Body composition and cardiovascular disease: Clinical implications beyond body mass index

The prevalence of obesity in the United States and the world has risen to epidemic/pandemic proportions. This increase has occurred despite great efforts by healthcare providers and consumers alike to improve the health-related behaviors of the population and a tremendous push from the scientific community to better understand the pathophysiology of obesity. This epidemic is all the more concerning given the clear association between excess adiposity and adverse health consequences such as cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The risks associated with overweight/obesity are primarily related to the deposition of adipose tissue, which leads to excess adiposity or body fatness. Furthermore, weight loss, specifically loss of body fat, is associated with improvement in obesity-related comorbidities. Before weight loss interventions can be recommended, however, patients must be assessed for their adiposity-related risk. Unfortunately, healthcare providers and systems have not done a good job of assessing for excess adiposity even in its simplest form, such as measuring body mass index (BMI). It is for these reasons that we must emphasize the importance of assessing adiposity in clinical practices. Although it can be argued that the entire population should be targeted as an important public health issue with a goal of prevention of weight gain and obesity, there are currently so many “at risk” individuals that simple strategies to identify and treat those individuals are necessary. We must identify those individuals at highest risk of comorbidities in order to identify those who might benefit the most from aggressive weight management. This scientific statement will first briefly review the epidemiology of obesity and its related comorbidities, supporting the need for improved assessment of adiposity in daily clinical practice. This will be followed by a discussion of some of the challenges and issues associated with assessing adiposity and then by a review …

Not all women diagnosed with PCOS share the same cardiovascular risk profiles

As reports show cardiovascular (CV) risks in first-degree relatives (FDR) of type2 diabetics, and autonomic imbalance predisposing to CV risks, in the present study we have assessed the contribution of sympathovagal imbalance (SVI) to CV risks in these subjects. Body mass index (BMI), waist-to-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in FDR of type2 diabetics (study group, n=293) and in subjects with no family history of diabetes (control group, n=405). The ratio of low-frequency (LF) to high-frequency (HF) power of HRV (LF-HF), a sensitive marker of SVI, was significantly increased (P<0.001) in the study group compared with the control group. The SVI in the study group was due to concomitant sympathetic activation (increased LF) and vagal inhibition (decreased HF). In the study group, the LF-HF ratio was significantly correlated with BMI, WHR, BHR, BP and RPP. Multiple regression analysis showed an independent contribution of LF-HF to hypertension status (P=0.000), and bivariate logistic regression showed significant prediction (odds ratio 2.16, confidence interval 1.130-5.115) of LF-HF to increased RPP, the marker of CV risk, in the study group. Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activity is present in FDR of type2 diabetics. Increased resting heart rate, elevated hypertension status, decreased HRV and increased RPP in these subjects make them vulnerable to CV risks. SVI in these subjects contributes to CV risks independent of the degree of adiposity.

Cardiovascular disease in HIV-positive patients

A growing body of evidence is pointing out the pathophysiological role of fat accumulation in different organs. Ectopic fat depots within heart, liver, skeletal muscle, kidney, and pancreas as well as around blood vessels might be more associated to cardiometabolic risk than classical variables, such as body mass index. Among different mechanisms, lipid metabolism appears to be particularly influenced by ectopic fat depots. Indeed, intracellular accumulation of nonesterified fatty acids, and triglycerides promotes endoplasmic reticulum stress, mitochondrial uncoupling, oxidative stress, and altered membrane composition/function, finally promoting inflammatory response and cell death. The dysfunctional adipose tissue was shown to induce both local and systemic effects, with relevant clinical consequences. Epicardial fat and myocardial steatosis have been associated with the development of atrial fibrillation and ventricular dysfunction. Similarly perivascular adipose tissue appears to trigger atherosclerosis and hypertension. Nonalcoholic fatty liver disease has been recognized both as the hepatic manifestation of metabolic syndrome and as a cardiovascular (CV) risk factor. Importantly, the renal sinus fat emerged as a potential player in kidney dysfunction. Finally, both skeletal muscle and pancreatic fat depots have been indicated as potential endocrine modulators of insulin resistance. Considering the global rise in the prevalence of obesity, the understanding of mechanisms underlying ectopic fat accumulation represents an urgent need, with potential clinical implications for CV risk stratification. Here, we attempt to update the current knowledge of the different ectopic fat depots, focusing on underlying mechanisms and potential clinical implications.

Obesity is increasingly recognized as a heterogeneous condition with variable cardiovascular risk in the setting of similar levels of body mass index. Ectopic fat depots may contribute to obesity-mediated vascular disease and explain part of this risk differential. This review will explore the current understanding of the biology of ectopic adipose tissue storage, its quantification and classification, and existing research supporting an association between ectopic fat and cardiovascular disease. Obesity is associated with significant cardiovascular morbidity and mortality, and is recognized as a major public health concern.1,2 Although useful clinically and in epidemiologic studies, the classification of obesity using body mass index (BMI) does not fully encompass the complex biology of excess adiposity. Excess body fat is now recognized as a heterogeneous condition in which individuals with similar levels of BMI may have distinct metabolic and cardiovascular disease risk.2 Variation in body fat distribution provides 1 potential explanation for some of the risk differential that persists after accounting for BMI and standard risk factors.3 The study of ectopic adipose tissue depots, which surround organs and blood vessels, focuses on the quantification of these different fat depots and their potential systemic and local consequences. Waist circumference was one of the earliest means of quantifying body fat distribution, and some clinical guidelines have recommended measurement of waist circumference to provide additional information regarding cardiovascular risk.4 However, waist circumference consists of both subcutaneous adipose (SAT) (classically nonectopic) and visceral adipose tissue (VAT) (classically ectopic). This is important because VAT is associated with more adverse levels of metabolic risk factors compared with SAT.5 In addition, seminal work in mice has shown that transplantation of SAT, but not VAT, to an intra-abdominal site resulted in beneficial effects on metabolism.6 Taken together, these findings suggest that information about …

The concept of the risk factor for chronic diseases, such as cardiovascular disorders, is derived from the application of epidemiological methods initially developed for infectious and nutritional deficiency diseases to chronic conditions to identify the factor(s) linked to the development of the chronic disease. Typically in infectious or nutritional deficiency conditions, a single causative agent or primary cause is identified. Thus, the cause of tuberculosis is the tubercle bacillus, and the cause of pellagra is niacin deficiency. However, for cardiovascular diseases, in which causes are usually complex and multifactorial, new concepts were required. For example, individuals with hypertension have a far greater risk for cardiovascular disease than those without hypertension, but many individuals with hypertension never have clinical sequelae, and many individuals with diagnosed cardiovascular diseases have no hypertension. One can also argue that many individuals who are exposed to the tubercle bacillus do not develop clinical tuberculosis, but the converse is not true; no one has tuberculosis without the tubercle bacillus. This provides a clear distinction between multifactorial diseases, such as coronary disease where the risk factor concept is paramount, and other health conditions. The initial application of the risk factor concept was well developed long before the term was coined. Early in the previous century, insurance companies noted that individuals with high blood pressure were at higher risk for premature mortality1 and therefore would be accepted for life insurance only on payment of an additional premium. Insurance companies also recognized the related risk factor of obesity, and imposed higher premiums on overweight clients. In this context, risk factors are used as predictors of disease and mortality. Surprisingly, insurance companies failed to recognize the enormous contribution of smoking to cardiovascular risk until later. Although the underlying concept had been widely discussed and applied, the term “risk factor” was …

Cardiovascular Protection in People With Diabetes.

Usefulness of Brachial Artery Flow-Mediated Dilation to Predict Long-Term Cardiovascular Events in Subjects Without Heart Disease

Objective: Cardiovascular (CV) risk stratification in patients with arterial hypertension is essential for tailoring adequate antihypertensive treatment. Only few data is available on CV risk stratification in primary care patients with arterial hypertension. The aim of this subanalysis from the Swiss Hypertension Cohort Study (HccH) was to evaluate the compliance of general practitioners with the ESH/ESC guidelines on CV risk stratification in arterial hypertension as well as potential gaps in the risk stratification process. Design and method: HccH is an ongoing prospective observational study which has been initiated in 2005 by the Institute for Primary Care of the University of Basel, Switzerland. Data collection is conducted by general practitioners in Switzerland. Eligible patients are adult men and women (age > = 18 years) with arterial hypertension. Inclusion criteria are antihypertensive treatment respectively a mean through sitting office blood pressure (OBPM) > = 140/90mmHg. Patient characteristics, OBPM, ambulatory blood pressure (ABPM), CV risk factors, asymptomatic target organ damage (OD), diabetes mellitus (DM), chronic kidney disease (CKD) and symptomatic CV and renal disease are recorded on an annual basis and CV risk analyzed according to the 2013 ESH/ESC Guidelines. Results: Baseline data from 1005 patients included into HccH are given in the following table:BMI: Body Mass Index; CHD: Coronary Heart Disease; CHF: Congestive Heart Failure; CKD: Chronic Kidney Disease; GFR: Glomerular Filtration Rate; PAD: Peripheral Artery Disease; TIA: Transitory Ischemic Attack; Smoking Status: Y: active smoker, N: never smoked, Ex: former smoker. Data given as mean ± SD or absolute numbers (% of recorded data) where applicable. Conclusions: Decisions about treatment and optimal therapy in hypertensive patients should be based on an individual overall CV risk. Therefore a complete performance of risk stratification is very important. Our preliminary analysis from HccH demonstrates that CV risk factors from medical history and clinical data, with the exception of ABPM, appear to be comprehensively recorded in primary care. Substantial gaps were revealed with regards to the assessment of asymptomatic OD, particularly microalbuminuria and left ventricular hypertrophy, indicating that overall CV risk may be significantly underestimated in primary care patients with arterial hypertension.

Measures for the prevention of cardiovascular diseases (CVD) are more effective if they are performed taking into account the risk factors of their development. Screening scales, which are helpful in determining the population risk, are used in primary prevention for cardiovascular (CV) risk stratification. The assessment of individual CV risk remains a problem. Biomarkers and instrumental investigations are used for its detailing. Carotid ultrasound is the main noninvasive method of vascular assessment. It allows assessing the intima-media thickness (IMT) and detecting the presence, location and morphology of atherosclerotic plaques (ASP), in other words, subclinical signs of atherosclerosis. Different views on the diagnosis of IMT and ASP in the carotid arteries and their value as predictors of CV and cerebrovascular diseases among individuals without CVD are presented in the article. Opinions about the benefits of IMT assessment for re-classification of patients with signs of subclinical atherosclerosis are also presented. The debate about the value of IMT in the CV risk stratification, and the feasibility of its assessment in clinical practice has not yet been completed. Assessment of IMT for CV risk stratification is most appropriate in patients with intermediate risk or with multiple risk factors of CVD. Consensus on primary CV prevention strategies in patients with intermediate risk of CVD is currently unavailable. Assessment of subclinical atherosclerosis by carotid ultrasound is important in such patients. The finding of increased carotid IMT should have an effect on the choice of hypolipidemic drug and intensity of treatment. However, the diagnosis of subclinical atherosclerosis is not built into the algorithm for determining the CV risk. This causes difficulties in choosing tactic of prophylactic intervention, especially for intermediate risk patients.

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Epicardial adipose tissue and cardiovascular diseases

The increase in stiffness of large arteries is one of the mechanisms that could play a role in the association between obesity and increased risk of cardiovascular (CV) events. Carotid–femoral pulse wave velocity (cfPWV), known as an independent CV risk factor, represents a validated measure of large arteries stiffness and a good proxy of arterial ageing. We aimed at evaluating which body composition parameters better correlated with cfPWV and whether this correlation differed between men and women. cfPWV was measured in all subjects with Sphigmocor by sequentially recording electrocardiogram–gated carotid and femoral artery waveforms; body composition was measured by bioimpedance analysis and waist circumference (W). Furthermore, each subject was characterized by sex, age, height, weight, body mass index (BMI), brachial blood pressure (BP) and heart rate. A linear correlation was used to define the relationship between cfPWV and parameters. Univariate and multivariate analysis were performed in male and female subgroups separately to select the main determinants of arterial stiffness, considering the following parameters: age, mean BP (mBP), BMI, W, fat mass (FM) and skeletal muscle mass (SMM). We enrolled 69 subjects (37 men, 32 women) with average age 34.5 years (min 19–max 76). cfPWV was significantly correlated with age (r = 0.65, p&amp;lt;.0001), and mBP (r = 0.38, p&amp;lt;.01). Among the body composition parameters, W, BMI and FM percentage were significantly correlated with cfPWV (respectively: r = 0.48, r = 0.42, r = 0.41; p&amp;lt;.0001). Multivariable regression analysis in men revealed that age and mBP were significant determinants of cfPWV (respectively: b = 0.042, p = 0.002; b = 0.051, p = 0.004). Conversely, multivariate analysis in women showed that age, FM and SMM are retained as main determinants of increased cfPWV (respectively: b = 0.079; p &amp;lt; 0.0001; b = 0.217, p = 0.012; b = 0.125, p = 0.011). Irrespectively of gender, age is the main determinant of arterial stiffness. Our results demonstrated that the relationship between adiposity and arterial stiffness is verified only in female subjects. This suggests that this relationship is influenced by complex and not fully known mechanisms. Moreover, technical factors (algorithm and indirect methods to assess body composition) contribute to uncertainty regarding which parameter exploring adiposity is more accurate in stratifying CV risk. The present study recalls attention on possible gender–specific determinants of arterial ageing.