...lack of SDB data in the National Health and Nutrition Examination Survey sample limits our ability to compare fully our 2 study populations, and our relatively small sample size limits more ...complex analyses. Table 1 Baseline Demographics and Characteristics Data are presented as mean ± SD for continuous variable and as percentages for categorical variables.BMI = body mass index; HDL = high-density lipoprotein; LDL = low-density lipoprotein; NFL = National Football League; NHANES = National Health and Nutrition Examination Survey; SDB = sleep-disordered breathing.
The 2013 American College of Cardiology/American Heart Association cardiovascular disease prevention guidelines represent an important step forward in the risk assessment and management of ...atherosclerotic cardiovascular disease in clinical practice. Differentiated risk prediction equations for women and black individuals were developed, and convenient 10-year and lifetime risk assessment tools were provided, facilitating their implementation. Lifestyle modification was portrayed as the foundation of preventive therapy. In addition, based on high-quality evidence from randomized controlled trials, statins were prioritized as the first lipid-lowering pharmacologic treatment, and a shared decision-making model between the physician and the patient was emphasized as a key feature of personalized care. After publication of the guidelines, however, important limitations were also identified. This resulted in a constructive scientific debate yielding valuable insights into potential opportunities to refine recommendations, fill gaps in guidance, and better harmonize recommendations within and outside the United States. The latter point deserves emphasis because when guidelines are in disagreement, this may result in nonaction on the part of professional caregivers or nonadherence by patients. In this review, we discuss the key scientific literature relevant to the guidelines published in the year and a half after their release. We aim to provide cohesive, evidence-based views that may offer pathways forward in cardiovascular disease prevention toward greater consensus and benefit the practice of clinical medicine.
The recently published American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for cardiovascular risk assessment provide equations to estimate the 10-year and lifetime ...atherosclerotic cardiovascular disease (ASCVD) risk in African Americans and non-Hispanic whites, include stroke as an adverse cardiovascular outcome, and emphasize shared decision making. The guidelines provide a valuable framework that can be adapted on the basis of clinical judgment and individual/institutional expertise. In this review, we provide a perspective on the new guidelines, highlighting what is new, what is controversial, and potential adaptations. We recommend obtaining family history of ASCVD at the time of estimating ASCVD risk and consideration of imaging to assess subclinical disease burden in patients at intermediate risk. In addition to the adjuncts for ASCVD risk estimation recommended in the guidelines, measures that may be useful in refining risk estimates include carotid ultrasonography, aortic pulse wave velocity, and serum lipoprotein(a) levels. Finally, we stress the need for research efforts to improve assessment of ASCVD risk given the suboptimal performance of available risk algorithms and suggest potential future directions in this regard.
Current body mass index (BMI) strata likely misrepresent the accuracy of true adiposity in older adults. Subjects with normal BMI with elevated body fat may metabolically have higher cardiovascular ...and overall mortality than previously suspected. We identified 4,489 subjects aged ≥60 years (BMI = 18.5 to 25 kg/m2 ) with anthropometric and bioelectrical impedance measurements from the National Health and Nutrition Examination Surveys III (1988 to 1994) and mortality data linked to the National Death Index. Normal weight obesity (NWO) was classified in 2 ways: creation of tertiles with highest percentage of body fat and body fat percent cutoffs (men >25% and women >35%). We compared overall and cardiovascular mortality rates, models adjusted for age, gender, smoking, race, diabetes, and BMI. The final sample included 1,528 subjects, mean age was 70 years, median (interquartile range) follow-up was 12.9 years (range 7.5 to 15.3) with 902 deaths (46.5% cardiovascular). Prevalence of NWO was 27.9% and 21.4% in men and 20.4% and 31.3% in women using tertiles and cutoffs, respectively. Subjects with NWO had higher rates of abnormal cardiovascular risk factors. Lean mass decreased, whereas leptin increased with increasing tertile. There were no gender-specific differences in overall mortality. Short-term mortality (<140 person-months) was higher in women, whereas long-term mortality (>140 person-months) was higher in men. We highlight the importance of considering body fat in gender-specific risk stratification in older adults with normal weight. In conclusion, NWO in older adults is associated with cardiometabolic dysregulation and is a risk for cardiovascular mortality independent of BMI and central fat distribution.
To study the relationship between body mass index (BMI) and central obesity and mortality in elderly patients with coronary artery disease (CAD).
We identified 7057 patients 65 years or older from 5 ...cohort studies assessing mortality risk using either waist circumference (WC) or waist-hip ratio (WHR) in patients with CAD from January 1, 1980, to December 31, 2008. Normal weight, overweight, and obesity were defined using standard BMI cutoffs. High WHR was defined as 0.85 or more for women and 0.90 or more for men. High WC was defined as 88 cm or more for women and 102 cm or more for men. Separate models examined WC or WHR in combination with BMI (6 categories each) as the primary predictor (referent = normal BMI and normal WC or WHR). Cox proportional hazards models investigated the relationship between these obesity categories and mortality.
Patients' mean age was 73.0±6.0 years (3741 53% women). The median censor time was 7.1 years. A normal BMI with central obesity (high WHR or high WC) demonstrated highest mortality risk (hazard ratio HR, 1.29; 95% CI, 1.14-1.46; HR, 1.29; 95% CI, 1.12-1.50, respectively). High WHR was also predictive of mortality in the overall (HR, 2.14; 95% CI, 1.93-2.38) as well as in the sex-specific cohort. In the overall cohort, high WC was not predictive of mortality (HR, 1.04; 95% CI, 0.97-1.12); however, it predicted higher risk in men (HR, 1.12; 95% CI, 1.01-1.24).
In older adults with CAD, normal-weight central obesity defined using either WHR or WC is associated with high mortality risk, highlighting a need to combine measures in adiposity-related risk assessment.
To investigate the relationship of body mass index (BMI) with total mortality, cardiovascular (CV) mortality, and myocardial infarction (MI) after coronary revascularization procedures (coronary ...artery bypass grafting CABG and percutaneous coronary intervention PCI).
Systematic search of studies was conducted using PubMed, CINAHL, Cochran CENTRAL, Scopus, and the Web of Science databases. We identified studies reporting the rate of MI, CV mortality, and total mortality among coronary artery disease patients' postcoronary revascularization procedures in various BMI categories: less than 20 (underweight), 20-24.9 (normal reference), 25-29.9 (overweight), 30-34.9 (obese), and 35 or more (severely obese). Event rates were compared using a random effects model assuming interstudy heterogeneity.
A total of 36 studies (12 CABG; 26 PCI) were selected for final analyses. The risk of total mortality (relative risk RR, 2.59; 95% CI, 2.09-3.21), CV mortality (RR, 2.67; 95% CI, 1.63-4.39), and MI (RR, 1.79; 95% CI, 1.28-2.50) was highest among patients with low BMI at the end of a mean follow-up period of 1.7 years. The risk of CV mortality was lowest among overweight patients (RR, 0.81; 95% CI, 0.68-0.95). Increasing degree of adiposity as assessed by BMI had a neutral effect on the risk of MI for overweight (RR, 0.92; 95% CI, 0.84-1.01), obese (RR, 0.99; 95% CI, 0.85-1.15), and severely obese (RR, 0.93; 95% CI, 0.78-1.11) patients.
After coronary artery disease revascularization procedures (PCI and CABG), the risk of total mortality, CV mortality, and MI was highest among underweight patients as defined by low BMI and CV mortality was lowest among overweight patients.
Objectives The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans. Background Endothelial dysfunction has been identified as ...an independent predictor of cardiovascular events. Whether fat gain impairs endothelial function is unknown. Methods A randomized controlled study was conducted to assess the effects of fat gain on endothelial function. Forty-three normal-weight healthy volunteers were recruited (mean age 29 years; 18 women). Subjects were assigned to gain weight (approximately 4 kg) (n = 35) or to maintain weight (n = 8). Endothelial function (brachial artery flow-mediated dilation FMD) was measured at baseline, after fat gain (8 weeks), and after weight loss (16 weeks) for fat gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition was measured by dual-energy X-ray absorptiometry and abdominal computed tomographic scans. Results After an average weight gain of 4.1 kg, fat gainers significantly increased their total, visceral, and subcutaneous fat. Blood pressure and overnight polysomnography did not change after fat gain or loss. FMD remained unchanged in weight maintainers. FMD decreased in fat gainers (9.1 ± 3% vs. 7.8 ± 3.2%, p = 0.003) but recovered to baseline when subjects shed the gained weight. There was a significant correlation between the decrease in FMD and the increase in visceral fat gain (rho = −0.42, p = 0.004), but not with subcutaneous fat gain (rho = −0.22, p = 0.15). Conclusions In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction. (Fat Gain and Cardiovascular Disease Mechanisms; NCT00589498 )
Obstructive sleep apnea (OSA) and obesity have been linked to systolic and diastolic dysfunction of the left ventricle. Right ventricular function is poorly understood in the 2 clinical conditions. ...Data from this study show that otherwise healthy obese patients with OSA had increased an left atrial volume index compared with similarly obese patients without OSA (16.3 ± 1.2 ml/m in obese patients without OSA vs 20.2 ± 1.0 ml/m in those with OSA, p = 0.02) and altered diastolic function reflected by changes in mitral annular late diastolic velocity (−5.7 ± 0.7 cm/s in obese patients without OSA vs −7.3 ± 0.7 cm/s in those with OSA, p = 0.007), mitral annular early diastolic velocity (−7.9 ± 0.6 cm/s in obese patients without OSA vs −6.4 ± 0.3 cm/s in those with OSA, p = 0.05), and early to late diastolic annular ratio >1 (82% of obese patients without OSA vs 26% of those with OSA, p = 0.001), which may be signs of early subclinical impairment of cardiac function. Importantly, healthy obese subjects had similarly increased left ventricular mass compared with obese patients with OSA but normal diastolic function and left atrial size. There was a trend toward abnormal right ventricular filling in patients with OSA, measured by altered superior vena cava diastolic velocity during expiration (−15 ± 2 cm/s in obese patients without OSA vs −10 ± 3 cm/s in those with OSA, p = 0.2) and a tendency toward diastolic dysfunction reflected by decreased lateral tricuspid annular early diastolic velocity (−7.2 ± 0.5 cm/s in obese patients without OSA vs −6.1 ± 0.5 cm/s in those with OSA, p = 0.1) beyond that seen in obesity alone. In conclusion, OSA independent of obesity may induce cardiac changes that could predispose to atrial fibrillation and heart failure.
Background High cardiorespiratory fitness and body mass index (BMI) are associated with decreased mortality in patients with coronary artery disease. Our objective was to determine the joint impact ...of fitness and adiposity measures on all-cause mortality in this subgroup. Methods Coronary artery disease patients (n = 855) enrolled in the Mayo Clinic cardiac rehabilitation program from 1993 to 2007 were included. Fitness levels were determined by cardiopulmonary exercise testing. Patients were divided into low and high fitness by sex-specific median values of peak oxygen consumption and total treadmill time. Adiposity was measured through BMI and waist-to-hip ratio (WHR). Results There were 159 deaths during 9.7 ± 3.6 years of mean follow-up. After adjusting for potential confounding factors, low fitness, shorter treadmill time, low BMI, and high WHR were significantly associated with increased mortality. Using low WHR–high fitness group as reference, significantly increased mortality was noted in low WHR–low fitness (hazard ratio 4.2, 95% CI, 1.8-9.8), centrally obese–high fitness (2.3, 1.0-5.4), and centrally obese–low fitness (6.1, 2.7-13.6) groups. Overweight–high fitness (2.2, 0.63-7.4), obese–high fitness (3.2, 0.88-11.4), and obese–low fitness (3.3, 0.96-11.4) subjects did not have a significantly different mortality as compared with the reference group of normal weight–high fitness subjects, whereas normal weight–low fitness (9.6, 2.9-31.8) and overweight–low fitness (6.8, 2.1-22.2) groups had significantly increased mortality. Conclusions Low fitness and central obesity were independently and cumulatively associated with increased mortality in coronary artery disease patients attending cardiac rehabilitation. The association of BMI with mortality is complex and altered by fitness levels.
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