Browsing by Subject "Hypertrophy, Left Ventricular"
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Item Association of African Ancestry with Electrocardiographic Voltage and Concentric Left Ventricular Hypertrophy: The Dallas Heart Study(2020-05-01T05:00:00.000Z) Alame, Aya J.; Drazner, Mark H.; Garg, Sonia; Kozlitina, JuliaBACKGROUND: 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). METHODS: 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. 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 concentricity^0.67, 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 concentricity^0.67: β, 0.05; P = .045; prevalent LVH: odds ratio, 1.2; 95% CI, 1.03-1.4; P = .02). CONCLUSION: 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.Item Association of African Ancestry with Left Ventricular Hypertrophy Assessed by Electrocardiographic Voltage and Cardiac Magnetic Resonance: The Dallas Heart Study(2018-01-23) Alame, Aya J.; Garg, Sonia; Kozlitina, Julia; Ayers, Colby; Drazner, Mark H.INTRODUCTION: Left ventricular hypertrophy (LVH) is more common in blacks than whites, despite adjusting for differences in blood pressure. Whether environmental or genetic factors lead to this increased prevalence of LVH in blacks is unknown. If genetic factors are involved, we hypothesized that the proportion of African ancestry among self-reported blacks would be associated with an increased risk of LVH in this ethnic group. METHODS: Participants from the Dallas Heart Study underwent genotyping, an electrocardiogram (ECG), and Cardiac Magnetic Resonance (CMR) imaging. Ancestral admixture proportions were estimated using genetic markers (Illumina Exome Chip) and ADMIXTURE software assuming 3 ancestral populations. In this analysis, we included participants that self-identified as black or white (n=2077). First, we tested the association of genetically inferred African ancestry (AFR) and self-reported black race, separately, using multivariable linear regression models, with three LVH phenotypes: 12-lead ECG voltage, LV concentricity0.67 (LV mass/volume0.67, a marker of concentric LVH), and LV Wall Thickness (LVWT). Next, we entered both AFR and black race into the same models to determine if the association of black race with LVH would be accounted for by AFR. Finally, we tested the association of AFR with LVH phenotypes among self-reported blacks. RESULTS: The study cohort consisted of 1,251 black and 826 white participants. Black race and AFR were individually associated with ECG voltage, LV concentricity0.67, and LVWT (Table 1). When AFR and black race were entered together into multivariable models, AFR, but not black race, was significantly associated with the LVH phenotypes (Table 1). Among self-reported blacks, AFR remained significantly associated with these LVH phenotypes (Table 1). CONCLUSIONS: The association of black race with LVH phenotypes can be captured more robustly with a genetic estimate of African ancestry. Further, within blacks, the proportion of AFR was associated with LVH phenotypes. These data support a genetic basis, related to African ancestry, for the increased prevalence of LVH in blacks.Item Compensatory left ventricular hypertrophy: relation of physiology to management(2002-09-05) Malloy, Craig R.Item The Etiology of LVH - A Review Of Genetic Predispositions(2006-08-15) Canham, Russell M.; Drazner, Mark H.My research fellowship was focused on assessing putative associations of polymorphisms in candidate genes with cardiovascular disease. Two previously well publicized associations were tested in the Dallas Heart Study (DHS), a stratified random population-sample of 6,101 Dallas County residents aged 18-65, with equivalent numbers of Black and non-Black women and men.1 The first putative association tested was whether two polymorphisms in adrenergic receptors (alpha 2CDel322-325 and ß1Arg389) synergistically increased the risk of heart failure in Blacks as reported by others (adjusted odds ratio, 10.1; 95% CI: 2.11 to 48.53; p=0.004).2 In the DHS, we found that these variant alleles were not associated with self-reported heart failure or traits commonly accepted to be precursors for systolic HF, including left ventricular hypertrophy, increased left ventricular volume, reduced ejection fraction, and left ventricular mass (LVM).3 The second putative association tested was whether polymorphisms in the alpha 2A-adrenergic receptor (DraI restriction fragment length protein) and the alpha 2C-adrenergic receptor (Del 322-325) increased the risk of hypertension in Blacks.4, 5 Again, we were unable to replicate these findings. We found that these variant alleles were not associated with hypertension in Blacks in the DHS, alone or in combination.6 Based on this experience, the present review was undertaken to analyze the genetic influence on a cardiovascular disease and determine whether lack of reproducibility of genetic association studies occurs commonly. Given the breadth of this topic, I have chosen to focus on association studies of putative polymorphisms with the development of the "complex" trait of left ventricular hypertrophy (LVH). LVH can be defined as increased LV mass in relation to body size. The geometric pattern of this increased LV mass in LVH is important.7 In response to pressure overload from conditions like hypertension, there is increased LV wall thickness leading to an increase in LV mass and the ratio of wall thickness to chamber dimension, the combination of which has been termed "concentric hypertrophy".8 When volume overload conditions prevail, there is an increase in the left ventricular chamber volume with resultant chamber dilatation leading to a decrease in the ratio of wall thickness to chamber dimension, a pattern called "eccentric hypertrophy".8 For purposes of this review, the focus will be largely on concentric hypertrophy. Although there are inherited monogenic causes of hypertrophy, ("familial hypertrophy cardiomyopathy"), established by linkage and family studies,9 that body of work will not be evaluated in this review. Rather, the reproducibility of associations in polymorphisms with LVH performed in reported studies will be examined. Evidence looking at the role of polymorphisms in exercise-induced hypertrophy ("physiological" hypertrophy) also will be assessed. The review will conclude with a summary of "lessons learned" from previous work in this area with the intent of providing clues to improve future association studies in this field.