Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The syndrome of peri-partum cardiac failure (PPCF) has been studied in 224 women seen in three years in Zaria, in northern Nigeria. A very high proportion were rural Hausa patients. There was a seasonal peak in July, and the incidence was about one per cent of deliveries. The risk increased with both age and parity. Symptoms began most commonly in the second week after delivery, and admission was commonest in the fourth. Typical signs of cardiac failure were found, and pulsus alternans, atrio-ventricular valvular incompetence, transient systemic hypertension and splenomegaly were common. The chest radiograph showed marked cardiomegaly, and extrasystoles and inverted T waves were often present in the electrocardiogram (ECG). Hypoalbuminaemia was common. Digoxin and diuretics were rapidly effective, causing a mean weight loss of 29 per cent in 15 days, resolution of hypertension, and a fall in the cardio-thoracic ratio (CTR) from 61 to 53 per cent. During the first year after diagnosis, the CTR became normal in 82 per cent of patients, and the ECG in 60 per cent. PPCF recurred, again with the same seasonal variation, after 19 per cent of subsequent pregnancies. During follow up for two to five years, 22 per cent of the women became hypertensive, and 11 per cent died. The prognosis was worst in those with an arrhythmia, hypertension, sustained cardiomegaly or aged 30 or more. Asymtomatic post-partum hypertension (PPHT) was found in 61 per cent of normal Hausa women, with a seasonal peak in May, especially in those with hypertension during pregnancy or labour, and twin pregnancies. Peri-partum cardiac failure may be due to the combined pressure load of PPHT, the volume load from eating the customary sodium-rich kanwa, and the cardiovascular demands of heat, both climatic and traditionally self-imposed.
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PMID:Peri-partum cardiac failure. 75 Oct 87

Cardiac failure is often associated with disturbances in cardiac output, autonomic nervous system activity, central and systemic venous pressures, and sodium and water metabolism. These disturbances influence the extent and pattern of tissue perfusion, may lead to tissue hypoxia and visceral congestion, and may alter gastrointestinal motility. By these mechanisms, cardiac failure potentially affects absorption and disposition characteristics of drugs, which may necessitate adjustment in dosage regimen for optimum therapy. Lignocaine is the drug which has been studied most extensively in cardiac failure. Volumes of distribution and clearance are decreased. As a drug whose metabolism is largely limited by liver blood flow, decreased blood flow to the liver accounts for some of the change in clearance, but impaired hepatic metabolism appears also to play a role in some patients. Accumulation of active metabolites of lignocaine and procainamide in patients with cardiac failure can influence therapeutic and toxic effects. Theophylline metabolism, which is largely independent of blood flow, appears to be reduced significantly in patients with severe cardiac failure and necessitates reduction of dosage. In the presence of severe cardiac failure, digoxin clearance may be less than anticipated on the basis of estimates of renal function. Quinidine plasma levels may be higher after single doses due to reduced volume of distribution. Quinidine metabolites are believed not to be pharmacologically active but may create confusion with nonspecific assays. Specific assays are recommended in cardiac failure, especially complicated by renal insufficiency. Data are lacking relating pharmacokinetic alterations to haemodynamic measurements in patients with cardiac failure. Whereas the direction of change in pharmacokinetic parameters may be predicted, variability in the magnitude of change is so great that determination of drug concentration in blood remains as essential adjunct to therapy.
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PMID:Pharmacokinetics in patients with cardiac failure. 79 48

In patients with dangerously elevated diastolic blood pressures, the titrated intravenous administration of sodium nitroprusside usually reduces blood pressure to near-normal levels in less than an hour. This rapid reduction of pressure is well tolerated by hypertensive patients and probably diminishes the morbidity from renal and cardiac failure and stroke. The side effects of sodium nitroprusside treatment are minimal.
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PMID:Treating acute hypertensive crisis with sodium nitroprusside. 83 90

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.
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PMID:Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure. 88 11

Vasodilative treatment of severe heart failure with infusions of phentolamine leads to ventricular unloading and in many cases brings about a dramatic improvement of the patient's condition. Phentolamine is the only one of the vasodilators so far used in the treatment of heart failure that has a positively inotropic effect. In contrast to sodium nitroprusside and nitroglycerin, it also increases stroke volume at normal filling pressures. Although vasodilative therapy has resulted in a notable decline in the mortality from severe heart failure among hospitalized patients, the long-term prognosis after discharge remains poor. One of the chief reasons is that there has hitherto been no effective orally administrable drug suitable for protracted therapy. Initial clinical studies with a newly developed slow-release formulation of phentolamine have shown that the preparation produces remarkably good effects in patients with chronic heart failure: systolic pressure rises, the amplitude of the blood pressure is augmented and there is an increase in urinary excretion accompanied with a corresponding reduction in weight. In practically all cases, there is a distinct decrease in the size of the heart and in pulmonary congestion.
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PMID:[Treatment of heart failure with phentolamine (Regitin)]. 89 48

In 12 patients with severe congestive heart failure (CHF) due to ischemic heart disease or nonischemic cardiomyopathy the hemodynamic response to intravenous infusion of sodium nitroprusside (N) was compared to that of dobutamine (D) 10 microgram/kg/min. D and N produced comparable increases in cardiac output (CO) (2.8 to 5.8 L/min and 2.9 to 5.0 L/min, respectively), but, compared to N, D caused a higher arterial pressure (99.3 vs 86.2 mm Hg, P less than 0.01) and heart rate (102.5 vs 95.3, P less than 0.05) and less reduction in pulmonary wedge pressure (PWP) (28.9 to 20.2 mm Hg vs 29.1 to 16.6 mm Hg, P less than 0.05). In five additional patients N and D were studied separately and then were infused together. The combination resulted in a higher CO, lower PWP and greater reduction in systemic and pulmonary vascular resistances than either drug alone. Brachial arterial infusion of nitroprusside produced prominent forearm vasodilation in a dose less than 10% of the systemic dose, whereas vasodilation with dobutamine was only modest even when 50% of the systemic dose was infused. Therefore, potent inotropic and vasodilator drugs produce similar and additive augmentation to left ventricular performance in heart failure. Reduction in vascular resistance with dobutamine probably is largely of reflex origin, but the vasodilation itself may be an important determinant of the rise in cardiac output.
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PMID:Comparative hemodynamic effects of inotropic and vasodilator drugs in severe heart failure. 90 77

Sodium nitroprusside is an excellent agent for lowering blood pressure in hypertensive emergencies, for producing controlled hypotension during anesthesia, and for treating acute myocardial infarction and chronic heart failure. Toxic effects of this drug have been reported and above-normal cyanide and thiocyanate concentrations have been observed in the blood of a small proportion of subjects receiving nitroprusside. Nitrite, syanide, and thiocyanate are major decomposition products of nitroprusside, resulting from an in vitro reaction with human blood. On the basis of the conversion mechanism, we suggest that, in the cyanide/thiocyanate cycle, only cyanide is directly responsible for any acute toxicity attributed to sodium nitroprusside. In this work, the extent of cyanide production by erythrocytes in vitro was studied. The rate of detoxification of cyanide by human liver in vitro was experimentally determined and data from a search for a possible inhibitor of the nitroprusside/hemoglobin reaction are presented. Also, the possible mechanism of the nitroprusside/hemoglobin reaction is discussed.
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PMID:Some aspects of sodium nitroprusside reaction with human erythrocytes. 92 83

The transcapillary escape rate of albumin (TERalb), i.e., the fraction of intravascular mass of albumin that passes to the extravascular space per unit of time, was determined from the disappearance of intravenously injected 125I-labeled human serum albumin during the first 60 minutes after injection in 10 subjects with chronic right heart failure. The investigation was repeated after sodium and water depletion. Before treatment TERalb was significantly elevated (mean 8.3 +/- 1.6% (SD)/hour, in comparison to values for normal subjects (mean 5.4 +/- 1.1%/hour, P less than 0.001). With treatment TERalb decreased significantly (mean 5.9 +/- 1.2%/hour, P less than 0.01). Right atrial pressure decreased from an average of 10 mm Hg to 6 mm Hg during treatment. A statistically significant, positive correlation was found between TERalb and right atrial pressure (r = 0.77, P less than 0.001). Our results best can be explained by increased filtration, mainly through the venous end of the microvasculature, due to the increased venous pressure in heart failure.
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PMID:Transcapillary escape rate of albumin and right atrial pressure in chronic congestive heart failure before and after treatment. 95 65

Results of studies have suggested that endotoxin and lowered coronary arterial perfusion pressures are detrimental to cardiac performance and lead to failure. Prevention of cardiac failure in the isolated canine heart preparation confronted with endotoxin and decreased coronary perfusion pressure was possible by perfusing these hearts with sodium nitroprusside. Prevention of failure was manifested by a lowered left ventricular endiastolic pressure and was associated with increased coronary flow and decreased coronary resistance with increased oxygen delivery and decreased oxygen extraction. Possible explanations for improved performance by dilator perfusion include increased delivery of oxygen and nutrients to myocardial tissue as well as a reduction of ventricular wall tension by dilating the coronary vascular skeleton. Prevention of extravasation of interstitial fluid into myocardial tissue by reducing overperfusion of potentially damaged coronary vessels could serve to maintain myocardial integrity and ventricular compliance. The potential use of such therapy warrants further study, with emphasis on evaluating the hemodynamics of the intact animal.
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PMID:The effects of coronary vasodilatation on cardiac performance during endotoxin shock. 95 69

The renal regulation of sodium is intertwined with the extracellular fluid volume (ECFV). Most adjustments in sodium elimination in man are accomplished via alterations in tubular reabsorption. The latter is sensitive to change in ECFV. An expanded ECFV results in less reabsorption and more excretion of sodium, and a contracted ECFV has the converse effect. There are direct and indirect mechanisms whereby ECFV influences sodium reabsorption. Patients with nephrotic syndrome, heart failure, and cirrhosis "behave" physiologically as normal individuals with a contracted ECFV. Water balance is normally determined by intake and losses in sweat which is always hypoosmotic to plasma, by evaporation from skin and lungs, and through renal excretion. The major factors that determine the ability to concentrate the urine are (1) the establishment of a concentrated environment around the collecting ducts, and (2) the elaboration and effects on the kidney of antidiuretic hormone. The evaluation of a patient with abnormalities of sodium and water rests initially and largely on clinical information. The clinical setting provides clues to anticipating, preventing, and interpreting distortions of body sodium and water. The laboratory can detect an abnormality, confirm or refute clinical assessment, and assist in the quantitative aspects of treatment and its efficacy.
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PMID:Sodium and water: an overview. 96 14


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