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

Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and its interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca++-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the dimunition in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.
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PMID:Cardiac metabolsim: its contributions to alcoholic heart disease and myocardial failure. 15 68

The role of dialysis in the treatment of patients with severe hypercalcemia is uncertain. The fourteen previously reported cases of hypercalcemia treated with either peritoneal or hemodialysis have been reviewed. Two additional patients treated with hemodialysis are described in this report. Because the use of large volumes of intravenous fluids was contraindicated, each of the patients received a low calcium bath (0-1 mEq calcium per liter) hemodialysis for three and a half hours. After dialysis, the serum calcium fell to normal in both and remained normal thereafter with treatment of the underlying disease (multiple myeloma in one and vitamin D intoxication in the other). Hemodialysis can clear up to 682 mg of calcium per hour as compared to 124 mg per hour for peritoneal dialysis and 82 mg per hour with forced saline diuresis. Low calcium bath hemodialysis is indicated when the presence of renal and/or cardiac failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients.
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PMID:Role of dialysis in the treatment of severe hypercalcemia: report of two cases successfully treated with hemodialysis and review of the literature. 16 Aug 52

Direct cardiac and vascular effects of the antikaliuretic diuretic potassium-canrenoate were measured in cardio-surgical patients during extracorporal circulation and immediatly after operations, each time in neuroleptanalgesia. During "steady state" extracorporeal circulation (aorta cross-clamped, constant flow rate of heart-lung-machine, constant hypothermia), in 13 patients no significant influence on peripheral circulation was found after i.v.-injection of 800 mg potassium-canrenoate. Neither arterial perfusion pressure (representing an arterial vascular reaction) nor changes in oxygenator-volume (indicating venous vasodilation or contraction) demonstrated significant differences in comparison to a control group. After cardiac surgery haemodynamic measurements were performed for a period of 60 minutes in 10 patients given 800 mg potassium-canrenoate. In comparison with a control group (n = 6), no significant differences in arterial pressure, heart rate, cardiac index and pulmonary arterial pressure were found. Left ventricular measurements, using a catheter tip manometer, revealed no direct positive inotropic effect of a single i.v.-injection of potassium-canrenoate. In acute myocardial failure during anaesthesia or in "low cardiac ouptut" following open heart surgery no improvement in myocardial contractility is obtained by i.v.-application of potassium-canrenoate; at the present there seems no alternative to other positive inotropic agents such as calcium, glucagon, dopamine, orciprenaline and epinephrine.
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PMID:[Extrarenal effects of potassium-canrenoate. Haemodynamic investigations during neuroleptanalgesia in cardiosurgical patients (author's transl)]. 31 42

Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.
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PMID:Effects of verapamil on myocardial performance in coronary disease. 36 90

On the basis of the data from the literature and own studies the genesis of acute cardiac insufficiency has been shown to be directly associated with a sharp decline in the effectiveness of intracellular energy transportation. A challenging factor in the transformation of the pathological process into acute cardiac insufficiency may consist in one of the three main types of influence: (1) hypoxia of the myocardium, (2) effects causing disorders in the calcium metabolism, and (3) additional mechanical loads on the already affected myocardium. The pattern of the observed ultrastructural changes may be used to a certain extent for the judgement on the type of effect which was most important in the genesis of acute cardiac insufficiency.
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PMID:[Ultrastructural basis of acute cardiac insufficiency not associated with rhythm disorders]. 36 23

1 This study has compared the diuresis produced by a single oral administration of 6 mg piretanide, 9 mg piretanide and 1 mg bumetanide in a group of nine patients with cardiac failure using a balanced randomized design. 2 The natriuresis and kaliuresis produced in the first 6 h after administration of piretanide 9 mg and bumetanide 1 mg were similar. Piretanide 6 mg produced a lesser response. 3 There was evidence of sodium and water conservation following the diuresis for up to 48 h with all three treatments. 4 The patterns of urate and calcium excretion were similar for the two diuretics.
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PMID:A single dose comparison of piretanide and bumetanide in congestive cardiac failure. 38 25

Serum and salivary digoxin concentrations were measured in 53 children and correlated with ECG variables and serum potassium, calcium and magnesium concentrations. In 73% of patients cardiac failure was controlled, while only 7,5% of patients had serum digoxin concentrations within the 'therapeutic range'. It is proposed that the adult therapeutic range of 1-2 ng/ml is not applicable to children, who can be controlled at lower concentrations and/or that a significant proportion of the children studied no longer required maintenance digoxin therapy.
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PMID:Serum and salivary digoxin concentrations in children. 55 Apr 20

A linear three-pool model of rhythm-inotropic phenomena in the cardiac muscle is proposed. Dynamics of accumulation and liberation of calcium from intracellular pools is described by differential equations. It has been shown by numerical experiments that rhythm-inotropic phenomena in the normal cardiac muscle and under cardiac insufficiency can be described qualitatively in terms of the concept on calcium recirculation in intracellular pools.
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PMID:[Modeling the effect of rhythm on the strength of myocardial contraction]. 67 76

In a group of 29 patients treated with digoxin for cardiac failure, only 16 showed increased calcium and potassium concentrations in saliva. There was no correlation in the 29 patients between serum digoxin levels and concentrations of salivary electrolytes. On the other hand, in 4 normal subjects treated with digoxin no change in salivary electrolytes was noted. It is concluded that modifications in salivary electrolytes seen in patients with cardiac failure treated with digitalis are not due to this drug. However, a retrospective clinical study showed a good correlation between clinical signs of cardiac failure and increased levels of salivary calcium, potassium and CaX Kproduct. It is suggested that this phenomenon is due to the well-known adrenergic stimulation in patients with cardiac failure.
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PMID:[Salivary electrolytes, digitalis glycosides and cardiac insufficiency]. 71 27

A 35-year-old patient who presented with recurrent chest infection, pulmonary oedema and cardiac failure was found to be grossly hypocalcaemic owing to previously undiagnosed hypoparathyroidism. The cardiac failure was not easily relieved by digoxin and diuretics but it quickly responded when the plasma calcium was restored to normal with dihydrotachysterol. With dihydrotachysterol as sole treatment for more than 2.5 years he had normal exercise tolerance and no features of cardiac failure.
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PMID:Hypocalcaemic cardiac failure. 72 84


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