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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous electrocardiographic criteria, which are largely dependent on fixed voltage thresholds, have been proposed for the diagnosis of left ventricular hypertrophy (LVH). Electrocardiographic criteria for LVH were examined in 4,684 subjects of the Framingham Heart Study who underwent echocardiographic study for LVH. Echocardiographic LVH was detected in 290 men (14.2%) and 465 women (17.6%). Electrocardiographic features of LVH were present in 2.9% of men (60/2,042) and 1.5% of women (39/2,642). The overall sensitivity of the electrocardiographic diagnosis of LVH was 6.9%, whereas specificity was 98.8%. Sensitivity of the electrocardiogram (ECG) for LVH was marginally lower in women than in men (5.6% vs. 9.0%, p = 0.075). Obesity was inversely associated with sensitivity (p less than 0.05, both sexes combined, sex-adjusted). Smoking was also inversely related to sensitivity (p = 0.001, both sexes combined, sex-adjusted). In contrast, sensitivity of the ECG increased with age (p less than 0.001, both sexes combined, sex-adjusted). These findings suggest that electrocardiographic detection of LVH can be improved by incorporating information about noncardiac factors that impact on electrocardiographic sensitivity for LVH, presumably by attenuating QRS voltage. New strategies that take into consideration sex, age, smoking status, and obesity might improve the sensitivity of the ECG without diminishing specificity.
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PMID:Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. 213 31

A pattern of left ventricular hypertrophy evident on the electrocardiogram is a harbinger of morbidity and mortality from cardiovascular disease. Echocardiography permits the noninvasive determination of left ventricular mass and the examination of its role as a precursor of morbidity and mortality. We examined the relation of left ventricular mass to the incidence of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in 3220 subjects enrolled in the Framingham Heart Study who were 40 years of age or older and free of clinically apparent cardiovascular disease, in whom left ventricular mass was determined echocardiographically. During a four-year follow-up period, there were 208 incident cardiovascular events, 37 deaths from cardiovascular disease, and 124 deaths from all causes. Left ventricular mass, determined echocardiographically, was associated with all outcome events. This relation persisted after we adjusted for age, diastolic blood pressure, pulse pressure, treatment for hypertension, cigarette smoking, diabetes, obesity, the ratio of total cholesterol to high-density lipoprotein cholesterol, and electrocardiographic evidence of left ventricular hypertrophy. In men, the risk factor-adjusted relative risk of cardiovascular disease was 1.49 for each increment of 50 g per meter in left ventricular mass corrected for the subject's height (95 percent confidence interval, 1.20 to 1.85); in women, it was 1.57 (95 percent confidence interval, 1.20 to 2.04). Left ventricular mass (corrected for height) was also associated with the incidence of death from cardiovascular disease (relative risk, 1.73 [95 percent confidence interval, 1.19 to 2.52] in men and 2.12 [95 percent confidence interval, 1.28 to 3.49] in women). Left ventricular mass (corrected for height) was associated with death from all causes (relative risk, 1.49 [95 percent confidence interval, 1.14 to 1.94] in men and 2.01 [95 percent confidence interval, 1.44 to 2.81] in women). We conclude that the estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors. An increase in left ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease.
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PMID:Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. 214 5

To elucidate the impact of increased afterload during physical and mental stress on myocardial hypertrophy, a homogeneous population of 73 patients with untreated mild-to-moderate essential hypertension were enrolled in the current study. Left ventricular mass and cross-sectional area, both determined by 2-D guided M-mode echocardiography, were related to blood pressure measured at rest as well as during various stress situations. Left ventricular mass and cross-sectional area correlated with systolic pressure at work site (r = 0.28 and r = 0.23 respectively, P less than .05) and systolic pressure at complete rest (r = 0.35 and r = 0.33, P less than .01). Neither the response in blood pressure to mental arithmetic or a bicycle exercise test performed in the laboratory, nor blood pressure during both stress tests were significantly related to the degree of left ventricular hypertrophy. In addition, patients with a hyperreactive response to mental arithmetic or to the physical stress test did not disclose a greater left ventricular mass than normoreactors. Examining the hemodynamic response pattern during mental arithmetic, we found that patients with vasoconstriction during mental stress had a greater left ventricular mass than individuals with vasodilation during mental stress (244 +/- 73 v 204 +/- 53 g, P less than .05), but this was due to the impact of obesity on left ventricular mass (analysis of covariance: F = 2.1, P = NS). Thus, blood pressure at work site and at rest, but not blood pressure during mental or physical stress, nor the response of blood pressure to both stress tests, was linked to the degree of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of hemodynamic reaction during stress to left ventricular hypertrophy in essential hypertension. 214 Jun 89

Left ventricular hypertrophy (LVH) has been studied as a condition predisposing to cardiovascular disease over a 34 year period in the Framingham study. Whether present on the electrocardiogramme, chest X-ray or echocardiography, LVH is a harbinger of cardiovascular disease. It increases the risks of coronary artery disease, cardiac failure, cerebral haemorrhage and peripheral arterial disease. Its contribution to global cardiovascular risk is three times greater than that of hypertension which is the principal cause of LVH. Age, blood pressure and obesity are the three essential factors predisposing to LVH. Each contributes independently to the development of electrocardiographic hypertrophy (ECG-LVH). Increased left ventricular mass detected by echocardiography is commoner with age but apparently as the consequence of an increased prevalence of hypertension, obesity, coronary artery and valvular heart disease with age. The increase of left ventricular mass with age seems largely to be due to fatty hypertrophy and to hypertension. The risk associated with ECG-LVH is particularly important when St-T wave changes are associated with increased voltage. The outcome and prognosis of ECG-LVH and of silent myocardial infarction are similar. When overt coronary artery disease is present, ECG-LVH further increases the risk of cardiovascular events. Electrocardiographic LVH carries a worse prognosis than radiographic LVH which corresponds to anatomic hypertrophy. As the two forms of LVH contribute independantly to the cardiovascular risk, it is probable that they result from different physiopathological mechanisms.
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PMID:[Prognostic implications of left ventricular hypertrophy in arterial hypertension]. 215 Apr 70

Systolic or diastolic hypertension, cigarette smoking, diabetes mellitus, left ventricular hypertrophy, age, prior stroke, transient cerebral ischemic attack, extracranial arterial disease, and coronary heart disease are risk factors for the most common type of geriatric stroke, atherothrombotic brain infarction (ABI). Also, by contributing to hypertension and diabetes mellitus, obesity predisposes to ABI. The relationship of abnormal serum lipids and of physical inactivity to ABI is unclear. Antihypertensive treatment decreases the incidence of fatal and nonfatal stroke in patients with systolic and diastolic hypertension. Cessation of smoking also decreases risk.
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PMID:Risk factors for geriatric stroke: identification and follow-up. 220 86

Based on postmortem records at the Wayne County Medical Examiners' Office from 1982 to 1986, autopsy results indicated that the deaths of 129 persons aged 20-34 resulted from heart disease: 51 of these deaths were attributed to atherosclerotic cardiovascular disease (ASCVD), 29 to hypertensive cardiovascular disease, 28 to cardiomyopathy, and 21 to other cardiac causes. The majority of the deaths due to ASCVD occurred among men, both black and white, followed by black women, and the incidence increased with age. All of these deaths due to ASCVD were sudden and accounted for all deaths due to ischemic heart disease in this age group among Wayne County residents. Diabetes mellitus, left ventricular hypertrophy, a history of seizures, and the recent ingestion of alcohol were all found to be associated with sudden death from ASCVD in this group. Obesity did not seem to be a significant factor. These data suggest that ASCVD is not rare as a cause of death in young adults and some of the risk factors identified in older subjects also operate in this age group.
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PMID:Atherosclerotic cardiovascular disease and sudden deaths among young adults in Wayne County. 222 Jul 3

Joint studies of the ALIMDA and Society of Actuaries, notably those of 1935, 1959 and 1979, established that there is a progressive rise in cardiovascular mortality with successive increments in blood pressure. This has provided the basis of underwriting. The converse is not true, or at least has not been true until very recently. Drugs that effectively reduce blood pressure have been available for several decades, but reduction and maintenance of blood pressure is still accomplished in only a minority of hypertensives. Long-term trials employing a combination of drugs, i.e., diuretics, vasodilators and reserpine and subsequently beta-blockers, almost without fail have not shown that treatment with these agents significantly reduces heart disease mortality and sudden death. This has been attributed, perhaps without basis, to an unfavorable countering effect of increased lipid levels, aggravating this risk factor, and other undesirable metabolic effect of diuretics, such as hypokalemia and depletion of body magnesium, increasing the propensity to ventricular arrhythmias, hyperglycemia, worsening diabetes, and hyperuricemia. A survey of 674 persons with hypertension seen personally during the period 1985-89, who were under the care of approximately that many physicians, reveals striking changes in drug prescription and use during this brief period that portend a major change in the outlook of hypertension. Two classes of drugs have increased rapidly in popularity: these are the angiotensin-converting enzyme inhibitors (ACE inhibitors) and the calcium blockers. Both classes of drugs effectively lower blood pressure and have minimal side effects with good compliance. They act not only to reduce peripheral vascular resistance, but also locally in the heart muscle to directly cause left ventricular hypertrophy to regress, an effect of great consequence. The drugs used in former trials such as the vasodilators and diuretics have no effect on left ventricular hypertrophy, unlike the ACE inhibitors and calcium antagonists. Left ventricular hypertrophy is the key lesion in hypertension and is only in part due to increased work load imposed by elevated pressure. It is associated with elevated blood pressure, but not closely and occurs independently; ventricular myocytes as well as myocytes of the vasculature being stimulated to growth by angiotensin and calcium, potentiating the effect of norepinephrine. Left ventricular hypertrophy greatly increases the propensity to ventricular arrhythmias and sudden death, and is a prime cause of cardiac mortality and sudden death not only in hypertension, but also in obesity, aging and diabetes, in which conditions left ventricular hypertrophy also is very common.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Major new developments affecting treatment and prognosis in hypertension. 235 5

Obesity has been documented to be an independent risk factor for sudden death and other cardiovascular mortality. The present study was designed to monitor and quantify cardiac arrhythmias in obese subjects with and without eccentric left ventricular hypertrophy, who were matched with regard to arterial pressure, age, sex, and height with lean subjects. Prevalence of premature ventricular (but not atrial) contractions was 30 times higher in obese patients with eccentric left ventricular hypertrophy compared with lean subjects. Similarly, obese patients with left ventricular hypertrophy scored higher with regard to the classification of Lown and Wolf than those without left ventricular hypertrophy and lean subjects having the same level of arterial pressure. Patients' class in the Lown and Wolf system correlated with ventricular diastolic diameter and left ventricular mass. Thus, heart enlargement of the eccentric type as a consequence of obesity predisposes to excessive ventricular ectopy. Echocardiographic assessment and electrocardiographic monitoring allow us to identify the patients who are at highest risk of more serious arrhythmias or possibly sudden death and to subject them to the most specific preventive and therapeutic measures.
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PMID:Overweight and sudden death. Increased ventricular ectopy in cardiopathy of obesity. 244 73

For the characterization of the left-ventricular thickness of the wall, of the diameter and of the functional parameters in obesity in a short-term investigation on 18 extremely adipose female normotonics and 17 normotonics with normal weight the echocardiographic investigation in the M-mode in the short parasternal axis was performed. The women with overweight had a by 28% (p less than 0.001) greater fractional shortening, a by 8% (p less than 0.01) greater ejection fraction, a by 23% (p less than 0.05) greater stroke volume and a by 34% (p less than 0.001) greater cardiac output as well as a by 13% smaller left-ventricular end-systolic volume than normotonic women with normal weight. Index of stroke volume and cardiac output did not differ. The women with overweight had a significantly larger left-ventricular end-diastolic diameter and a thicker interventricular septum as well as a larger thickness of the left-ventricular posterior wall in the systole. The results allowed the conclusion that changed left-ventricular parameters both with regard to the form and to the function in obesity per se might be the expression of the physiological adaptation to an increased requirement and the borderlines to the transition into a disturbed left-ventricular function and development of a left-ventricular hypertrophy were not fixed. Long-term studies should bring further explanation concerning these problems.
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PMID:[The relation of anthropometric parameters and echocardiography findings in the evaluation of left ventricular form and function in extreme obesity]. 252 19

The effect of obesity and weight reduction upon circulating concentrations of atrial natriuretic peptide was assessed in an experimental model of the disease. Obese rats weighing in excess of 750 g were compared with formerly obese animals subjected to a 15-week period of caloric restriction resulting in a 40% reduction in body weight. Mean adipocyte size was significantly reduced with weight loss, as was estimated body fat. Mean arterial blood pressure remained normotensive for both groups, but a significant reduction in heart rate was associated with weight reduction. Circulating atrial natriuretic peptide was significantly elevated in the lean rats, which also exhibited decreased plasma renin activity and a negative sodium balance. Analysis of heart to body weight ratios implied that an obesity-associated, volume-induced cardiac hypertrophy remained even after the normalization of body fat. These results suggest that the diuresis and natriuresis accompanying weight reduction may be facilitated by atrial natriuretic peptide, which was elevated in part due to a persistent left ventricular hypertrophy following the transition from the obese to lean condition.
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PMID:Effect of experimental obesity and subsequent weight reduction upon circulating atrial natriuretic peptide. 252 48


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