Left ventricular hypertrophy phenotype to predict incident atrial fibrillation: The Multi-Ethnic Study of Atherosclerosis.

BACKGROUND AND AIM: Left ventricular hypertrophy (LVH) has been shown to be associated with the occurrence of atrial fibrillation (AF). However, the predictive value of the LVH phenotype for incident AF remains uncertain. This study aimed to investigate the predictive value of LVH phenotype for incident AF. METHODS AND RESULTS: This study utilized the Multi-Ethnic Study of Atherosclerosis (MESA) data. LVH was defined by cardiac magnetic resonance measured LV mass index. Isolated LVH was determined as LVH without elevated cardiac biomarker and malignant LVH was determined as LVH with at least 1 elevated biomarker. Receiver-operating characteristic (ROC) analysis was performed to calculate areas under the curves (AUC) for predicting AF. A total of 4983 community-dwelling participants were included, with a mean age of 61.5 years. 279 (5.6 %) had isolated LVH, and 222 (4.5 %) had malignant LVH. During a median follow-up of 8.5 years, 272 incident AF was observed. Compared to participants without LVH and elevated cardiac biomarkers, those with isolated LVH (HR, 1.82; 95 % CI, 1.03-3.20) and malignant LVH (HR, 4.13; 95 % CI, 2.77-6.16) had a higher risk of incident AF. Malignant LVH carried a 1.5-fold increased risk of AF compared to isolated LVH (HR: 2.48, 95 % CI: 1.30-4.73). Including the LVH phenotype in the CHARGE-AF model improved model discrimination (AUC increase: 0.03, p < 0.001). CONCLUSIONS: The risks of AF incidence varied across LVH phenotypes. Malignant LVH carried the highest risk among LVH phenotypes. LVH phenotype provides incremental predictive value over the variables included in the CHARGE-AF model.

Life-Course Cumulative Burden of Body Mass Index and Blood Pressure on Progression of Left Ventricular Mass and Geometry in Midlife: The Bogalusa Heart Study.

RATIONALE: Data are limited regarding the influence of life-course cumulative burden of increased body mass index (BMI) and elevated blood pressure (BP) on the progression of left ventricular (LV) geometric remodeling in midlife. OBJECTIVE: To investigate the dynamic changes in LV mass and LV geometry over 6.4 years during midlife and to examine whether the adverse progression of LV geometric remodeling is influenced by the cumulative burden of BMI and BP from childhood to adulthood. METHODS AND RESULTS: The study consisted of 877 adults (604 whites and 273 blacks; 355 males; mean age=41.4 years at follow-up) who had 5 to 15 examinations of BMI and BP from childhood and 2 examinations of LV dimensions at baseline and follow-up 6.4 years apart during adulthood. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI and systolic BP (SBP). After adjusting for age, race, sex, smoking, alcohol drinking, and baseline LV mass index, the annual increase rate of LV mass index was associated with all BMI measures (ß=0.16-0.36, P<0.05 for all), adult SBP (ß=0.07, P=0.04), and total AUC of SBP (ß=0.09, P=0.01) but not with childhood and incremental AUC values of SBP. All BMI and SBP measures (except childhood SBP) were significantly associated with increased risk of incident LV hypertrophy, with odds ratios of BMI (odds ratio=1.85-2.74, P<0.05 for all) being significantly greater than those of SBP (odds ratio=1.09-1.34, P<0.05 for all except childhood SBP). In addition, all BMI measures were significantly and positively associated with incident eccentric and concentric LV hypertrophy. CONCLUSIONS: Life-course cumulative burden of BMI and BP is associated with the development of LV hypertrophy in midlife, with BMI showing stronger associations than BP. Visual Overview: An online visual overview is available for this article.

Relationship of a new anthropometric index with left ventricular hypertrophy in hypertensive patients among the Han Chinese.

BACKGROUND: This study aimed to assess the relationship of a new anthropometric index with left ventricular hypertrophy (LVH) in hypertensive patients among the Han Chinese. METHODS: The study is a community-based cross-sectional study that included 4639 patients with hypertension and integrated clinical and echocardiographic data. Left ventricular (LV) mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of left ventricular mass indexed (LVMI) over 49.2 g/m2.7 for men and 46.7 g/m2.7 for women. Quartiles of a body shape index (ABSI), body roundness index (BRI), waist circumference (WC), and body mass index (BMI) were used regarding LVH prevalence. The logistic regression model was used to determine the odds ratio (OR) and 95% confidence intervals (CI) of the new anthropometric index and LVH. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive ability of the obesity indices for LVH risk. RESULTS: The prevalence of LVH increased across quartiles for ABSI, BRI, BMI, and WC. Comparing the lowest with the highest quartile, adjusted OR (95% CI) for LVH were significantly different for BRI 3.86 (3.12-4.77), BMI 3.54 (2.90-4.31), and WC 2.29 (1.88-2.78). No association was observed for ABSI. According to ROC analysis, the area under the curve (AUC) of BRI was (AUC: 0.653, 95% CI 0.637-0.669), BMI (AUC: 0.628, 95% CI 0.612-0.644), WC (AUC: 0.576, 95% CI 0.559-0.593), ABSI (AUC: 0.499, 95% CI 0.482-0.516). CONCLUSIONS: This study shows that LVH prevalence increased per quartile across the Han Chinese population with hypertension for ABSI, BRI, BMI, and WC. There is a significant association between BRI and LVH in hypertensive people, while ABSI was not. BRI showed potential for use as an alternative obesity measure in the assessment of LVH.

Prevalence and Cumulative Risk of Familial Idiopathic Dilated Cardiomyopathy.

Importance: 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. Objective: 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. Design, Setting, and Participants: 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. Exposures: The presence of DCM in a proband. Main Outcomes and Measures: 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. Results: 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]). Conclusions and Relevance: 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. Trial Registration: ClinicalTrials.gov Identifier: NCT03037632.

Association between insulin resistance and left ventricular hypertrophy in asymptomatic, Black, sub-Saharan African, hypertensive patients: a case-control study.

BACKGROUND: Conflicting information exists regarding the association between insulin resistance (IR) and left ventricular hypertrophy (LVH). We described the associations between obesity, fasting insulinemia, homeostasis model assessment of insulin resistance (HOMA-IR), and LVH in Black patients with essential hypertension. METHODS: A case-control study was conducted at the Centre Médical de Kinshasa (CMK), the Democratic Republic of the Congo, between January and December 2019. Cases and controls were hypertensive patients with and without LVH, respectively. The relationships between obesity indices, physical inactivity, glucose metabolism and lipid disorder parameters, and LVH were assessed using linear and logistic regression analyses in simple and univariate exploratory analyses, respectively. When differences were observed between LVH and independent variables, the effects of potential confounders were studied through the use of multiple linear regression and in conditional logistic regression in multivariate analyses. The coefficients of determination (R2), adjusted odds ratios (aORs), and their 95% confidence intervals (95% CIs) were calculated to determine associations between LVH and the independent variables. RESULTS: Eighty-eight LVH cases (52 men) were compared against 132 controls (81 men). Variation in left ventricular mass (LVM) could be predicted by the following variables: age (19%), duration of hypertension (31.3%), body mass index (BMI, 44.4%), waist circumference (WC, 42.5%), glycemia (20%), insulinemia (44.8%), and HOMA-IR (43.7%). Hypertension duration, BMI, insulinemia, and HOMA-IR explained 68.3% of LVM variability in the multiple linear regression analysis. In the logistic regression model, obesity increased the risk of LVH by threefold [aOR 2.8; 95% CI (1.06-7.4); p = 0.038], and IR increased the risk of LVH by eightfold [aOR 8.4; 95 (3.7-15.7); p < 0.001]. CONCLUSION: Obesity and IR appear to be the primary predictors of LVH in Black sub-Saharan African hypertensive patients. The comprehensive management of cardiovascular risk factors should be emphasized, with particular attention paid to obesity and IR. A prospective population-based study of Black sub-Saharan individuals that includes the use of serial imaging remains essential to better understand subclinical LV deterioration over time and to confirm the role played by IR in Black sub-Saharan individuals with hypertension.

The burden, correlates and outcomes of left ventricular hypertrophy among young Africans with first ever stroke in Tanzania.

BACKGROUND: Left ventricular hypertrophy is a pathophysiological response often due to chronic uncontrolled hypertension. Our primary aim was to investigate the magnitude, correlates and outcomes of left ventricular hypertrophy as a surrogate maker for chronic uncontrolled hypertension in young adults ≤ 45 years with stroke. Our secondary aim was to determine the accuracy of electrocardiography using Sokolow-Lyon and Cornell criteria in detecting left ventricular hypertrophy compared to echocardiography. METHODS: This cohort study recruited young strokes who had undergone brain imaging, electrocardiography and transthoracic echocardiography at baseline. The modified Poisson regression model examined baseline correlates for left ventricular hypertrophy. The National Institute of Health Stroke Scale assessed stroke severity and the modified Rankin Scale assessed outcomes to 30-days. Performance of electrical voltage criterions was estimated using receiver operator characteristics. RESULTS: We enrolled 101 stroke participants. Brain imaging revealed ischemic strokes in 60 (59.4%) and those with intracerebral hemorrhage, 33 (86.8%) were localized to the basal ganglia. Left ventricular hypertrophy was present in 76 (75.3%:95%CI 65.7%-83.3%), and 30 (39.5%) and 28 (36.8%) had moderate or severe hypertrophy respectively. Young adults with premorbid or a new diagnosis of hypertension were more likely to have left ventricular hypertrophy, 47 (61.8%), and 26 (34.2%). On multivariable analysis, left ventricular hypertrophy was independently associated with not being on anti-hypertensive medications among hypertensives participants {adjusted risk ratio 1.4 (95%CI:1.04-1.94). The mean National Institute of Health Stroke score was 18 and 30-day mortality was 42 (43.3%). The sensitivity and specificity for Sokolow-Lyon in detecting left ventricular hypertrophy was 27% and 78%, and for Cornell was 32% and 52% respectively. CONCLUSIONS: We identified a high proportion of left ventricular hypertrophy in young adults with stroke associated with chronic undertreated hypertension. While the study methodology does not allow us to determine causation, this association and knowledge of pathophysiological processes supports the notion that chronic hypertension is a major risk factor for young strokes associated with high mortality. Our findings did not support the use of the electrical voltage criteria for detecting left ventricular hypertrophy. We recommend low cost interventions like blood pressure screening and treatment to reduce this burden.

Racial Differences in the Influence of Risk Factors in Childhood on Left Ventricular Mass in Young Adulthood.

OBJECTIVE(S): To examine racial differences in the relationship between cardiovascular (CV) risk factors measured since age 10 years and left ventricular mass index (LVMI) in adulthood in the National Heart, Lung, and Blood Institute Growth and Health Study. STUDY DESIGN: Longitudinal investigation with CV risk factors measured throughout childhood and LVMI measured in adulthood. In total, 556 black and white girls were recruited from schools in the greater Cincinnati area. Analyses examined traditional CV risk factors at baseline, follow-up, and over time (ie, area under the curve [AUC]). LVMI was collected with 2-dimensional guided echocardiographic imaging at a mean age of 25.7 ± 1.7 years. RESULTS: Black girls had higher adiposity and insulin and lower heart rate across time (all P < .05). Blacks had higher LVMI compared with whites in adulthood. Major determinants of young adult LVMI, were race, body mass index z score AUC, systolic blood pressure z score AUC, percent body fat by skin fold AUC, heart rate AUC, and an interaction between race and heart rate (model R2 = 0.40, P < .0001). CONCLUSIONS: The major determinants of LVMI in young female adults are race, adiposity, and systolic blood pressure.

An Investigation of Selection Bias in Estimating Racial Disparity in Stroke Risk Factors.

Selection due to survival or attrition might bias estimates of racial disparities in health, but few studies quantify the likely magnitude of such bias. In a large national cohort with moderate loss to follow-up, we contrasted racial differences in 2 stroke risk factors, incident hypertension and incident left ventricular hypertrophy, estimated by complete-case analyses, inverse probability of attrition weighting, and the survivor average causal effect. We used data on 12,497 black and 17,660 white participants enrolled in the United States (2003-2007) and collected incident risk factor data approximately 10 years after baseline. At follow-up, 21.0% of white participants and 23.0% of black participants had died; additionally 22.0% of white participants and 28.4% of black participants had withdrawn. Individual probabilities of completing the follow-up visit were estimated using baseline demographic and health characteristics. Adjusted risk ratio estimates of racial disparities from complete-case analyses in both incident hypertension (1.11, 95% confidence interval: 1.02, 1.21) and incident left ventricular hypertrophy (1.02, 95% confidence interval: 0.84, 1.24) were virtually identical to estimates from inverse probability of attrition weighting and survivor average causal effect. Despite racial differences in mortality and attrition, we found little evidence of selection bias in the estimation of racial differences for these incident risk factors.

Evaluation of left ventricular remodelling in young Afro-Caribbean athletes.

BACKGROUND: Cardiac adaptation to intense physical training is determined by many factors including age, gender, body size, load training and ethnicity. Despite the wide availability of ECG analysis, with a higher presence of abnormalities in different races, echocardiographic studies on young Afro-Caribean (AA) and Caucasian athletes (CA) are lacking in literature. We aimed to assess the effect in the secondary LV remodelling of load training in young AA players compared to matched CA players. METHOD: Seventy-seven AA and 53 CA matched soccer players (mean age 17.35 ± 0.50 and 18.25 ± 0.77 y) were enrolled. They were evaluated with echocardiography. A subgroup of 30 AA and 27 CA were followed up for a period of 4 years. The myocardial contractile function was evaluated by speckle-tracking echocardiographic global longitudinal strain (GLS). RESULTS: No significant differences were found in weight and height and in blood pressure response to maximal ergometer test in either group. In AA a higher level of LV remodelling, consisting in higher LV wall thickness, higher interventricular septum (IVS) and posterior wall (PW) thickness were found (IVS: 10.04 ± 0.14 and 9.35 ± 0.10 in AA and CA respectively, p < 0.001. PW: 9.70 ± 0.20 and 9.19 ± 0.10 mm in AA and CA respectively, p < 0.05). Strain data showed no significant differences between the two groups (22.35 ± 0.48 and 23.38 ± 0.69 in AA (n = 27) and CA (n = 25), respectively). At the beginning of the follow-up study AA showed a significantly higher left ventricular remodelling (IVS = 9.29 ± 0.3 and 8.53 ± 0.12 mm in AA and CA respectively, p < 0.002. PW = 9.01 ± 0.2 and 8.40 ± 0.20 in AA and CA respectively, p = 0.1). During the next four years of follow-up we observed a regular parallel increase in LV wall thickness and chamber diameters in both groups, proportionally to the increase in body size and LV mass. (IVS = 10.52 ± 0.17 and 9.03 ± 0.22 mm in AA and CA respectively, p < 0.001. PW: 10.06 ± 0.17 and 8.26 ± 0.19 mm in AA and CA respectively, p < 0.001). CONCLUSION: The study shows that the ventricular remodelling observed in AA appears to be a specific phenotype already present in pre-adolescence. These data also suggest that genetic/ethnic factors play a central role in left ventricular remodelling during the first years of life in elite athletes.

APOL1 nephropathy risk variants do not associate with subclinical atherosclerosis or left ventricular mass in middle-aged black adults.

Prior studies reported associations of APOL1 nephropathy risk variants with subclinical atherosclerosis. However, these findings were limited to older individuals with high comorbidities. To evaluate this in younger individuals, we calculated associations of APOL1 risk variants (high risk [2 risk variants] vs. low risk [0-1 risk variant]) with prevalent, incident, or progressive coronary artery calcification, a carotid intima media thickness over the 90th percentile, and left ventricular hypertrophy in 1315 black participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. The mean age of this cohort was 44.6 years and their mean estimated glomerular filtration rate was 102.5 ml/min/1.73m2. High-risk participants were found to be younger and have a higher prevalence of albuminuria than low-risk participants. In Poisson regression models adjusted for comorbidities and kidney function, the risk of prevalent coronary artery calcification (relative risk [95% confidence interval] 1.12 [0.72,1.71]), the incident coronary artery calcification (1.50 [0.87,2.59]), and the progression of coronary artery calcification (1.40 [0.88,2.23]) did not significantly differ in high vs. low-risk participants. Furthermore, the risk of carotid intima media thickness over the 90th percentile (1.28 [0.78,2.10]) and left ventricular hypertrophy (1.02[0.73,1.43]) did not significantly differ in high vs. low-risk participants in fully-adjusted models. Thus, APOL1 risk variants did not associate with subclinical markers of atherosclerosis or left ventricular hypertrophy in middle-aged black adults with preserved kidney function.

Association of left ventricular hypertrophy with cognitive decline and dementia risk over 20 years: The Atherosclerosis Risk In Communities-Neurocognitive Study (ARIC-NCS).

BACKGROUND: Left ventricular hypertrophy (LVH) is an indicator of organ damage largely due to hypertension. We assessed whether LVH was associated with dementia and cognitive function in the Atherosclerosis Risk in Communities study. METHODS: Our analysis included 12,665 individuals (23% black race, 56% female, mean age 57) who attended visit 2 in 1990-1992. Cornell voltage (SV3 + RaVL) was derived from 12-lead electrocardiograms and dichotomized as LVH using sex-specific criteria (>28 mm men; >22 mm women). Incident dementia was defined by expert review using a predetermined algorithm, and cognitive function was measured longitudinally using 3 tests. A Cox model was used to evaluate the association between time-dependent LVH and dementia adjusted for time-varying covariates from 1990 to 2013. Linear regression models fit with generalized estimating equations were used to evaluate LVH with cognitive function. RESULTS: During a mean follow-up of 18 years, we identified 544 participants with LVH and 1,195 dementia cases. LVH was associated with a higher risk of dementia: multivariable hazard ratio = 1.90; 95% CI: 1.47-2.44. Those with LVH had lower cognitive scores at baseline; however, there was no difference in the rate of cognitive decline over 20 years in those with LVH versus those without LVH. CONCLUSIONS: In this population-based study, LVH measured during midlife was associated with an increased risk of incident dementia; however, LVH was not associated with additional cognitive decline. These results underscore the need for hypertension control to prevent subclinical brain injury.

Identification of a novel loss-of-function mutation of the GLA gene in a Chinese Han family with Fabry disease.

BACKGROUND: Fabry disease is an X-linked recessive lysosomal disorder caused by deficient enzymatic activity of α-galactosidase A (α-Gal A). The insufficient enzymatic activity leads to excessive accumulation of glycosphingolipids, the substrates of the enzyme, in lysosomes in organs and tissues. Mutations in the α-Gal A gene (GLA, Xq22) have been proven to be responsible for Fabry disease. METHODS: In this study, we report a four-generation pedigree with left ventricular hypertrophy and chronic renal failure that was diagnosed by sequencing the GLA gene. An over expression system was constructed to evaluate the function of the detected mutation. RESULTS: We identified a novel mutation in exon 6 of the GLA gene, p.Asn278Lys, which completely co-segregated with the disease phenotype. The protein level of α-Gal A was significantly lower in the variant group than in the wild-type group; additionally, the pharmacological chaperone 1-deoxy-galactonojirimycin (DGJ) effectively normalized the enzyme activity of α-Gal A and its decline at the protein level. CONCLUSIONS: This study is the first to report a novel loss-of-function mutation, p.Asn278Lys, in exon 6 of the GLA gene as a genetic aetiology for Fabry disease. In addition, we analysed the feasibility of DGJ as a therapeutic approach for this particular GLA mutation.

Diabetes mellitus and insulin resistance associate with left ventricular shape and torsion by cardiovascular magnetic resonance imaging in asymptomatic individuals from the multi-ethnic study of atherosclerosis.

BACKGROUND: Although diabetes mellitus (DM) and insulin resistance associate with adverse cardiac events, the associations of left ventricular (LV) remodeling and function with compromised glucose metabolism have not been fully evaluated in a general population. We used cardiovascular magnetic resonance (CMR) to evaluate how CMR indices are associated with DM or insulin resistance among participants before developing cardiac events. METHODS: We studied 1476 participants who were free of clinical cardiovascular disease and who underwent tagged CMR in the Multi-Ethnic Study of Atherosclerosis (MESA). LV shape and longitudinal myocardial shortening and torsion were assessed by CMR. A higher sphericity index represents a more spherical LV shape. Multivariable linear regression was used to evaluate the associations of DM or homeostasis model assessment-estimated insulin resistance (HOMA-IR) with CMR indices. RESULTS: In multiple linear regression, longitudinal shortening was lower in impaired fasting glucose than normal fasting glucose (NFG) (0.36% lower vs. NFG, p < 0.05); torsion was greater in treated DM (0.24 °/cm greater vs. NFG, p < 0.05) after full adjustments. Among participants without DM, greater log-HOMA-IR was correlated with greater LV mass (3.92 g/index, p < 0.05) and LV mass-to-volume ratio (0.05 /index, p < 0.01), and lower sphericity index (- 1.26/index, p < 0.01). Greater log-HOMA IR was associated with lower longitudinal shortening (- 0.26%/index, p < 0.05) and circumferential shortening (- 0.30%/index, p < 0.05). Torsion was positively correlated with log-HOMA-IR until 1.5 of log-HOMA-IR (0.16 °/cm/index, p = 0.030).), and tended to fall once above 1.5 of log-HOMA-IR (- 0.50 °/cm/index, p = 0.203). The sphericity index was associated negatively with LV mass-to-volume ratio (- 0.02/%, p < 0.001) and torsion (- 0.03°/cm/%, p < 0.001). CONCLUSIONS: Glucose metabolism disorders are associated with LV concentric remodeling, less spherical shape, and reduced systolic myocardial shortening in the general population. Although torsion is higher in participants who are treated for DM and impaired insulin resistance, myocardial shortening was progressively decreased with higher HOMA-IR and torsion was increased only with less severe insulin resistance. CLINICAL TRIAL REGISTRATION: Multi-Ethnic Study of Atherosclerosis (MESA): A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org/ . Study Start Date: January 1999 ( NCT00005487 ).

Air Pollution, Cardiovascular Outcomes, and Social Disadvantage: The Multi-ethnic Study of Atherosclerosis.

BACKGROUND: Social factors may enhance health effects of air pollution, yet empirical support is inconsistent. The interaction of social and environmental factors may only be evident with long-term exposures and outcomes that reflect long-term disease development. METHODS: We used cardiac magnetic resonance imaging data from the Multi-Ethnic Study of Atherosclerosis to assess left-ventricular mass index (LVMI) and left-ventricular ejection fraction (LVEF). We assigned residential concentrations of fine particulate matter (PM2.5), oxides of nitrogen, and nitrogen dioxide in the year 2000 to each participant in 2000 using prediction models. We examined modifying roles of four measures of adversity: race/ethnicity, racial/ethnic residential segregation, and socioeconomic status and psychosocial adversity as composite indices on the association between air pollution and LVMI or LVEF. RESULTS: Compared with whites, blacks showed a stronger adjusted association between air pollution and LVMI. For example, for each 5 µg/m greater PM2.5 level, whites showed a 1.0 g/m greater LVMI (95% confidence interval = -1.3, 3.1), while blacks showed an additional 4.0 g/m greater LVMI (95% confidence interval = 0.3, 8.2). Results were similar for oxides of nitrogen and nitrogen dioxide with regard to black race and LVMI. However, we found no evidence of a modifying role of other social factors or ethnic groups. Furthermore, we found no evidence of a modifying role for any social factors or racial/ethnic groups on the association between air pollution and LVEF. CONCLUSIONS: Our results suggest that racial group membership may modify the association between air pollution and cardiovascular disease.

Fibrosis and coronary perfusion - a cardiovascular disease risk in an African male cohort: The SABPA study.

Low-grade inflammation has been correlated with risk factors of cardiovascular diseases (CVD). Whether the pro-inflammatory and thrombotic ratio (fibrosis) may contribute to CVD is not known. We therefore aimed to assess whether Cornell Product left ventricular hypertrophy (LVH) is associated with fibrosis and coronary perfusion (silent ischemia) in a bi-ethnic male cohort from South Africa. A cross sectional study was conducted including 165 African and Caucasian men between the ages of 20-65. Fasting blood samples were obtained to measure fibrinogen, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α). Ambulatory blood pressure, ECG and 12 lead ECG measures were obtained to determine silent ischemic events (ST events) and LVH, respectively. Africans revealed more silent ischemia, higher 24 h blood pressure, inflammatory, coagulation as well as fibrosis levels than Caucasians. In a low-grade inflammatory state (CRP > 3 mg/l), Africans revealed higher fibrosis (p ≤ 0.01) values, but lower IL-6 and TNF-α values than Caucasians. Linear regression analyses in several models demonstrated positive associations between silent ischemia and fibrosis [Adj. R(2) 0.23; ß 0.35 (95% CI 0.13, 0.58), p ≤ 0.01]. In a low-grade inflammatory state (CRP>3mg/l), fibrinogen predicted AV-block in African men [OR 3.38 (95% CI 2.24, 4.53); p = 0.04]. Low-grade inflammation may induce AV-block through mechanisms involving fibrosis and ischemia to increase the burden on the heart in African men.

Life Course Socioeconomic Position and Subclinical Disease: The Jackson Heart Study.

OBJECTIVES: African Americans experience higher rates of cardiovascular disease (CVD) and lower childhood and adult socioeconomic position (SEP). Research that examines the associations of multiple measures of SEP with subclinical CVD markers among African Americans is limited. METHODS: Data from the Jackson Heart Study (JHS) were used to examine cross-sectional associations of childhood SEP and adult SEP with subclinical markers among 4,756 African American participants (mean age 54, 64% female), adjusting for age, health behaviors and CVD risk factors. Subclinical markers included prevalent left ventricular hypertrophy (LVH), peripheral artery disease (PAD), coronary artery calcification (CAC), and carotid intima-media thickness (CIMT). RESULTS: The prevalence of LVH, PAD and CAC was 7%, 6% and 45%, respectively. The mean CIMT was .72 ± .17 mm. In fully-adjusted models, having a college education was inversely associated with PAD (OR, .27; 95% CI .13,.56) and CIMT (ß=-29.7, P<.01). Income was inversely associated with LVH after adjustment for health behaviors (OR, .49 95% CI .25,.96), though associations attenuated in the fully-adjusted model. Measures of childhood SEP (material resources and mother's education) were not consistently associated with subclinical disease measures other than a positive association between material resources and CIMT. CONCLUSIONS: Subclinical disease markers were patterned by adult SEP measures among African Americans.

Left ventricular hypertrophy and cardiovascular disease risk prediction and reclassification in blacks and whites: the Atherosclerosis Risk in Communities Study.

BACKGROUND: Left ventricular hypertrophy (LVH) is a major independent predictor of cardiovascular disease (CVD) survival and is more prevalent in blacks than whites. In a large biracial population, we evaluated the ability of electrocardiography (ECG)-determined LVH (ECG-LVH) to reclassify CVD/coronary heart disease (CHD) events beyond traditional risk factors in blacks and whites. METHODS: The analysis included 14,489 participants (mean age 54 ± 5.7 years; 43.5% men; 26% black) from the ARIC cohort, with baseline (1987-1989) ECG, followed up for 10 years. Predicted risk for incident CVD and CHD were estimated using the 10-year Pooled Cohort and Framingham risk equations (base models 1A/1B), respectively. Models 2A and 2B included respective base model plus LVH by "any" of 10 traditional ECG-LVH criteria. Net reclassification improvement (NRI) was calculated, and the distribution of risk was compared using models 2A and 2B versus models 1A and 1B, respectively. RESULTS: There were 792 (5.5%) 10-year Pooled Cohort CVD events and 690 (4.8%) 10-year Framingham CHD events. Left ventricular hypertrophy defined by any criteria was associated with CVD and CHD events (hazard ratio [95% CI] 1.62 [1.38-1.90] and 1.56 [1.32-1.86], respectively]. Left ventricular hypertrophy did not significantly reclassify or improve C statistic in models 2A/B (C statistics 0.767/0.719; NRI = 0.001 [P = not significant]), compared with the base models 1A/B (C statistics 0.770/0.718), respectively. No racial interactions were observed. CONCLUSIONS: In this large cohort of black and white participants, ECG-LVH was associated with CVD/CHD risk but did not significantly improve CVD and CHD events risk prediction beyond the new Pooled Cohort and most used Framingham risk equations in blacks or whites.

Acculturation is associated with left ventricular mass in a multiethnic sample: the Multi-Ethnic Study of Atherosclerosis.

BACKGROUND: Acculturation involves stress-related processes and health behavioral changes, which may have an effect on left ventricular (LV) mass, a risk factor for cardiovascular disease (CVD). We examined the relationship between acculturation and LV mass in a multiethnic cohort of White, African-American, Hispanic and Chinese subjects. METHODS: Cardiac magnetic resonance assessment was available for 5004 men and women, free of clinical CVD at baseline. Left ventricular mass index was evaluated as LV mass indexed by body surface area. Acculturation was characterized based on language spoken at home, place of birth and length of stay in the United States (U.S.), and a summary acculturation score ranging from 0 = least acculturated to 5 = most acculturated. Mean LV mass index adjusted for traditional CVD risk factors was compared across acculturation levels. RESULTS: Unadjusted mean LV mass index was 78.0 ± 16.3 g/m(2). In adjusted analyses, speaking exclusively English at home compared to non-English language was associated with higher LV mass index (81.3 ± 0.4 g/m(2) vs 79.9 ± 0.5 g/m(2), p = 0.02). Among foreign-born participants, having lived in the U.S. for ≥ 20 years compared to < 10 years was associated with greater LV mass index (81.6 ± 0.7 g/m(2) vs 79.5 ± 1.1 g/m(2), p = 0.02). Compared to those with the lowest acculturation score, those with the highest score had greater LV mass index (78.9 ± 1.1 g/m(2) vs 81.1 ± 0.4 g/m(2), p = 0.002). There was heterogeneity in which measure of acculturation was associated with LV mass index across ethnic groups. CONCLUSIONS: Greater acculturation is associated with increased LV mass index in this multiethnic cohort. Acculturation may involve stress-related processes as well as behavioral changes with a negative effect on cardiovascular health.

Pulmonary hyperinflation and left ventricular mass: the Multi-Ethnic Study of Atherosclerosis COPD Study.

BACKGROUND: Left ventricular (LV) mass is an important predictor of heart failure and cardiovascular mortality, yet determinants of LV mass are incompletely understood. Pulmonary hyperinflation in chronic obstructive pulmonary disease (COPD) may contribute to changes in intrathoracic pressure that increase LV wall stress. We therefore hypothesized that residual lung volume in COPD would be associated with greater LV mass. METHODS AND RESULTS: The Multi-Ethnic Study of Atherosclerosis (MESA) COPD Study recruited smokers 50 to 79 years of age who were free of clinical cardiovascular disease. LV mass was measured by cardiac magnetic resonance. Pulmonary function testing was performed according to guidelines. Regression models were used to adjust for age, sex, body size, blood pressure, and other cardiac risk factors. Among 119 MESA COPD Study participants, the mean age was 69±6 years, 55% were male, and 65% had COPD, mostly of mild or moderate severity. Mean LV mass was 128±34 g. Residual lung volume was independently associated with greater LV mass (7.2 g per 1-SD increase in residual volume; 95% confidence interval, 2.2-12; P=0.004) and was similar in magnitude to that of systolic blood pressure (7.6 g per 1-SD increase in systolic blood pressure; 95% confidence interval, 4.3-11; P<0.001). Similar results were observed for the ratio of LV mass to end-diastolic volume (P=0.02) and with hyperinflation measured as residual volume to total lung capacity ratio (P=0.009). CONCLUSIONS: Pulmonary hyperinflation, as measured by residual lung volume or residual lung volume to total lung capacity ratio, is associated with greater LV mass.

Assessing the performance of the Framingham Stroke Risk Score in the reasons for geographic and racial differences in stroke cohort.

BACKGROUND AND PURPOSE: The most well-known stroke risk score is the Framingham Stroke Risk Score (FSRS), which was developed during the higher stroke risk period of the 1990s and has not been validated for blacks. We assessed the performance of the FSRS among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study to determine whether it is useful in both blacks and whites. METHODS: Expected annualized stroke rates from the FSRS were compared with observed stroke rates overall and within strata defined by FSRS risk factors (age, sex, systolic blood pressure, use of antihypertensive medications, diabetes mellitus, smoking, atrial fibrillation, left ventricular hypertrophy, and prevalent coronary heart disease). RESULTS: Among 27 748 participants stroke-free at baseline, 715 stroke events occurred over 5.6 years of follow-up. FSRS-estimated incidence rates of stroke were 1.6× higher than observed for black men, 1.9× higher for white men, 1.7× higher for black women, and 1.7× higher for white women. This overestimation was consistent among most subgroups of FSRS factors, although the magnitude of overestimation varied by the risk factor assessed. CONCLUSIONS: Although higher FSRS was associated with higher stroke risk, the FSRS overestimated the observed stroke rates in this study, particularly in certain subgroups. This may be because of temporal declines in stroke rates, secular trends in prevention treatments, or differences in populations studied. More accurate estimates of event rates are critical for planning research, including clinical trials, and targeting health-care efforts.