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Query: UMLS:C0028754 (obesity)
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Left ventricular hypertrophy (LVH) has assumed an important role in clinical medicine as a result of the clinical implications of this often asymptomatic finding. Epidemiological data from the Framingham Heart Study have permitted an examination of prevalence, incidence, underlying predisposing factors and prognosis of LVH. Although LVH is an infrequent finding on the electrocardiogram, it is a forerunner of coronary disease, congestive heart failure, stroke and even peripheral arterial disease. Despite being strongly related to hypertension, LVH remains associated with excess risk for adverse cardiovascular morbid and fatal outcomes, even after adjusting for blood pressure. The risks associated with LVH are comparable with those of myocardial infarction. The recent introduction of echocardiography at the Framingham Heart Study has permitted the development of new criteria for LVH based on M-mode determined left ventricular mass. Unlike its electrocardiographic counterpart, echocardiographically determined LVH is a common finding, occurring in over 15% of the general population. Echocardiographic LVH is related to hypertension, obesity, valvular heart disease, coronary disease and advancing age. Ambulatory ECG results in subjects with echocardiographic LVH demonstrate increased risk for ventricular arrhythmias, which have been shown in other clinical settings to predict risk for sudden cardiac death. Preliminary data from Framingham and elsewhere suggest that echocardiographic LVH is associated with increased risk for cardiovascular disease morbidity and all-cause mortality.
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PMID:Left ventricular hypertrophy. Epidemiological insights from the Framingham Heart Study. 297 14

Obesity and hypertension are two major risk factors for the cardiovascular system. Whereas arterial hypertension increases afterload to the left ventricle, obesity produces an increase in stroke volume and increases preload. As a result of this double burden, the heart adapts with eccentric left ventricular hypertrophy. Contractility becomes impaired early in the course of obesity hypertension, and ventricular ectopy is observed. As a consequence, the obese hypertensive patient is at a high risk for congestive heart failure and sudden death. Despite the synergistic effects of obesity and hypertension on the heart, patients appear to be relatively protected from nephrosclerosis and coronary artery disease. These epidemiologic observations are supported by the pathophysiologic changes that take place in obesity hypertension. At any given level of arterial pressure, cardiac output and renal blood flow are elevated in obese hypertensive patients, whereas systemic and renal vascular resistance are decreased when compared to lean hypertensive patients. Because total peripheral resistance is considered the hemodynamic hallmark of arterial hypertension, systemic vascular complications may be less pronounced in obesity hypertension. Weight loss decreases preload, afterload to the left ventricle, and the sympathetic drive to the heart. Protecting the heart from these hypertrophic stimuli should be a major goal of preventive cardiology.
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PMID:Obesity hypertension. 330 13

Quantitative electrocardiographic (ECG) and vectorcardiographic (VCG) analysis was carried out in 113 newly diagnosed, middle-aged, non-insulin-dependent diabetics (61 men, 52 women) and 125 non-diabetic control subjects (56 men, 69 women) in order to explore changes attributable to non-coronary heart disease (diabetic cardiomyopathy) in diabetics. Diabetic men had a prolonged PQ interval and women a more negative P-terminal force and a more leftward frontal QRS axis than their non-diabetic counterparts, but no other significant differences we found between diabetic and non-diabetic subjects in various quantitative ECG and VCG variables when the effect of confounding factors (age, obesity, coronary heart disease, hypertension, drugs) was taken into account. The more negative P-terminal force and left axis deviation in diabetic women could be explained by a concomitant left ventricular hypertrophy among them. Non-insulin-dependent (type 2) diabetes, which is commonly preceded by a long duration of asymptomatic hyperglycaemia, is not associated, early in its clinical course, with major ECG and VCG abnormalities suggestive of diabetic cardiomyopathy.
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PMID:Quantitative electrocardiographic and vectorcardiographic study on newly-diagnosed non-insulin-dependent diabetic and non-diabetic control subjects. 334 19

Although cardiovascular disease remains the leading cause of death in the United States, its incidence has decreased steadily during the past 20 years. This trend is largely attributable to improved detection and management of cardiovascular risk factors. The pioneering work of the Framingham Heart Study, which has followed subjects since the late 1940s, has helped shed light on the risks conferred by factors such as advancing age, hypertension, smoking, elevated serum cholesterol, diabetes, left ventricular hypertrophy, and obesity. As a result of this ongoing investigation, clinicians have gained a better understanding of the ways in which cardiovascular risks can be modified so that mortality rates will hopefully continue to decline.
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PMID:Cardiovascular risks: new insights from Framingham. 339 38

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

The relationship of blood pressure to fasting and postglucose serum insulin and lipid levels was examined in 133 (70 men, 63 women) newly diagnosed, non-insulin-dependent diabetic patients and 144 (62 men, 82 women) non-diabetic control subjects. In addition, the frequency of left ventricular hypertrophy by ECG criteria and left ventricular mass determined by M-mode echocardiography in diabetic patients were compared to that in non-diabetic subjects. Fasting serum insulin showed a significant correlation with systolic and diastolic blood pressure levels in male non-diabetic subjects, but not in male and female diabetic or in female non-diabetic subjects. Postglucose serum insulin levels showed no significant correlations with systolic or diastolic blood pressure levels in men, but in female diabetic and non-diabetic subjects significant correlations were found in particular with systolic blood pressure level. The correlations between serum insulin and blood pressure levels could not be accounted for by obesity. In male and female diabetic subjects serum triglycerides correlated positively with systolic and diastolic blood pressure levels even after adjustment for obesity. No significant difference was found in the prevalence of left ventricular hypertrophy based on ECG criteria between diabetic and non-diabetic subjects, but female diabetic subjects showed in echocardiography an increased left ventricular mass related to body surface area compared to their non-diabetic counterparts. Elevated systolic blood pressure and high postglucose serum insulin levels showed an independent, significant association with left ventricular mass in female diabetic subjects.
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PMID:Relationship of blood pressure and left ventricular mass to serum insulin levels in newly diagnosed non-insulin-dependent (type 2) diabetic patients and in non-diabetic subjects. 355 63

Most hypertensive subjects are overweight, and as a consequence have an increased prevalence of hypercholesterolaemia, impaired glucose tolerance, and left ventricular hypertrophy. Reduction of the blood pressure by antihypertensive drugs without control of the obesity leaves these additional risk factors for cardiovascular disease uncorrected. Weight reduction has a substantial and sustained antihypertensive effect, removes or reduces the need for drug treatment, corrects the associated risk factors, and is clearly the more rational approach to management.
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PMID:Obesity and hypertension. 369 50

The heart may play an active, passive, or incidental role in the pathogenesis of hypertension. Echocardiography probably contributes little to understanding of active mechanisms, although it may provide important information relative to structural and functional adaptive changes associated with development of left ventricular hypertrophy. Moreover, because other clinical conditions frequently coexist with hypertensive heart disease, echocardiography may provide another dimension in the assessment of obesity, coronary heart disease, mitral valve prolapse, idiopathic hypertrophic subaortic stenosis, and asymmetric septal hypertrophy in the overall problem. Critical in this understanding are the subtle changes that occur in the individual patient, reflecting the natural history of the disease or response to its treatment. Since technical problems preclude echocardiographic evaluation in all patients with hypertension, particular care must be exercised in making epidemiologic generalizations.
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PMID:Future directions in the use of echocardiography. 380 1

The studied group comprised 82 children with simple obesity. In the group the character and frequency of ECG changes in 12 conventional leads were analyzed. A correlation was established between the character and frequency of these changes and the degree of overweight and obesity duration. In children with simple obesity a considerable prevalence was observed of disturbances of sinus rhythm, impairment of intraventricular conduction and signs of left ventricular hypertrophy. The observed changes were more frequent in children with over 5 years of obesity duration. No correlation was demonstrated between the incidence of these changes and the degree of overweight.
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PMID:Assessment of the character and incidence of electrocardiographic changes in children with simple obesity. 383 6

Hypoxia is the major cause of pulmonary hypertension and right ventricular hypertrophy in chronic obstructive pulmonary disease, cystic fibrosis, kyphoscoliosis, chronic mountain sickness, and the obesity-hypoventilation and sleep apnea syndromes. Pulmonary hypertension develops in these patients because the long-standing vasoconstriction produced by hypoxia causes muscular hypertrophy of the pulmonary arteries and arterioles. These pathologic changes may regress if alveolar hypoxia is corrected and hypoxic pulmonary vasoconstriction is continuously inhibited. Intermittent inhibition of hypoxic pulmonary vasoconstriction does not reverse these pathologic changes. Since patient noncompliance with oxygen therapy makes it difficult to achieve continual relief of alveolar hypoxia, a drug that inhibits hypoxic vasoconstriction may be useful. Experimental findings indicate that hypoxic pulmonary vasoconstriction requires calcium influx and can be inhibited by certain slow-channel calcium blockers. Studies also demonstrate that slow-channel calcium antagonists can attenuate the pulmonary hypertension and right ventricular hypertrophy produced in rats by chronic hypoxia. Recently, two studies have shown that nifedipine inhibits hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. If further studies demonstrate that these short-term effects are sustained, certain slow-channel calcium blockers may become a useful adjuvant to low-flow oxygen therapy in the treatment of hypoxic pulmonary hypertension.
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PMID:Calcium channel blockers in hypoxic pulmonary hypertension. 397 91


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