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Premature Parental Cardiovascular Disease and Subclinical Disease Burden in the Offspring.

ABSTRACT: Background Offspring of parents with premature cardiovascular disease (CVD) have an increased risk of developing subclinical and clinical CVD. It is unclear whether this association differs by vascular beds in the offspring or by the age cut points used to define premature parental CVD. Methods and Results Using 3 generations of Framingham Heart Study participants, we assessed prevalent coronary artery calcification, the progression of coronary artery calcification over 6.1 years (median), carotid intima media thickness and the ankle-brachial index in 1046 offspring of parents with premature CVD before age 70 years, in 1618 offspring with both parents free of CVD and in 923 offspring with parents with CVD after age 70 years. We used different age cut points (55, 60, 65, and 70 years) to define premature parental CVD. In multivariable-adjusted models, offspring of parents with premature CVD (onset before age 65 years) displayed greater odds for prevalent coronary artery calcification (odds ratio [OR], 1.81; 95% CI, 1.35-2.43), higher carotid intima media thickness (OR, 1.50; 95% CI, 0.92-2.44) and lower ankle-brachial index (OR, 1.89; 95% CI, 1.00-3.58). These associations were generally consistent across different age cut points used to define premature parental CVD. The association with the progression of coronary artery calcification was less consistent. Conclusions Parental premature CVD is associated with increased subclinical CVD burden in the offspring, with consistent relations across different vascular beds and for different age cut points used to define premature parental CVD. Future studies should evaluate whether screening for subclinical CVD traits is warranted in offspring with premature parental CVD.

SUBMITTER: Lieb W

PROVIDER: S-EPMC7727015 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Premature Parental Cardiovascular Disease and Subclinical Disease Burden in the Offspring.

Lieb Wolfgang W Song Rebecca J RJ Vasan Ramachandran S RS Xanthakis Vanessa V

Journal of the American Heart Association 20200908 18

Background Offspring of parents with premature cardiovascular disease (CVD) have an increased risk of developing subclinical and clinical CVD. It is unclear whether this association differs by vascular beds in the offspring or by the age cut points used to define premature parental CVD. Methods and Results Using 3 generations of Framingham Heart Study participants, we assessed prevalent coronary artery calcification, the progression of coronary artery calcification over 6.1 years (median), carot ...[more]

PMID: 32896212

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Project description:BackgroundWhether high burden of subclinical vascular disease (SVD) is associated with increased premature mortality among middle-aged adults is not adequately understood. The association of midlife SVD burden with premature mortality among middle-aged adults free of clinical cardiovascular disease (CVD) could provide further insights into stratifying premature death beyond clinical CVD.ObjectiveTo determine whether high burden of subclinical vascular disease is associated with increased premature mortality among middle-aged adults.DesignWe leveraged data from the Atherosclerosis Risk in Communities Study.ParticipantsThirteen thousand eight hundred seventy-six community-dwelling blacks and whites aged 45-64 years from the Atherosclerosis Risk in Communities Study.Main measuresEach SVD measure-ankle-brachial index, carotid intima-media thickness, and electrocardiogram-was scored 0 (no abnormalities), 1 (minor abnormalities), or 2 (major abnormalities). An index was constructed as the sum of three measures, ranging from 0 (lowest burden) to 6 (highest burden). We used the Cox proportional-hazards model to determine the association of SVD burden with premature mortality (death before age 70) among persons free of clinical CVD. We then tested the difference in point estimates between SVD and clinical CVD.Key resultsAmong persons without CVD, the premature death was 1.7, 2.1, 2.5, and 3.8 per 1000 person-years among those with an SVD score of 0 (lowest burden), 1, 2, and 3-6 (highest burden), respectively. After multivariable-adjustment, highest SVD burden (score = 3-6; HR = 1.47) was significantly associated with premature death among persons initially without CVD. In the model where persons with and without CVD were included, high SVD burden (score: 3-6 vs. 0) and CVD did not have hugely different association with premature death (HR = 1.49 vs. 1.68; P = 0.32 for comparison).ConclusionsMidlife SVD burden was associated with premature mortality and it could stratify premature death beyond clinical CVD. It is important to take SVD into account when designing interventions for reducing premature mortality.

Project description:Background The extent to which cardiovascular disease (CVD) risk factors across the menopause explain racial/ethnic differences in subclinical vascular disease in late midlife women is not well documented and was explored in a multi-ethnic cohort. Methods and Results Participants (n=1357; mean age 60 years) free of clinical CVD from the Study of Women's Health Across the Nation had common carotid artery intima-media thickness, interadventitial diameter, and carotid plaque presence assessed by ultrasonography on average 13.7 years after baseline visit. Early to late midlife time-averaged cumulative burden of traditional CVD risk factors calculated using serial measures from baseline to the ultrasound visit were generally less favorable in black and Hispanic women compared with white and Chinese women, including education and smoking status and time-averaged cumulative blood pressure, high-density lipoprotein cholesterol, and fasting insulin. Independent of these risk factors, BMI, and medications, common carotid artery intima-media thickness was thicker in black women, interadventitial diameter was wider in Chinese women, yet plaque presence was lower in black and Hispanic women compared with white women. CVD risk factor associations with subclinical vascular measures did not vary by race/ethnicity except for high-density lipoprotein cholesterol on common carotid artery intima-media thickness; an inverse association between high-density lipoprotein cholesterol and common carotid artery intima-media thickness was observed in Chinese and Hispanic but not in white or black women. Conclusions Race/ethnicity did not particularly moderate the association between traditional CVD risk factors measured across the menopause transition and late midlife subclinical vascular disease. Unmeasured socioeconomic, cultural, and nontraditional biological risk factors likely play a role in racial/ethnic differences in vascular health and merit further exploration.

Project description:Background Although there is research on the impact of social determinants of health (SDOHs) on cardiovascular health, most existing evidence is based on individual SDOH components. We evaluated the impact of cumulative SDOH burden on cardiovascular risk factors, subclinical atherosclerosis, and incident cardiovascular disease events. Methods and Results We included 6479 participants from the MESA (Multi-Ethnic Study of Atherosclerosis). A weighted aggregate SDOH score representing the cumulative number of unfavorable SDOHs, identified from 14 components across 5 domains (economic stability, neighborhood and physical environment, community and social context, education, and health care system access) was calculated and divided into quartiles (quartile 4 being the least favorable). The impact of cumulative SDOH burden on cardiovascular risk factors (hypertension, diabetes, dyslipidemia, smoking, and obesity), systemic inflammation, subclinical atherosclerosis, and incident cardiovascular disease was evaluated. Increasing social disadvantage was associated with increased odds of all cardiovascular risk factors except dyslipidemia. Smoking was the risk factor most strongly associated with worse SDOH (odds ratio [OR], 2.67 for quartile 4 versus quartile 1 [95% CI, 2.13-3.34]). Participants within SDOH quartile 4 had 33% higher odds of increased high-sensitivity C-reactive protein (OR, 1.33 [95% CI, 1.11-1.60]) and 31% higher risk of all cardiovascular disease (hazard ratio, 1.31 [95% CI, 1.03-1.67]), yet no greater burden of subclinical atherosclerosis (OR, 1.01 [95% CI, 0.79-1.29]), when compared with those in quartile 1. Conclusions Increasing social disadvantage was associated with more prevalent cardiovascular risk factors, inflammation, and incident cardiovascular disease. These findings call for better identification of SDOHs in clinical practice and stronger measures to mitigate the higher SDOH burden among the socially disadvantaged to improve cardiovascular outcomes.

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Premature Parental Cardiovascular Disease and Subclinical Disease Burden in the Offspring.

Publications

Premature Parental Cardiovascular Disease and Subclinical Disease Burden in the Offspring.

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