - JAMA Cardiology

SN - 2380-6583

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