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This study has been designed to evaluate whether duration and severity of obesity can influence left ventricular function response to exercise in obese subjects without other known cardiovascular risk factors such as hypertension, diabetes or hyperlipoproteinemia. A total of 29 obese subjects were included and they were divided, according to their body mass index and to Garrow's criteria as follows: Overweight or mildly obese subjects: body mass index from 25 to 30 kg/m2; moderately obese subjects: body mass index30 and40 kg/m2. Both obese groups were further subdivided according to their duration of obesity evaluated by accurate anamnesis in subgroup A (duration of obesity less than 120 months) and subgroup B (duration of obesity more than 120 months). Left ventricular ejection fraction was detected by blood pool gated radionuclide angiocardiography both at rest and after symptom-limited bicycle ergometer procedure. At peak exercise left ventricular ejection fraction increased significantly (p0.05) only in overweight subjects. Exercise produced an increase of left ventricular ejection fraction in 14 overweight and in 5 moderately obese subjects and a decrease in 2 moderately obese subjects. At peak exercise mean heart rate and mean blood pressure increased significantly (p0.001) in both groups. When obese subjects were subgrouped according to duration of obesity, left ventricular ejection fraction increased significantly (p0.05) only in overweight subjects with duration of obesity less than 120 months. Duration of obesity correlated inversely with percent change in left ventricular ejection fraction (EF) at peak exercise (delta EF) (r = -0.59; p0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Letter to Editor

Obesity and overweight have great clinical and social significance and are associated with a number of medical and surgical complications. We attempt here to summarize current knowledge on the subject and describe the research we are presently carrying out in this field. After a brief introduction, definition, and discussion of etiopathogenesis, the indexes of ponderal excess and epidemiology are illustrated. The cardiovascular adjustments and the relationships between obesity and hypertension, ischemic heart disease and congestive heart failure are then treated. One aim of our investigation was to study the modifications of an entire set of biological and clinical parameters which could concretely formulate and/or identify some pathophysiological links between obesity and heart disease. We thus studied obese subjects with hypertension, diabetes and multiple cardiovascular risk factors. We also studied a group of asymptomatic obese subjects, whom we define as "the healthy obese". Our results, supported by the medical literature, led to the conclusion that obesity is an important and/or independent cardiovascular risk factor. We think, however, that it would be prudent to await for the results of interventional trials and follow-up studies involving a large number of young, healthy obese subjects in order to monitor the most important biological variables over the long term.

The metabolic syndrome (MS) is a common metabolic disorder that has been recently related to the increasing prevalence of obesity. The disorder is defined in various ways, but in the near future a new definition(s) will be applicable worldwide. The pathophysiology has been largely attributed, in the past years, to insulin-resistance, even if several epidemiological and pathophysiological data are attractive to indicate visceral obesity as a main factor in the occurrence of the MS, promoting new definitions and re-valuation of the pathogenesis of this syndrome. In this review, we have analyzed the role of visceral obesity in the new definition of the MS such as the pathophysiological role of the abnormal fat distribution in the occurrence of this syndrome. In view of this, relationships between visceral obesity, free fatty acids, dyslipidaemia and insulin-resistance have been reported. In addition, the effects of some adipocytokines and other proinflammatory factors produced by fat accumulation on the appearance of the MS have been also emphasized. Finally, according to recommendations of several international societies, the role of the life-style change and of the weight loss in the prevention and treatment both of obesity and of other associated risk factors has been analyzed.

Several studies have shown a significant association of obesity with cardiovascular morbidity and mortality. The present study was carried out to investigate central and systemic haemodynamics in overweight and moderate obese, but otherwise healthy subjects, and in a lean control group to determine whether obesity can influence left ventricular performance per se. In this study an attempt has been made to eliminate misleading factors, such as diabetes, lipid abnormalities and hypertension. A total of 67 subjects, 44 with overweight or moderate obesity and 23 lean healthy subjects, were included. Patients were divided into three groups according to BMI levels and Garrow's criteria as follows: lean control group (BMI less than 25 kg/m2); overweight (BMI from 25 to 30 kg/m2); moderate obese (BMI greater than 30 less than 40 kg/m2). Overweight and moderate obese subjects were further subgrouped according to duration of obesity (DO) in subgroup A (DO less than 98 months) and in subgroup B (DO greater than 98 months). Haemodynamic assessment was performed using first pass radionuclide angiocardiography. When compared with lean subjects, overweight and moderate obese subjects were characterized by a significant increase in cardiac output (CO), stroke volume (SV), end diastolic volume (EDV), end systolic volume (ESV), total blood volume (TBV) and total plasma volume (TPV) and by a significant decrease in left ventricular ejection fraction (EF); some of these changes appeared to be related to the degree of obesity. In overweight and moderate obese subjects, total peripheral resistance (TPR) was lower than in lean controls, but this difference was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension and obesity are associated with an increased risk of clinical cardiovascular complications due to atherosclerosis. Moreover has been reported that hypertension may predispose to atheroma development. In the present review some common aspects to hypertension and atherosclerosis including smooth muscle cell proliferation, endothelial damage and intervention of growth factors have been analyzed. Additional data have to be provided to explain if the connections between hypertension and atherosclerosis could be considered two effects with one unknown cause. In addition some aspects related to obesity and atherosclerosis have been dissected. In particular we have reported our results indicating that young obese subjects without risk factors for cardiovascular disease have already several markers of cardiovascular damage i.e. atherogenetic lipid pattern, pro-thrombotic and hypofibrinolitic pattern without sign of coagulation and/or platelet in vivo activation, increased plasma endothelin and catecholamine values, rised fasting and after OGTT insulin levels. In view of this more extensively data have to be necessary to support the opinion that obesity and atherosclerosis could be two associated conditions evolving during the time to develop cardiovascular disease or events.