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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to elaborate criteria for the assessment of the severity of pulmonary hypertension and cor pulmonale in patients with chronic bronchitis and to give rationale for expert medical evaluation of the working capacity of such patients. 94 patients (89 males and 5 females) aged 20 to 60 with chronic bronchitis were examined. Basing on the clinical, x-ray, ECG, VCG and echocardiography data, the gravity of cor pulmonale was assessed by the degree of right ventricular hypertrophy (absent, mild, marked, dramatically marked), changes in the right ventricular echo dimensions and the stage of heart failure, and by the lung vital capacity (in percent of the predicted value). The rationale for expert medical evaluation of patients with associated cor pulmonale and chronic bronchitis is described.
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PMID:[The medical disability evaluation of patients with pulmonary hypertension and cor pulmonale]. 182 62

Epidemiologic studies have revealed that in arterial hypertension left ventricular hypertrophy is an important risk factor for cardiac failure. Accordingly antihypertensive therapy should aim at preventing or regressing left ventricular hypertrophy. Reduction of blood pressure does not necessarily induce reversal of left ventricular hypertrophy. Vasodilators like hydralazine and minoxidil, which lead to augmented plasma levels of norepinephrine, were not able to diminish left ventricular hypertrophy. In contrast, a sympatholytic therapy with methyldopa caused a reversal of left ventricular muscle mass. These experimental findings in spontaneously hypertensive rats led to the hypothesis that catecholamines control the onset and progression of myocardial hypertrophy mostly independent of blood pressure. This hypothesis was supported by the experimental findings, that subhypertensive dosages of norepinephrine induce left ventricular hypertrophy and that this hormone promotes alpha-receptor mediated growth of isolated myocytes. Recent studies have revealed that also the renin-angiotension-system has trophic effect on the myocardium. Clinical investigations have documented regression of cardiac hypertrophy due to antihypertensive therapy with sympatholytic drugs, ACE-inhibitors, calcium-channel blockers and beta-receptor blockers. Diuretics failed to decrease left ventricular muscle mass along with blood pressure normalization.
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PMID:[ACE inhibition: mechanisms of cardioprotection in heart hypertrophy]. 183 Sep 11

Among dialysis patients, only 23% have a normal echocardiogram, about 10% have recurrent or chronic congestive heart failure, and 17% have asymptomatic ischemic heart disease. The predisposing factors for congestive heart failure are dilated cardiomyopathy, hypertrophic hyperkinetic disease, and ischemic heart disease. Dilated cardiomyopathy, a disorder of systolic function, includes among its risk factors age, hyperparathyroidism, and smoking. Hypertrophic disease results in diastolic dysfunction, and its predictors include age, hypertension, aluminum accumulation, anemia, and, perhaps, hyperparathyroidism. Ischemic heart disease is due to the presence of coronary artery disease and also to nonatherosclerotic disease caused by the reduction in coronary vasodilator reserve and altered myocardial oxygen delivery and use. The clinical outcome of congestive heart failure is comparable to that of nonrenal patients with medically refractory heart failure. Left ventricular hypertrophy is an important independent determinant of survival. A subset have hyperkinetic disease with severe hypertrophy and have a bad survival, as low as 43% have a 2-yr survival after the first admission to hospital with cardiac failure. The prognosis for those with dilated cardiomyopathy is less severe but is worse than those with normal echocardiogram. The survival of patients with symptomatic ischemic heart disease was little different from that of patients without symptoms, suggesting that the underlying cardiomyopathies had an adverse impact on survival independent of ischemic disease. Much research needs to be undertaken on the risk factors, natural history, and therapy of the various types of cardiac disease prevalent in dialysis patients.
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PMID:The natural history of myocardial disease in dialysis patients. 183 84

In heart failure, many alterations occur in the ventricle as a whole, as well as in the myocardial cell. In the first part of this review we report on the macroscopic structure of the left ventricle by analysing the relation between left ventricular dilatation and left ventricular hypertrophy in terms of ventricular wall stress. Peak systolic stress in dilated ventricles of patients with compensated heart failure does not differ from values obtained in normal ventricles, whereas the systolic stress-time integral is increased by more than 40%. The stress-time integral is a major determinant of myocardial oxygen consumption, and its reduction by peripheral vasodilation leads to a proportional decrease in left ventricular oxygen consumption. In contrast, the phosphodiesterase inhibitor, enoximone, decreases the stress-time integral without a proportional decrease in myocardial oxygen consumption, due to the competition between positive inotropic effect with increased oxygen consumption and a vasodilating effect with decreased oxygen consumption. Beta-1 adrenoceptor agonists increase myocardial oxygen consumption. In the second part of this review we report on the functional alterations of the following subcellular and molecular structures in the failing myocardium: (1) adrenoceptors and G-proteins; (2) sarcoplasmic reticulum with an altered force-frequency relationship; (3) the acto-myosin system with decreased velocity of shortening and increased economy of force generation. On the basis of these alterations, a disadvantageous chain of events develops in the failing myocardial cell.
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PMID:The heart in heart failure. Ventricular and myocardial alterations. 183 95

The progression of cardiac hypertrophy and failure is associated with marked changes in cardiac autonomic innervation, and there are sympathetic-parasympathetic interactions in the regulation of cardiac function. Although the indexes of sympathetic innervation have been found to be depressed with the development of heart failure, those of parasympathetic innervation have not yet been fully investigated. In order to better understand changes in markers of autonomic innervation associated with cardiac hypertrophy and failure, we measured the myocardial acetylcholine (ACh) store as a parasympathetic marker and the norepinephrine (NE) store as a sympathetic marker in pressure-overloaded right ventricular hypertrophy in rats. Two weeks after the injection of monocrotaline, significant right ventricular hypertrophy occurred. Three weeks after, severe right ventricular hypertrophy with no sign of heart failure occurred, and 4 weeks after, overt heart failure developed. In the right heart of monocrotaline rats, NE concentrations tended to increase at 1 week, returned to baseline at 2 weeks, decreased to one-half of the control values at 3 weeks, and then fell to 14% of the controls at 4 weeks. ACh concentrations in the right heart tended to increase at 1 week and exhibited a significant increase (136% and 129% of the controls in the right atrium and ventricle, respectively) at 2 weeks. As with NE, ACh concentrations in the right atrium and ventricle decreased to 76% and 54% of the controls at 3 weeks, and continued to decrease to 22% and 24% of the controls at 4 weeks after monocrotaline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered myocardial acetylcholine and norepinephrine concentrations in right ventricular hypertrophy and failure. 183 70

Left ventricular hypertrophy may be considered the result of an interaction of a myriad of factors, including hemodynamic overload; age, race, and gender of the patient; the stage of hypertensive disease; and other coexisting diseases. This concept is similar to the multifactorial "mosaic of hypertension" described by Page. In addition, the increased left ventricular mass in hypertension may reflect the disposition of collagen tissue and the participation of a myriad of myocytic growth factors, as well as drug therapy. The resultant left ventricular hypertrophy confers increased cardiovascular risk that is independent of the height of arterial pressure. The mechanisms that account for that risk are not yet well understood but include reduced adaptive myocardial reserve, enhanced predisposition to cardiac dysrhythmias and cardiac failure, accelerated atherosclerosis, and reduced (absolute and relative) coronary flow and flow reserve, as well as other possibilities. At present much work is directed to the demonstration of pharmacological reversal of hypertrophy. However, even with that demonstration of reduced cardiac mass with therapy, it will be necessary to show improved risk at the reduced mass that is independent of the reduction of arterial pressure as well as of the effects of those drugs on cardiac rhythm, flow, metabolism, and direct effects on the cardiac myocyte itself.
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PMID:The heart in hypertension: a 1991 overview. 183 56

Left ventricular hypertrophy in arterial hypertension occurs in over 50% of patients. The detection of such high incidence has been facilitated by the introduction of echocardiography into diagnostic studies. Both earlier electrocardiographic findings and later echocardiographic results show that cardiac hypertrophy leads to an increased mortality and predisposes to cardiac arrhythmias, ischemic heart disease including myocardial infarction and heart failure. The development of hypertrophy is mediated by hemodynamic factors such as elevated blood pressure due to increased peripheral vascular resistance, ejection fraction, increased cardiac output, blood viscosity, as well as by non-hemodynamic factors. Of the latter ones the contribution of a genetic factor is discussed, whereas the role of para- and autocrine cardiac function manifested by local production and action of catecholamines as well as the renin-angiotensin system has been proved. Blockade of these systems makes possible prevention of the development of cardiac hypertrophy or its regression. Such results have been obtained both in experimental studies and in humans with hypertension treated with selected drugs. Regression of hypertrophy is accompanied by an improvement in systolic and especially diastolic cardiac function, the impairment of which is usually diagnosed prior to the detection of hypertrophy. The improvement in cardiac function and possibility of preventing consequences of hypertrophy help us to evaluate the efficacy of hypotensive drugs and their preferential use in this regard. There are also changes in recently recommended models of pharmacological treatment in arterial hypertension.
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PMID:[Hypertrophy and function of the left heart ventricle in hypertension]. 183 84

The pathogenesis of essential hypertension may possibly involve a deficiency in, or a decreased response to, endogenous vasodilator and natriuretic factor(s). Searching for hereditary or familial defects, it is plausible to evaluate blood pressure (BP) regulating factors in (yet) normotensive offspring of hypertensive parents (OHyp), some of whom are in fact in a stage of prehypertension. Studies by our group demonstrated that compared with healthy offspring of normotensive parents, OHyp have plasma atrial natriuretic (ANF) factor levels that are unaltered on a low salt intake but often fail to increase normally in response to a high salt intake. Plasma levels of cyclic GMP, the presumed second messenger of ANF, also may tend to be decreased in certain OHyp. On the other hand, renal excretory responses of cyclic GMP and electrolytes to ANF infused in "physiological" dose were unchanged in some OHyp tested so far. In borderline to moderate, uncomplicated essential hypertension, plasma ANF levels are often "normal." This may be inappropriately low relative to the existing BP, although the relationship of circulating ANF to atrial pressures in essential hypertension remains to be clarified. A conversion to higher plasma ANF values may occur with cardiac complications such as left ventricular hypertrophy, enlargement, dysfunction, or overt heart failure. Acute or short-term elevation of circulating ANF within the physiological and pathophysiological range by ANF infusion produces an exaggerated natriuresis and lowers BP in essential hypertensive patients. We postulate a syndrome of ANF deficiency, characterized by an impaired response of circulating ANF to high salt intake and by low cyclic GMP levels in certain yet normotensive offspring of essential hypertensive parents and by inappropriately "normal" plasma ANF in some patients with uncomplicated essential hypertension. At the stage of prehypertension, a disturbance in the ANF - cyclic GMP pathway may be expressed primarily at the circulatory rather than at the renal level. Hypertension-prone humans also tend to have an exaggerated vascular reactivity to norepinephrine. Whether the two disturbances may be interrelated is presently unknown. Both defects may potentially predispose to the development of essential hypertension. Relative ANF deficiency, an enhanced natriuretic response to ANF, and a sustained antihypertensive effect of infused ANF may represent a rational basis for treatment of essential hypertension with agents that activate the ANF system.
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PMID:Developing essential hypertension: a syndrome involving ANF deficiency? 183 26

The effect of left-ventricular afterload on cardiac performance was investigated in normotensive Wistar rats and in spontaneously hypertensive rats (10 months old) with a left-ventricular hypertrophy of 54%. The measurements were performed on a modified heart-lung preparation in which left-ventricular afterload could be adjusted arbitrarily. In the heart in situ, left-ventricular afterload limits not only the mechanical conditions of the contraction, but also influences coronary perfusion pressure. With decreasing afterload stroke volume and pressure-volume work initially increases. Simultaneously coronary resistance decreases considerably so that coronary flow increases, although coronary perfusion pressure is reduced. However, when perfusion pressure falls short of a critical value, coronary flow cannot be maintained despite maximal coronary dilatation and stroke volume decreases, i.e., stroke volume, pressure-volume work and coronary flow run through an optimum with decreasing afterload. A reduction in coronary perfusion pressure below a certain value yields acute heart failure in all preparations. The minimal aortic mean pressure without reaching cardiac insufficiency was in the spontaneously hypertensive rats with 65 mm Hg significantly higher than in the control animals with 35 mm Hg, although the minimal coronary resistance was identical in both groups. The elevated critical coronary perfusion pressure of the spontaneously hypertensive rats can be explained by the increased O2-demand of the hypertrophied hearts.
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PMID:The effect of decreased left-ventricular afterload on cardiac performance in the normal and hypertrophied rat heart. 183 47

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


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