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

Case reports on three patients with Fabry's disease. Two of them involved necroptic examination, in one case the authors examined bioptic specimens of a 9-years old boy's skin. The material was processed by light microscopy, by electron microscopy, and by chromatography [in one case]. The two fatal cases showed accumulation of glycolipid mainly in cardiac muscle cells, the cause of heart failure. The authors describe the morphology of granules and give a list of their tinction and histochemical properties.
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PMID:[Fabry's disease]. 677 52

Although vasodilators are used with increasing frequency for the treatment of heart failure and myocardial ischemia, their direct effects on cardiac muscle have not been completely characterized. To delineate the action of vasodilators on mammalian myocardium, the chronotropic and inotropic effects of vasodilators on isolated guinea-pig atria (n = 163) have been determined. The spontaneous frequency and the peak rate of isometric force development at a fixed frequency of 200/min were used as indexes of chronotropy and inotropy. The potency series for negative chronotropy was diltiazem greater than D600 greater than verapamil greater than lidoflazine greater than bepridil greater than prenylamine greater than perhexiline greater than nifedipine. The potency series for negative inotropy differed substantially, exhibiting the sequence nifedipine greater than D600 greater than verapamil greater than bepridil greater than lidoflazine greater than prenylamine greater than perhexiline greater than diltiazem. Therefore, nifedipine acted as an "inoselective" and diltiazem as a "chrono-selective" depressant. Other vasodilators, including papaverine, nitroglycerin, nitroprusside, adenosine, dipyridamole, diazoxide and hydralazine exerted no or negligible negative chronotropic or inotropic effects even at high concentration (10(-5) M). Therefore, only vasodilators classified among the calcium antagonists proved to have appreciable direct myocardial effects. This supports the view that these drugs constitute a category of agents distinct from classical vasodilators.
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PMID:Inotropic and chronotropic effects of vasodilators. 680 62

Clinico-hemodynamic features as well as arterial hypertension outcome in 92 patients with hypertensive disease accompanied by atherosclerosis and atherosclerotic hypertension, who had suffered acute stroke in arteria caroticus interna areas 0.5-19 years before were followed up for 6 years. The minimal number of lethal outcomes fell within the first 3 years after stroke when hyperkinetic circulation was seen in all the patients. The lethality increase caused by repeated strokes (4-5 years after the first stroke was connected with gradual development of cardiac muscle pathology manifested by cardiac rhythm disorders or coronary and cardiac insufficiency in the patients with hypertensive disease in conjunction with atherosclerosis. Regressive course of arterial hypertension occurred in the patients with atherosclerotic hypertension 2 years after stroke. The frequency of repeated strokes did not increase in these patients. The lethality caused by cardiac muscle infarction was not increasing in the post-stroke period.
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PMID:[Course and outcome of arterial hypertension after stroke]. 682 44

A method is suggested of evaluating the cardiac internal hydraulic resistance R0 and maximal blood flow at zero post load Q0. R0 in intact dogs is 11.9 mm/Hg/l/min and Q0 is 27.1 l/min. In the condition of acute cardiac insufficiency and under the effect of large adrenaline doses these parameters were, respectively, 8.8 mm Hg/l/min, 7.0 mm Hg/l/min and 36.9 l/min, 38.8 l/min. The reducing of of R0 reflect the reduction of rigidity of the myocardial wall, and the increase of Q0 reflects the increase of the cardiac muscle inotropism connected with the compensatory increase of the catecholamines level in blood.
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PMID:[Experimental study of the output characteristics of the left heart ventricle]. 685 95

Newly hatched male White Pekin ducklings were fed furazolidone (FZ) at dosage of 750 mg/kg of feed for 4 weeks. Selected ducklings with advanced lesions of FZ-induced congestive cardiomyopathy were used for ultrastructural study of the myocardial alterations. Semithin sections of plastic-embedded blocks of myocardium from these dilated hearts revealed diffuse myocytolysis, characterized by pale sarcoplasm and lack of cross-striations in affected myocytes. Evidence of myocardial necrosis, inflammation, or fibrosis was not observed. Ultrastructural study revealed that the principal alteration in cardiac muscle cells was diffuse myofibrillar lysis. The sarcoplasm of affected myocytes had scattered masses of free thick and thin myofilaments, clumps of Z-band material, and accumulations of cytoskeletal filaments. Numerous polyribosomes were present in the areas of lysis of contractile material, as were other normal-appearing organelles. Myofibrillar lysis may have resulted from FZ-induced decreased synthesis, increased degradation, or disaggregation of contractile proteins. Ducklings with FZ-induced congestive cardiomyopathy offer an attractive model for studies of the biochemical and ultrastructural alterations of myofibrillar lysis and drug-induced cardiac failure.
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PMID:Furazolidone-induced congestive cardiomyopathy in ducklings: myocardial ultrastructural alterations. 687 5

The mechanisms of oedema in cor pulmonale remain unexplained. On the basis of a small number of studies, cor pulmonale is not caused by cardiac muscle failure, at least in early oedematous phases. Progressive and persistent elevation of pulmonary vascular resistance may exceed the pumping capacity of the right ventricle in later stages. Alternative explanations for the sharp fall in renal blood flow as oedema appears should be sought. The renin-angiotensin-aldosterone system seems causally related to oedema. The curious position of hypercapnia remains an enigma. Surprisingly few studies of hypercapnia, renal blood flow and renal hormones are reported. Redistribution of body water from intracellular to the extracellular space may be in part due to the need to buffer extracellular respiratory acidosis caused by hypercapnia. It provides an explanation for one form of hypercapnic oedema. Cyclical loss and gain of tissue mass seems more evident in cor pulmonale than ischaemic or valvular heart failure.
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PMID:Oedema in cor pulmonale. 703 67

Myotonia atrophica, a neuromuscular disease marked by autosomal dominant transmission and delayed relaxation of skeletal muscle, has been associated with cardiac failure, conduction abnormality and mitral prolapse (MVP). In order to determine the relaxation rate of cardiac muscle, left ventricular (LV) size and function, and the presence of MVP, 30 patients with myotonia atrophica were studied using digitized M-mode echocardiography (MME). Intracardiac conduction intervals were determined by noninvasive His bundle recording (HBR) from surface electrodes using a high-resolution, R-wave triggered, signal averaging computer. Neurologically unaffected first-degree relatives of the patients with myotonia atrophica were also studied to determine if cardiac abnormalities may be present in the absence of neurologic manifestations of the disease. Peak normalized diastolic endocardial velocity in patients with myotonia atrophica (3.7 +/- 0.8 sec-1) did not differ from unaffected first-degree relatives (3.8 +/- 0.8 sec-1) or normal subjects (3.6 +/- 0.8 sec-1). Systolic LV function and LV dimensions on MME were normal in both groups. However, MVP was present in 7 of 24 (29%) of patients who could be evaluated, but not in unaffected first-degree relatives. Despite normal LV systolic and diastolic function, infranodal intracardiac conduction was prolonged in patients with myotonia atrophica (average HV interval 50 +/- 5 SD msec) but not in neurologically unaffected relatives (average HV interval 40 +/- 5 msec). Delay in proximal intracardiac conduction was also found in patients with myotonia atrophica (average PH interval 140 +/- 20 msec) but not in neurologically unaffected relatives (average PH interval 115 +/- 6 msec). Hence cardiac findings in myotonia atrophica include proximal and distal conduction delay by external HBR even in the absence of abnormality of the standard 12-lead ECG. There may also be an increased frequency of MVP; however, early diastolic relaxation of the LV is unimpaired, and cardiac manifestations of myotonia are not transmitted independently of neurologic abnormality.
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PMID:Left ventricular relaxation, mitral valve prolapse, and intracardiac conduction in myotonia atrophica: assessment by digitized echocardiography and noninvasive His bundle recording. 709 Sep 87

Histological, electron microscopic, and physiological studies on the myocardium of rats and dogs in severe forms of compression syndrome (6-9 hours of compression and 2-4-7 hours after decompression) revealed three groups of morphological changes underlying cardiac insufficiency: (1) predominantly microcirculatory disorders with mild changes in cardiomyocytes detectable in bradycardia. Under these conditions the development of cardiac weakness may be based on both calcium overloading and reflectory weakening of the heart activity; (2) combination of microcirculatory disorders with marked hypoxic damage of the cardiomyocytes structure detectable under conditions of tachycardia may be an independent cause of the cardiac muscle weakness; (3) changes in the structures of cardiomyocytes responsible for nervous impulses conduction: sarcolemma and its derivatives. Under this condition, the probable cause of cardiac disorders may be electrolyte imbalance accompanying postcompression toxemia.
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PMID:[Ultrastructural bases of heart failure in the early period of the prolonged crush syndrome]. 712 30

A case of fatal familial intrahepatic cholestasis (Byler disease) developed a neuromuscular syndrome similar to that in experimental vitamin E deficiency and abetalipoproteinemia, and died of hepatic and cardiac failure. Serum vitamin E level was extremely low. Autopsy revealed intrahepatic cholestatic cirrhosis without obliterative lesions in the bile duct system and marked splenomegaly with splenoma-like nodules. The other pathological lesions were considered to be due to chronic vitamin E deficiency as follows:1. Mitochondrial changes especially of the hepatocyte and cardiac muscle. 2. Cardiomyopathy. 3. Myopathy. 4. Vasculopathy. 5. Systemic lipofuscinosis. 6. Lesions of the reproductive and endocrine organs. 7. Kyphoscoliosis and pes cavus. 8. Systemic neuroaxonal dystrophy with peripheral neuropathy.
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PMID:Pathology of chronic vitamin E deficiency in fatal familial intrahepatic cholestasis (Byler disease). 713 26

Phenol appears in high concentrations in renal failure with uremia. The effects of this material on contractile activity of isolated cardiac muscle were studied in right ventricular moderator band (MB) of piglets and papillary muscle (PM) of cats and kittens. The muscles were bathed in modified Krebs solution containing 5.6 mM glucose at 30 C and gassed with 95% O2 and 5% CO2. They were paced at 24 contractions per minute, isometrically at Lmax. Over the range 2.5-119.0 mg%, phenol produced dose-related decreases in both developed tension (DT) and maximal rate of tension development (max dT/dt) in MB of piglets. In contrast, the dose-dependent negative inotropic effect of phenol was not detected in feline PM until concentrations in excess of 12.5 mg% were used. Increasing extracellular Ca2+ from 2.5 to 5.0 mM as well as the addition of norepinephrine (3.94 x 10(-7) M) attenuated the phenol-induced cardiac depression in porcine MB. There were no further changes in either DT or max dT/dt when the extracellular Ca2+ was increased to 10 mM. These findings demonstrate that phenol elicits a direct negative inotropic effect on mammalian cardiac muscle that is modified by calcium and norepinephrine. Phenol may participate in the biochemical alterations leading to cardiac failure and death in uremia.
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PMID:Negative inotropic effects of phenol on isolated cardiac muscle. 721 19


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