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The relationship between the degree of obesity and the incidence of cardiovascular disease (CVD) was reexamined in the 5209 men and women of the original Framingham cohort. Recent observations of disease occurrence over 26 years indicate that obesity, measured by Metropolitan Relative Weight, was a significant independent predictor of CVD, particularly among women. Multiple logistic regression analyses showed that Metropolitan Relative Weight, or percentage of desirable weight, on initial examination predicted 26-year incidence of coronary disease (both angina and coronary disease other than angina), coronary death and congestive heart failure in men independent of age, cholesterol, systolic blood pressure, cigarettes, left ventricular hypertrophy and glucose intolerance. Relative weight in women was also positively and independently associated with coronary disease, stroke, congestive failure, and coronary and CVD death. These data further show that weight gain after the young adult years conveyed an increased risk of CVD in both sexes that could not be attributed either to the initial weight or the levels of the risk factors that may have resulted from weight gain. Intervention in obesity, in addition to the well established risk factors, appears to be an advisable goal in the primary prevention of CVD.
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PMID:Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. 621 30

Evidence is abundant supporting the premise that left ventricular hypertrophy in hypertension is related primarily to the hemodynamic factor of the increased left ventricular afterload associated with the disease. However, evidence is rapidly accumulating that additional, nonhemodynamic factors are associated not only with development of left ventricular hypertrophy but also with its regression that is related to antihypertensive therapy. Included among these mechanisms are humoral factors, including a variety of participating (or inhibited) circulating pressor mechanisms (e.g., angiotensin, catecholamines); sexual factors; aging; racial factors; and the role of obesity and coexisting diseases. Precisely how each factor is translated into the biochemical events associated with development of hypertrophy remains to be clarified, as do the explanatory mechanisms of why certain depressor agents produce regression of ventricular hypertrophy, whereas other agents with more salutary hemodynamic effects do not. This paper discusses the rationale and evidence underlying each of these factors.
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PMID:Hemodynamics and other determinants in development of left ventricular hypertrophy. 622 19

The left ventricle adapts to an increased afterload such as that produced by arterial hypertension with concentric left ventricular hypertrophy. However, this adaptive process can be modified by a variety of physiologic and pathophysiologic states. Progressive aging, black race, and perhaps disorders with an increased sympathetic outflow seem to accelerate left ventricular hypertrophy. Obesity and other high cardiac output states predominantly produce dilatation of the left ventricle, and their combination with arterial hypertension results in eccentric left ventricular hypertrophy. Similarly, endurance exercise increases left ventricular volume more than wall thickness, whereas isometric exercise produces an increase in wall thickness only. The presence or absence of some physiologic and pathogenetic factors has direct implication on the assessment of what constitutes a "normal" left ventricular structure and function. Left ventricular hypertrophy has been shown to increase ventricular ectopic impulse generation and to put patients at a high risk of sudden death. Moreover, the increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements. Thus, the presence of left ventricular hypertrophy has to be considered as an ominous sign rather than as a benign adaptive process.
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PMID:Clinical determinants and consequences of left ventricular hypertrophy. 622 96

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases sixfold to eightfold with the occurrence of LVH. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left ventricular filling and contractility. Hypertension, obesity, advanced age, valvular heart disease, and other pathologic disorders that cause an increase in the hemodynamic burden can lead to LVH. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.
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PMID:Left ventricular hypertrophy: a pressure-independent cardiovascular risk factor. 750 40

Obese subjects are at an increased risk of becoming hypertensive and vice versa. Essential hypertension and obesity are commonly accompanied by insulin resistance (defined as impaired insulin-mediated glucose disposal) and hyperinsulinaemia. In the offspring of patients with essential hypertension, insulin resistance and hyperinsulinaemia, as well as related increases in serum low density lipoproteins and triglycerides, often occur prior to the development of essential hypertension, overweight or central redistribution of body fat. Moreover, once obesity, and in particular central obesity, is present, insulin resistance is more marked in hypertensive than in normotensive obese subjects. Hyperinsulinaemia and/or insulin resistance in turn promote body fat deposition and impaired glucose tolerance. This cycle helps to explain why a familial predisposition to essential hypertension poses an increased risk of developing not only hypertension but also dyslipidaemia, obesity and non-insulin-dependent (type 2) diabetes. It is still unclear whether insulin resistance and/or hyperinsulinaemia also promote hypertension per se. Regardless of insulin's exact pathogenic role, obesity and/or a high dietary intake of carbohydrates, salt, etc. can induce several potential pressor mechanisms: 1) higher plasma noradrenaline (norepinephrine) and adrenaline (epinephrine) levels, suggesting a higher sympathetic tone in obese than in nonobese subjects, and in hypertensive obese than in normotensive obese subjects; 2) similarly, a tendency to hyperaldosteronism, with largely normal plasma renin activity, in obese hypertensive patients; 3) enhanced sensitivity of blood pressure to salt; 4) increased total blood volume (although it is normal relative to body surface area), leading to increased cardiac output and eventually eccentric left ventricular hypertrophy; and 5) increased cytosolic free Ca++ levels and reduced intracellular Mg++ levels in the blood cells of obese hypertensive patients and patients with non-insulin-dependent diabetes, although this finding cannot necessarily be extrapolated to cationic levels in vascular muscle cells. Total peripheral vascular resistance is usually low in normotensive obese subjects and rises with the development of hypertension; compared with lean patients with essential hypertension, obese hypertensive patients tend to have a slightly lower level of total peripheral vasoconstriction and a slightly higher cardiac output. Considering the intimate association between essential hypertension and obesity, as well as the prevalence and prognostic relevance of this combination, the spectrum of accompanying metabolic and cardiovascular abnormalities deserves careful consideration in the evaluation of therapeutic care for such patients.
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PMID:The pathogenesis of hypertension in obese subjects. 751 75

Hypertensive patients with left ventricular hypertrophy (LVH) have a higher degree of hyperinsulinaemia than hypertensive patients without LVH. Obese patients with LVH have also been demonstrated to have a very low glucose disappearance rate after an intravenous glucose bolus. No studies have investigated the difference in insulin action and substrate oxidation in hypertensive patients with and without LVH. For this reason 36 subjects were enrolled for our study: (1) healthy control subjects (n = 10); (2) hypertensive patients without LVH (n = 12); and (3) hypertensive patients with LVH (n = 14). All subjects underwent an oral glucose tolerance test (OGTT, 75 g of glucose) and a euglycaemic hyperinsulinaemic glucose clamp (insulin infusion rate, 7.1 pmol (kg min)-1 for 120 min). In this latter test indirect calorimetry allowed substrate oxidation determination. Echocardiographic methods allowed LVH assessment. Hypertensive patients with LVH had the lowest insulin-mediated nonoxidative glucose metabolism compared to hypertensive patients without LVH (P < 0.01) and to healthy subjects (P < 0.001). In the whole group of hypertensive patients (n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels (r = 0.44 P < 0.005), insulin-mediated whole body glucose disposal (r = -0.41 P < 0.01) and nonoxidative glucose metabolism (r = -0.33 P < 0.04) independently of age, body weight, systolic blood pressure and plasma catecholamines levels. In conclusion, our data provide evidence that LVH in hypertensive patients is associated with a worsening in nonoxidative glucose metabolism.
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PMID:Left ventricular hypertrophy is associated with a stronger impairment of non-oxidative glucose metabolism in hypertensive patients. 755 72

A follow-up study of hypertension was carried out among adults, in the age group between 25 to 64 years, in a rural population of Gurgaon district, Haryana, five years after an initial community based epidemiological survey of the same population. The progress of 77 out of 98 hypertensives detected at the initial survey could be reassessed. The treatment and severity of hypertension found at the initial survey has been compared with that observed on follow-up. The percentage of cases with blood pressure (BP) controlled on treatment increased from 2.6 percent to 45.4 percent on follow-up. An electrocardiogram could be obtained in 66 out of 77 subjects reexamined and was abnormal in 21 cases (31.8%). The electrocardiographic abnormalities found were: myocardial infarction in one, left ventricular hypertrophy in 5, left ventricular hypertrophy with ischaemic ST-T changes in 6, isolated ST-T abnormalities in 5 and conduction defects or arrhythmias in 4 cases. In a cohort of 1,334 subjects who were normotensive at the initial survey, 19 new cases were detected to have hypertension. The overall annual incidence of hypertension was 2.8/1000 (male: 3.8/1000 and female: 2.4/1000). In these hypertensives, a family history of hypertension was present in 10.5 percent and obesity in 42.1 percent.
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PMID:A 5-year follow-up study of hypertension in a rural community. 759 Aug 38

Patients with morbid obesity have high rates of sudden, unexpected cardiac death. The mechanism of death in these patients is uncertain. Twenty-eight patients with morbid obesity (22 sudden cardiac deaths, 6 unnatural deaths) were compared to 11 age-matched nonobese patients with traumatic deaths. Heart weight, left ventricular cavity diameter, left and right ventricular wall thickness, ventricular septal thickness, epicardial fat thickness, and extent of coronary artery atherosclerosis were determined; myocyte size, nuclear size, and degree of interstitial fibrosis were calculated morphometrically. Mean heart weights in the patients with morbid obesity were increased but remained constant as a percentage of body weight. Of the gross parameters, only heart weight and left ventricular cavity size were independent predictors of obesity. Of microscopic parameters, only nuclear area was an independent predictor of obesity. Of 22 patients with morbid obesity, dilated cardiomyopathy was the most frequent cause of sudden cardiac death in (10 patients), followed by severe coronary atherosclerosis (6), concentric left ventricular hypertrophy without left ventricular dilatation (4), pulmonary embolism (1), and hypoplastic coronary arteries (1). The cardiomyopathy of morbid obesity is characterized by cardiomegaly, left ventricular dilatation, and myocyte hypertrophy in the absence of interstitial fibrosis. It is the most common cause of sudden cardiac death in these patients.
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PMID:Sudden death as a result of heart disease in morbid obesity. 763 12

Left ventricular hypertrophy (LVH) is an early complication of hypertension. To a certain degree, this process counteracts the parietal stress induced by high blood pressure. Genetic factors, obesity, high salt diet and different growth factors, notably angiotensin II and noradrenaline, can also predispose to hypertrophic cardiomyopathy. Left ventricular mass is increased on echocardiography in about 20% of hypertensive subjects. LVH is initially associated with a change in myocardial diastolic function and later with abnormal systolic function. It is a major risk factor, a cause of cardiac failure, reduction in coronary reserve and of ventricular arrhythmias. Treatment of hypertension is associated with regression of LVH and preservation or improvement in myocardial diastolic and systolic functions. The decrease in left ventricular mass could reduce the incidence of cardiovascular complications in hypertension.
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PMID:[Physiopathology of left ventricular hypertrophy]. 764 13

The management of essential hypertension can no longer be directed toward an isolated reduction in arterial pressure. Optimal reduction in the risk factors associated with hypertension and cardiovascular disease hopefully will reduce coronary heart disease, angina, fatal and nonfatal myocardial infarction, left ventricular hypertrophy, congestive heart failure, and sudden death. Hypertension is a genetic and acquired syndrome that consists of dyslipidemia, insulin resistance and carbohydrate intolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and ion transport abnormalities (membranopathy). The selection of pharmacologic agents should improve the components of the hypertensive syndrome by utilizing the "subsets of hypertension approach" to treatment.
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PMID:The management of hypertension and associated risk factors for the prevention of long-term cardiac complications. 769 47


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