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Query: UMLS:C0028754 (obesity)
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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 six- to eightfold with the presence 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 disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.
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PMID:Left ventricular hypertrophy: an independent risk factor. 172 10

Left ventricular hypertrophy (LVH) is one of the less common but ominous risk factors for coronary disease, stroke and cardiac failure. The chief determinants of LVH, aside from age, are elevated blood pressure, obesity, stature and glucose intolerance. Cardiac valve disease and chronic heart disease (CHD) also cause LVH. Downward trends in the prevalence of LVH over four decades indicate that LVH is preventable, and this has coincided with improved hypertension control. When evidence of LVH disappears, the risk of all-cause, cardiovascular and CHD mortality is substantially reduced. Cardiovascular events occur incrementally in relation to left ventricular mass with no discernible critical value identifying pathological hypertrophy. LVH as evidenced by electrocardiogram (ECG-LVH), manifested by repolarization abnormality as well as increased voltage, was a lethal finding; with 5 years, 33% of men and 21% of women were dead. ECG-LVH was associated with ventricular ectopy and a sudden death risk comparable to that of CHD or cardiac failure. ECG-LVH was associated with a 3-15-fold increase of cardiovascular events with greatest risk ratios for cardiac failure and stroke. However, CHD is the predominant clinical sequel. No other risk factor approaches LVH in potency. Anatomical (echocardiographic or X-ray) LVH and ECG-LVH each independently contribute to the risk of cardiovascular disease, and having both confers a greater risk than having either alone. LVH is a clinical finding which should be taken seriously and corrected as soon as detected. It should not be regarded as an innocuous adaptive process, augmenting cardiac function.
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PMID:Left ventricular hypertrophy as a risk factor: the Framingham experience. 183 65

Evaluation without catheterization of patients with valvular heart disease implies that diagnosis based upon non-invasive techniques alone are qualitatively and quantitatively correct. The diagnosis should indicate not only the valvular lesion in question but should give information about associated conditions that could influence management decisions (whether to operate or not or whether to modify the intended operation). A review of the literature shows that in mitral stenosis (MS), both pressure gradient and valve area can be obtained non-invasively (rest/exercise). These data, combined with the ultrasound appearance of the valve, subvalvular apparatus, chamber sizes, assessment of associated regurgitation and eventual pulmonary hypertension, permit a complete evaluation of the MS patient. Thus, it can be concluded that in experienced hands, the large majority of patients with MS can be assessed reliably non-invasively for clinical screening and for valve surgery. Excluding those in whom coronary angiography is mandatory, cardiac catheterization should be required only infrequently (in less than 10%). Cardiac catheterization should, however, be carried out in patients in whom technical reasons make ultrasound examinations incomplete (obesity or respiratory disease), and in patients in whom there is a discrepancy between the physical signs and the Doppler ultrasound.
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PMID:Does mitral stenosis need invasive investigation? 193 32

In 85 patients (22 with myocardial infarct and 63 with valvular heart disease) echocardiographical examination simultaneously by classical and transesophageal methods was done. The transesophageal method was better in assessing the aortic valve and similar to the classical method in reference to the mitral valve. Heart contractility assessment was better with the classical method. Transesophageal echocardiography is the method of choice in patients in whom classical echocardiography cannot be done (obesity, emphysema, chest deformation).
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PMID:[Transesophageal and classical echocardiography in myocardial infarction and heart valve disease (comparison study)]. 194 59

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

Early detection of heart failure requires criteria by which to define the initial stages of a syndrome which often has an insidious onset and which may progress slowly for many years. The most specific definitions of heart failure are those obtained towards the end of the disease process, but reliance upon these means that, although few cases are misclassified, only manifest cases can be detected. Since prevention is the ultimate goal, early detection of subjects at risk and a wider understanding of the pathophysiological mechanisms and risk factors are necessary. The principal causes of heart failure in the Western world are coronary artery disease and hypertension; valvular heart disease and other cardiac disorders are relatively uncommon causes. The major risk factors are obesity, tobacco smoking and diabetes mellitus, and in a prospective large-scale study we have also shown that individuals who develop manifest symptoms of heart failure often have a long history of exercise-induced dyspnoea. Clearly, identification of the early symptoms of heart failure and prompt treatment of risk factors such as hypertension and obesity are important objectives. However, a better understanding of the underlying biochemical and structural abnormalities would help to define more appropriate preventive treatments.
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PMID:Improving the detection and diagnosis of congestive heart failure. 280 86

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

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

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. 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. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. 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:Hypertension and left-ventricular hypertrophy. 856 18

In an effort to combat obesity, several medications have been developed. The nonamphetamine anorectics, such as phentermine, fenfluramine, and dexfenfluramine, have been recommended as first-line drug therapy for the treatment of obesity once diet and exercise alone have failed. Numerous studies have shown that these agents can promote weight loss when combined with diet restriction and exercise. Although fenfluramine and dexfenfluramine lack the abuse potential of amphetamine and its congeners, these agents are associated with drug interactions and adverse effects. Concomitant administration of fenfluramine or dexfenfluramine with medications that enhance serotonin levels (e.g., antidepressants, monoamine oxidase inhibitors, and migraine medications) can precipitate serotonin syndrome. Sudden discontinuation of fenfluramine or dexfenfluramine after prolonged administration can precipitate withdrawal depressive symptoms. Primary pulmonary hypertension, a potentially fatal disorder, has been reported to occur approximately 30 times more frequently in patients receiving anorectic agents for more than 3 months compared to the general population. More recently, the association of these popular anorectics with valvular heart disease has caused increased concerns about their use. The risks of primary pulmonary hypertension, valvular heart disease, and the occurrence of convulsions, coma, and death in overdose appear to be equally likely with dexfenfluramine and fenfluramine. In addition, many patients who lose weight while taking these anorectics rapidly regain it after the medication has been discontinued.
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PMID:A close look at fenfluramine and dexfenfluramine. 954 1


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