Body Fat Distribution and Risk of Cardiovascular Disease

Abstract

E pidemiological, clinical, and mechanistic preclinical studies conducted in the field of cardiovascular medicine have led to remarkable progress in our understanding of nonmodifiable and modifiable risk factors for cardiovascular disease (CVD). For instance, although the prevalence of CVD had reached devastating levels in the 1950s, proper focus on the major CVD risk factors first identified at the time, such as smoking, hypertension, and high cholesterol levels, has allowed these risk factors to be targeted both at the clinical level and through public health policies. 1 As a consequence, coronary heart disease mortality has decreased by Ϸ50% over the past 50 years. 2 Ford et al 2 have suggested that better screening and medical management of these CVD risk factors and the medical procedures developed to treat the various acute manifestations of CVD have had a favorable impact on its related mortality rates. However, the current overconsumption of processed and energy-dense food products of poor nutritional value combined with our sedentary lifestyle have contributed to the emergence of new drivers of CVD risk: obesity and type 2 diabetes mellitus ( Figure 1). 3,4 It has been proposed that our medical progress at tackling CVD could be offset, at least to a certain extent, by the dramatic consequences of our toxic lifestyle, which includes poor nutrition or excess caloric consumption and a sedentary lifestyle, both leading to obesity and type 2 diabetes mellitus. 2 Thus, the mosaic of modifiable CVD risk factors has evolved over the past 50 years with, on the one hand, less influence of smoking, and of untreated hypertension and high cholesterol, as well, but, on the other hand, an increased prevalence of sedentary overweight/obese patients having either type 2 diabetes mellitus or a constellation of metabolic abnormalities linked to insulin resistance: the so-called metabolic syndrome. 5

Visceral Adiposity and Left Ventricular Mass and Function in Patients With Aortic Stenosis: The PROGRESSA Study

“…26 The use of imaging techniques such as CT and magnetic resonance imaging have improved our ability to precisely and reliably quantify individual differences in body fat distribution and to selectively distinguish subcutaneous adiposity from visceral abdominal adipose tissue. 27 The results of this study therefore suggest that excess visceral adipose tissue distribution may represent an early index of dangerous ectopic lipid deposition linked to altered myocardial lipid metabolism and eventually to impaired ventricular geometry and function. Other studies reported that the metabolic abnormalities linked to visceral obesity (i.e.…”

“…metabolic syndrome and type-2 diabetes) are associated with increased prevalence of aortic valve calcification, 28, 29 faster progression of AS, 30 and faster degeneration of aortic bioprosthetic valves. 31 As lifestyle modification programs including regular physical activity have been shown to mobilize visceral adipose tissue and ectopic fat depots, 27 it is suggested that lifestyle modification interventions may represent interesting early options to halt or slow disease progression at both the valvular and ventricular levels in patients with AS. Considering the limited therapeutic options for AS, randomized trials may be conducted to test the added value of prevention program targeting excess visceral/ectopic adiposity for the reduction of disease progression rate and cardiovascular events.…”

“Broken” autonomic cardiac circadian clock in obese adolescents: evidence and implications

“…However, when circadian curves of estimated high-frequency components detected in obese and control subjects are compared, it becomes clear that the difference in the two curves is greater for magnitude in the daytime period between 6.00 a.m. and 2.00 p.m. This time window includes the early morning hours known to be associated with a pronounced adrenergic overdrive to the heart and peripheral vessels, and with a greater risk of sudden arrhythmic death, particularly in obese patients [2,7].…”

“…First, unfortunately, no data are available on the relationships between the high-frequency/ low-frequency heart rate patterns and waist-to-hip ratio, which is a sensitive marker of body fat distribution [7]. This information is needed to determine whether the observed cardiac autonomic dysregulation was more pronounced in people with visceral fat obesity, or people with peripheral fat obesity, as it has been reported in obese adults [8,9].…”

“…This information is needed to determine whether the observed cardiac autonomic dysregulation was more pronounced in people with visceral fat obesity, or people with peripheral fat obesity, as it has been reported in obese adults [8,9]. More importantly, these missing data would have given the researchers an opportunity to more closely link the autonomic dysfunction to the metabolic alteration, which is a hallmark of the central type of body fat depot, i.e., insulin resistance [7,8]. The second limitation refers to the fact that the neural alterations reported in the present study strictly refer to cardiac autonomic drive and not to the overall cardiovascular autonomic function.…”