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

One to two per cent of children and up to 11% of adolescent have arterial hypertension. In most cases children and adolescent are not recognized to be hypertensive because physicians do not routinely measure blood pressure. Often the diagnosis is recognized only when the pediatric patients develop a complication: seizure, stroke, heart failure or paraplegia. Renovascular hypertension in children and adolescents is more common than all of the other causes combined, except for coarctation of the aorta. The diagnosis is not so easy and includes the usual history, physical examination (signs and symptoms of coarctation of the isthmic or abdominal aorta or of an abdominal mass or of one of the adrenal causes of hypertension), laboratory studies, abdominal ultrasound study and chest x-ray. Sometime a CAT can be usefull. The next steps are the early and rapid-sequence IVP, renal angiography and peripheral and renal renin activity. The management of renovascular hypertension in children and adolescent includes a conservative approach (percutaneous transluminal renal angioplasty or renal embolization), rarely used in pediatric age, and the surgical treatment. This latter includes all the surgical procedures of renal revascularization and, in unilateral renal parenchymal diseases, the nephrectomy or a partial nephrectomy. The postoperative results are very good in a high percentage of cases. In bilateral cases, the revascularization surgical procedures improve or normalize also the impaired renal function.
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PMID:[Renovascular hypertension in childhood]. 182 81

Antioxidant enzyme activities, including superoxide dismutase, glutathione peroxidase and catalase, are known to be altered under various physiological and pathophysiological conditions. There is a significant increase in some of these activities in the myocardium during stable hyperfunctional heart hypertrophy subsequent to pressure overload, as well as after exercise training in rats. Hearts with increased antioxidant capacity have been reported to be more resistant to in vivo and in vitro oxidative stress. On the other hand, cardiomyopathy and heart failure under a variety of conditions are accompanied by increased free radicals and lipid peroxidation. These data lead to the hypothesis that maintained or improved function during compensated heart hypertrophy may be supported by an increased antioxidant capacity, and a relative deficit in this 'antioxidant reserve' may contribute in the decompensated state.
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PMID:A relative deficit in antioxidant reserve may contribute in cardiac failure. 213 50

A complex approach to the whole range of diseases of the heart in alcoholics is presented. The authors are concerned with different variants of cardiac diseases induced by chronic alcoholism, understood and referred to in the light of the WHO concept as "alcoholic diseases of the heart". These conditions fall within the category of specific diseases of the myocardium, which in the stage of evident manifestations of cardiac insufficiency and dilation of the cavities are termed alcoholic cardiomyopathies. Although the etiology is not yet fully understood, the direct toxic effects of ethanol and acetaldehyde upon the structure and function of the myocardium due to the decreased functional activity of alcohol dehydrogenase and catalase are known to be involved in the development of alcoholic diseases of the heart. In chronic alcoholism the changes in the myocardium become increasingly irreversible. Moleculo-biological, biochemical, clinical, and morphological changes on cardiomocytes arising after the extensive effect of alcohol on different systems of the body are described in detail. The specific characteristics of clinical manifestations of different alcoholic diseases of the heart are analyzed and the currently used therapeutic procedures are discussed in relation to the clinical form and stage of the disease in the light of close cooperation with micrological departments.
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PMID:[Heart diseases in alcoholics]. 233 55

Enzymes in the human myocardium following sudden death were examined for activity in a quantitative histoenzymological study, these were NAD-dependent dehadrogenases of succinate (SDG), lactate (LDG), beta-hydroxybutyrate (beta-HOBDG), alpha-glycerophosphate (alpha-GPDG), alcohol (ADG), glucoso-6-phosphate (G-6-PDG), and NAD-diaphorase (NADse), and catalase. Autopsies were performed within 3 h after death. beta-HOBDG and LDG were found to show an increase in activity in the cardiomyocytes of sudden death subjects with coronary heart disease without apparent changes. In the myocardium from death subjects with coronary heart disease and large postinfarct cardiosclerosis, the activity of the enzymes was directly related to the severity of myocardial hypertrophy and signs of chronic heart failure. As myocardial hypertrophy developed, the enzyme activity increased; when there appeared signs of chronic heart failure it decreased. The myocardium from sudden death subjects with alcoholic cardiomyopathy showed diminished redox enzyme activity and higher activity of the enzyme utilizing alcohol (ADG and catalase). The findings suggest that changes in the enzyme activity in the myocardium are of various type and depend on previous cardiac abnormalities.
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PMID:Quantitative histoenzymological characteristics of the myocardium in sudden cardiac death. 252 98

The present study has examined early cellular effects of chronic adriamycin administration to dogs using a protocol (1 mg/kg/week to a total cumulative dose of 240 mg/m2) producing significant but small reductions in ejection fraction and stroke volume as determined echocardiographically prior to the development of clinical or radiological manifestations of heart failure. At this early phase of cardiomyopathy, significant reduction (P less than 0.05) in sarcoplasmic reticulum Ca2+, K+-ATPase was observed without any change in mitochondrial, lysosomal or sarcolemmal marker enzymes. Myocardial calcium (P less than 0.01) and glutathione (P less than 0.001) levels were increased significantly. Detailed analysis of myocardial phospholipid profiles failed to show any significant differences between control and treated dogs. In contrast, red cell membranes showed increased phosphatidylcholine (PC) and decreased phosphatidylserine (PS) contents, resulting in a significant increase in PC/PS ratio (P less than 0.05). No significant changes were detected in activities of catalase, superoxide dismutase or glutathione peroxidase in erythrocytes or myocardial tissue from control and adriamycin-treated animals. A significant (P less than 0.05) elevation in plasma sialic acid was observed following adriamycin treatment. Our results suggest that early adriamycin-induced damage is unlikely to result from alterations in cellular processes protecting tissues against oxidant injury. Regression analysis indicated that, of the various abnormalities observed, only the elevated myocardial calcium levels and the increases in plasma sialic acid correlated with the degree of myocardial functional impairment. Our findings suggest the presence of sarcolemmal alterations in Ca2+ handling in early adriamycin-induced myocardial injury and indicate that measurement of plasma sialic acid should be further investigated as a possible noninvasive indicator of impending adriamycin cardiotoxicity.
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PMID:Adriamycin cardiomyopathy: implications of cellular changes in a canine model with mild impairment of left ventricular function. 299 97

A case of cardiac failure in a 54 year old man with a diffuse total arteriovenous aneurysm of the liver is reported. The aneurysm was arteriolarvenous, without a wide bore localised fistula. It occupied the whole hepatic mass, including the territories of the right subphrenic and anterior collateral of the gastroduodenal artery. The cause of cardiac failure was the elevated cardiac output, 15 1/min, which fell to 6 1/min at each peroperative occlusion of the hepatic artery. After ligature of this vessel, the cardiac output stabilised at 9 1/min and remained at this value 4 months after surgical cure. This case is comparable to the neonatal cardiac failure due to multinodular hepatic angioma with respect to the clinical, angiographic and CAT scan characteristics, and the surgical cure of the high cardiac output syndrome. Some of the histological features were suggestive, in places, of the structure of hepatic cavernoma, which makes the exact pathological classification of this diffuse aneurysm difficult; the closest possibility being an involuted from of diffuse capillary hemangioma of childhood allowing such long survival and, occasionally taking on the appearances of a cavernoma. Permanent surgical cure by ligature of the hepatic artery was an additional rare feature of this case.
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PMID:[Curable asystole in an adult caused by a diffuse and complete arteriovenous aneurysm of the liver. Cure by ligation of the hepatic artery]. 640 47

During radiotherapy of thoracic tumors, the heart is often included in the primary treatment volume, and chronic impairment of myocardial function occurs. The cellular biomolecules are altered directly by radiation or damaged indirectly by free radical production. The purpose of this investigation was to evaluate the biochemical and functional responses of the rat heart to a single high dose of radiation. The effect of 20 Gy local X irradiation was determined in the heart of Wistar rats under general anesthesia. Mechanical performances were measured in vitro using an isolated perfused working heart model, and cardiac antioxidant defenses were also evaluated. Hearts were studied at 1 and 4 months after irradiation. This single dose of radiation induced a marked drop in the mechanical activity of the rat heart: aortic output was significantly reduced (18% less than control values) at 1 month postirradiation and remained depressed for the rest of the experimental period (21% less than control 4 months after treatment). This suggests the development of myocardial failure after irradiation. The decline of functional parameters was associated with changes in antioxidant defenses. The decrease in cardiac levels of vitamin E (-30%) was associated with an increase in the levels of Mn-SOD and glutathione peroxidase (+45.5% and +32%, respectively, at 4 months postirradiation). However, cardiac vitamin C and catalase levels remained constant. Since these antioxidant defenses were activated relatively long after irradiation, it is suggested that this was probably due to the production of free radical species associated with the development of inflammation.
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PMID:Effect of in vivo heart irradiation on the development of antioxidant defenses and cardiac functions in the rat. 756 73

Hypertrophy and heart failure were induced by placing a mildly constrictive band around the ascending aorta in young guinea pigs. Based on heart weight, left ventricular wall thickness, hemodynamic data, and other clinical signs, these animals were found to have physiological hypertrophy at 10 wk and congestive heart failure (CHF) at 20 wk. Hearts from these two groups of animals were examined for superoxide dismutase (SOD), glutathione peroxidase (GSHPx), and catalase activities as well as lipid peroxidation and glutathione [reduced glutathione (GSH)/oxidized glutathione (GSSG)] levels. There was an age-dependent increase in SOD activity and GSH content in sham controls. SOD activity was 28% higher in the 10-wk-hypertrophy group and 46% lower in the CHF group than in respective sham controls. GSHPx activity increased significantly in the hypertrophied hearts, whereas in the failing hearts, the activity was not different from the 20-wk controls but was significantly lower than in the hypertrophied hearts. Catalase activity did not change at either stage. GSH content in the hypertrophied hearts was significantly higher compared with sham controls. In the CHF group, GSH content was significantly lower and GSSG content was significantly higher than in sham controls. Lipid peroxidation, as indicated by malondialdehyde content, was significantly decreased in the hypertrophy group but increased toward control levels in the failure group. It is proposed that a relative deficit in myocardial antioxidant capacity as well as in the redox state may play a role in the pathogenesis of cardiac failure.
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PMID:Antioxidant changes in hypertrophied and failing guinea pig hearts. 818 5

Coarctation of the abdominal aorta in rats for 10 wk increased the heart weight-to-body weight ratio by 36% and peak left ventricular systolic pressure by 75%; there was no apparent change in the end-diastolic pressure, and animals did not show any clinical signs of heart failure. These hypertrophied (H) hearts showed increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) with no change in catalase. Lipid peroxide content as indicated by the malondialdehyde (MDA) level was lower in H hearts. There was no apparent difference in either Na+ and Ca2+ content or high-energy phosphates between sham (S) and H hearts. Control and H hearts were subjected to 10 min of ischemia (I) and 15 min of reperfusion (R). Contractile failure and rise in resting tension due to I, in both S and H hearts, were comparable. On reperfusion, H hearts showed better recovery of the developed force and resting tension as well as reduced incidence of arrhythmias when compared with corresponding S hearts. Both SOD and GSHPx activities were depressed due to I-R, but these activities were significantly higher in reperfused H hearts. Reperfused H hearts also showed a better maintenance of the ultrastructure and Na+ and Ca2+ contents, recovery of high-energy phosphates, and reduced MDA levels compared with S hearts. Supplementation of the perfusion medium with SOD (120 U/ml) and catalase (80 U/ml) significantly attenuated the I-R injury in S hearts, and the response in many ways was comparable to H hearts. The study documents the therapeutic potential of increased myocardial endogenous antioxidants against oxidative stress.
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PMID:Increase in endogenous antioxidant enzymes protects hearts against reperfusion injury. 836 52

Two cases of aortocaval fistula are described in patients with an otherwise asymptomatic abdominal aortic aneurysm. Both presented because of cardiac symptoms, one with chest pain and acute heart failure and electrocardiogram signs of acute coronary ischaemia, the other with a long history of chronic cardiac failure resistant to therapy. In the first case the fistula was proven by means of a CAT scan. Positive proof of a fistula or leakage is important because asymptomatic aneurysms should not be operated on in cardiac compromised patients. On the other hand, if an aortocaval fistula is present, operation is necessary to prevent fatal cardiac failure.
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PMID:"Asymptomatic" ruptured aneurysm: a report of two cases of aortocaval fistula presenting with cardiac failure. 851 21


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