This study prospectively investigates the contribution of pregnancy complications and other reproductive age risk factors on the risk of subsequent cardiovascular disease death. Participants were 14 ...403 women in the Child Health and Development Studies pregnancy cohort drawn from the Kaiser Permanente Health Plan in California. Only women with nonmissing parity and no previously diagnosed heart conditions were included. A total of 481 had observed preeclampsia, and 266 died from cardiovascular disease. The median age at enrollment was 26 years, and the median follow-up time was 37 years. Cardiovascular disease death was determined by linkage with the California Department of Vital Statistics. Observed preeclampsia was independently associated with cardiovascular disease death (mutually adjusted hazard ratio2.14 95% CI1.29 to 3.57). The risk of subsequent cardiovascular disease death was notably higher among women with onset of preeclampsia by 34 weeks of gestation (hazard ratio9.54 95% CI4.50 to 20.26). At 30 years of follow-up and a median age of 56 years, the cumulative cardiovascular disease death survival for women with early preeclampsia was 85.9% compared with 98.3% for women with late preeclampsia and 99.3% for women without preeclampsia. Women with preeclampsia had an increased risk of cardiovascular disease death later in life, independent of other measured risk factors. These findings reinforce previously reported recommendations that a history of preeclampsia should be used to target women at risk for cardiovascular disease. Additionally, women with preeclampsia earlier in pregnancy may be particularly at risk for cardiovascular disease death and could be targeted for early and intensive screening and intervention.
The risk of developing coronary heart disease differs by sex, and accumulating evidence suggests that sex differences exist in the effect of coronary risk factors on vascular risk. So far, the ...existence of a sex difference in the association between BMI and coronary heart disease has not been systematically studied. Since sexual dimorphisms in body composition exist, we postulated that the association between BMI and coronary heart disease would differ between women and men.
We did systematic searches of PubMed and Embase up to Feb 20, 2015, for studies of the longitudinal association between BMI and coronary heart disease in women and men from population-based cohorts. We excluded studies if they contained duplicate data from the same study, reported estimates only for Z scores or percentiles of BMI, did not report estimate uncertainty, did not report sex-specific estimates, recruited mainly individuals with a previous history of cardiovascular disease or from within selected populations, and those for which the full text was not available in English. We also included individual participant data from four large studies. Study results were pooled using random-effect models with inverse variance weighting. Our predefined primary endpoint was the pooled women-to-men ratio of the age-adjusted hazard ratios (HRs), or equivalent, relating (continuous and categorical) BMI to coronary heart disease.
We reviewed a total of 8561 original entries twice for inclusion in the analysis, of which 32 published studies were eligible for inclusion. Data from 95 cohorts, 1,219,187 participants, and 37,488 incident cases of coronary heart disease were included. Higher BMI was significantly associated with age-adjusted coronary heart disease: for a one-unit (kg/m(2)) increment in BMI; the HR was 1·04 (95% CI 1·03-1·05) in women and 1·05 (1·04-1·07) in men. Compared with people of a normal weight, the age-adjusted HR of coronary heart disease for the underweight group was 1·25 (1·05-1·49) in women and 1·09 (0·91-1·23) in men; for the overweight group 1·20 (1·12-1·29) in women and 1·22 (1·12-1·32) in men; and for the obese group 1·61 (1·42-1·82) in women and 1·60 (1·43-1·79) in men. Overall, these associations did not differ between the sexes. The women-to-men ratios of the HRs were 0·99 (95% CI 0·98-1·00) for a one-unit increment in BMI, 1·10 (0·91-1·32) for the underweight group, 0·99 (0·92-1·07) for the overweight group, and 1·06 (0·95-1·17) for the obese group, relative to the normal weight group. Similar results were obtained after multiple adjustment and in a range of sensitivity analyses.
Increased BMI, measured either continuously or categorically, has the same deleterious effects on the risk of coronary heart disease in women and men across diverse populations.
None.
Debate over the cardiometabolic risk associated with metabolically healthy obesity (MHO) continues. Many studies have investigated this relationship by examining MHO at baseline with longitudinal ...follow-up, with inconsistent results.
The authors hypothesized that MHO at baseline is transient and that transition to metabolic syndrome (MetS) and duration of MetS explains heterogeneity in incident cardiovascular disease (CVD) and all-cause mortality.
Among 6,809 participants of the MESA (Multi-Ethnic Study of Atherosclerosis) the authors used Cox proportional hazards and logistic regression models to investigate the joint association of obesity (≥30 kg/m2) and MetS (International Diabetes Federation consensus definition) with CVD and mortality across a median of 12.2 years. We tested for interaction and conducted sensitivity analyses for a number of conditions.
Compared with metabolically healthy normal weight, baseline MHO was not significantly associated with incident CVD; however, almost one-half of those participants developed MetS during follow-up (unstable MHO). Those who had unstable MHO had increased odds of CVD (odds ratio OR: 1.60; 95% confidence interval CI: 1.14 to 2.25), compared with those with stable MHO or healthy normal weight. Dose response for duration of MetS was significantly and linearly associated with CVD (1 visit with MetS OR: 1.62; 95% CI: 1.27 to 2.07; 2 visits, OR: 1.92; 95% CI: 1.48 to 2.49; 3+ visits, OR: 2.33; 95% CI: 1.89 to 2.87; p value for trend <0.001) and MetS mediated approximately 62% (44% to 100%) of the relationship between obesity at any point during follow-up and CVD.
Metabolically healthy obesity is not a stable or reliable indicator of future risk for CVD. Weight loss and lifestyle management for CVD risk factors should be recommended to all individuals with obesity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Context:
Sex hormones may influence adipose tissue deposition, possibly contributing to sex disparities in cardiovascular disease risk.
Objective:
We hypothesized that associations of sex hormone ...levels with visceral and subcutaneous fat differ by sex.
Design, Setting, and Participants:
Participants were from the Multi-Ethnic Study of Atherosclerosis with sex hormone levels at baseline and visceral and subcutaneous fat measurements from computed tomography at visit 2 or 3 (n = 1835).
Main Outcome Measures:
Multivariable linear regression was used to investigate the relationships between sex hormones and adiposity. Testing for interaction by sex, race/ethnicity, and age was conducted.
Results:
In adjusted models, there was a modest significant positive association between estradiol and visceral fat in both sexes (percent difference in visceral fat for 1% difference in hormone 95% confidence interval in women, 5.44 1.82, 9.09; and in men, 8.22 0.61, 16.18). Higher bioavailable T was significantly associated with higher visceral and subcutaneous fat in women and with the reverse in men (women, 14.38 10.23, 18.69; men, −7.69 −13.06, −1.00). Higher dehydroepiandrosterone was associated with higher visceral fat in women (7.57 1.71, 13.88), but not in men (−2.47 −8.88, 4.29). Higher SHBG was associated with significantly lower levels of adiposity in both sexes (women, −24.42 −28.11, −20.55; men, −27.39 −32.97, −21.34). There was no significant interaction by race/ethnicity or age.
Conclusion:
Sex hormones are significantly associated with adiposity, and the associations of androgens differ qualitatively by sex. This heterogeneity may help explain the complexity of the contribution of sex hormones to sex differences in cardiovascular disease.
Background
As the debate continues about whether obesity in metabolically healthy individuals is associated with poor outcomes or not, investigating the association between the obesity phenotypes and ...markers of subclinical myocardial injury will help identify those at risk for future cardiovascular events (cardiovascular disease CVD).
Hypothesis
We hypothesize that obesity phenotypes including metabolically healthy obesity (MHO) is associated with subclinical myocardial injury (SC‐MI).
Methods
This analysis included 3423 participants (57.85 ± 13.06 years, 53.3% women) without known CVD from National Health and Nutrition Examination Survey (NHANES) III. Multivariable logistic regression models were used to examine the cross‐sectional association between four obesity phenotypes (metabolically healthy nonobese (MHNO) reference, metabolically unhealthy nonobese (MUNO), MHO, and metabolically unhealthy obese (MUO) with SC‐MI. SC‐MI was defined from the 12‐lead electrocardiogram as cardiac infarction/injury score ≥ 10 units. Metabolic syndrome (MetS) was defined according to the International Diabetes Federation consensus definition. Obesity was defined as body mass index ≥30 kg/m2.
Results
MUO was associated with higher odds of SC‐MI compared with MHNO (odds ratio OR, 1.53; 95% confidence interval CI, 1.22‐1.92, P = 0.0005). This association was stronger in men vs women (OR 95% CI: 2.20 1.58‐2.07 vs 1.08 0.79‐1.48), respectively; interaction P‐value = 0.002) but was consistent in subgroups stratified by age and race. There was no significant association of MHO or MUNO with SC‐MI compared with MHNO, but there was a trend toward higher odds of SC‐MI in the MUNO group (P‐value for trend across MHNO, MUNO, and MUO = 0.0002).
Conclusions
Our findings suggest that a combination of obesity and MetS confers worse prognosis and early preventive strategies aimed at weight loss and management of MetS components may decrease the risk of future poor outcomes.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Background The relationship between alcohol consumption and ectopic fat distribution, both known factors for cardiovascular disease, remains understudied. Therefore, we aimed to examine the ...association between alcohol consumption and ectopic adiposity in adults at risk for cardiovascular disease. Methods and Results In this cross-sectional analysis, we categorized alcohol intake among participants in MESA (Multi-Ethnic Study of Atherosclerosis) as follows (drinks/day): <1 (light drinking), 1 to 2 (moderate drinking), >2 (heavy drinking), former drinking, and lifetime abstention. Binge drinking was defined as consuming ≥5 drinks on 1 occasion in the past month. Visceral, subcutaneous, and intermuscular fat area, pericardial fat volume, and hepatic fat attenuation were measured using noncontrast computed tomography. Using multivariable linear regression, we examined the associations between categories of alcohol consumption and natural log-transformed fat in ectopic depots. We included 6756 MESA participants (62.1±10.2 years; 47.2% women), of whom 6734 and 1934 had chest computed tomography (pericardial and hepatic fat) and abdominal computed tomography (subcutaneous, intermuscular, and visceral fat), respectively. In adjusted analysis, heavy drinking, relative to lifetime abstention, was associated with a higher (relative percent difference) pericardial 15.1 95% CI, 7.1-27.7, hepatic 3.4 95% CI, 0.1-6.8, visceral 2.5 95% CI, -10.4 to 17.2, and intermuscular 5.2 95% CI, -6.6 to 18.4 fat but lower subcutaneous fat -3.5 95% CI, -15.5 to 10.2). The associations between alcohol consumption and ectopic adiposity exhibited a J-shaped pattern. Binge drinking, relative to light-to-moderate drinking, was also associated with higher ectopic fat. Conclusions Alcohol consumption had a J-shaped association with ectopic adiposity. Both heavy alcohol intake and binge alcohol drinking were associated with higher ectopic fat.
Background
Visceral adipose tissue (VAT) is associated with incident heart failure (HF) and HF with preserved ejection fraction, yet it is unknown how pericardial and abdominal adiposity affect HF ...and mortality risks in Black individuals. We examined the associations of pericardial adipose tissue (PAT), VAT, and subcutaneous adipose tissue (SAT) with incident HF hospitalization and all‐cause mortality in a large community cohort of Black participants.
Methods and Results
Among the 2882 Jackson Heart Study Exam 2 participants without prevalent HF who underwent body computed tomography, we used Cox proportional hazards models to examine associations between computed tomography–derived regional adiposity and incident HF hospitalization and all‐cause mortality. Fully adjusted models included demographics and cardiovascular disease risk factors. Median follow‐up was 10.6 years among participants with available VAT (n=2844), SAT (n=2843), and PAT (n=1386). Fully adjusted hazard ratios (95% CIs) of distinct computed tomography–derived adiposity measures (PAT per 10 cm
3
, VAT or SAT per 100 cm
3
) were as follows: for incident HF, PAT 1.08 (95% CI, 1.02–1.14) and VAT 1.04 (95% CI, 1.01–1.08); for HF with preserved ejection fraction, PAT 1.13 (95% CI, 1.04–1.21) and VAT 1.07 (95% CI, 1.01–1.13); for mortality, PAT 1.07 (95% CI, 1.03–1.12) and VAT 1.01 (95% CI, 0.98–1.04). SAT was not associated with either outcome.
Conclusions
High PAT and VAT, but not SAT, were associated with incident HF and HF with preserved ejection fraction, and only PAT was associated with mortality in the fully adjusted models in a longitudinal community cohort of Black participants. Future studies may help understand whether changes in regional adiposity improves HF, particularly HF with preserved ejection fraction, risk predictions.
Registration
URL:
https://www.clinicaltrials.gov
; Unique identifier: NCT00005485.
Objective
Although increasing evidence suggests that visceral adipose tissue (VAT) is a major underlying cause of metabolic syndrome (MetS), few studies have measured VAT at multiple time points in ...diverse populations. VAT and insulin resistance were hypothesized to differ by MetS status within BMI category in the Insulin Resistance Atherosclerosis Study (IRAS) Family Study and, further, that baseline VAT and insulin resistance and increases over time are associated with incident MetS.
Methods
Generalized estimating equations were used for differences in body fat distribution and insulin resistance by MetS status. Mixed effects logistic regression was used for the association of baseline and change in adiposity and insulin resistance with incident MetS across 5 years, adjusted for age, sex, race/ethnicity, and family correlation.
Results
VAT and insulin sensitivity differed significantly by MetS status and BMI category at baseline. VAT and homeostatic model assessment of insulin resistance (HOMA‐IR) at baseline (VAT odds ratio OR = 1.16 95% CI: 1.12‐2.31; HOMA‐IR OR = 1.85 95% CI: 1.32‐2.58) and increases over time (VAT OR = 1.55 95% CI: 1.22‐1.98; HOMA‐IR OR = 3.23 95% CI: 2.20‐4.73) were associated with incident MetS independent of BMI category.
Conclusions
Differing levels of VAT may be driving metabolic heterogeneity within BMI categories. Both overall and abdominal obesity (VAT) may play a role in the development of MetS. Increased VAT over time contributed additional risk.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Objective
This study aimed to investigate the association of metabolically healthy obesity (MHO) and other obesity phenotypes with electrocardiographic (ECG) markers to understand the ...pathophysiological basis of increased cardiovascular disease (CVD) risk associated with these phenotypes.
Methods
A total of 3,700 participants (58.7 ± 13.6 years, 52% women) without CVD from the third National Health and Nutrition Examination Survey (NHANES III) were included. Logistic regression was used to examine the cross‐sectional association between obesity phenotypes (metabolically healthy without obesity MHNO; reference, metabolically unhealthy without obesity, MHO, and metabolically unhealthy obesity) with ECG markers (PR interval, P‐wave duration, QRS duration, and QT interval).
Results
Higher odds of prolonged PR interval, P‐wave duration, and QRS duration were observed among all phenotypes compared with MHNO, with the highest in participants with obesity with or without metabolic syndrome. However, for QT interval, the trend of association with obesity phenotypes was as follows, from the strongest to the least strong: metabolically unhealthy obesity, metabolically healthy without obesity, and then MHO, compared with MHNO.
Conclusions
An association of obesity phenotypes with ECG abnormalities further raises doubt about the concept of MHO as a healthy state. Variations in associations with ECG markers may suggest that metabolic syndrome and obesity have a different relationship with different CVD outcomes and may explain some of the inconsistent CVD estimates for MHO.
Full text
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
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