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 present study was designed to investigate the effect of the calcium-channel antagonist gallopamil on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Twenty-four adult patients with coronary artery disease and significant proximal stenosis of the left anterior descending coronary artery (LAD) were randomly assigned to receive gallopamil or placebo under double-blind conditions. Patients with recent myocardial infarction, apparent collateralization of the LAD, myocardial failure, sinoatrial or atrioventricular block, severe hepatic disease, or renal failure were excluded from the study. PTCA was performed with use of at least two balloon inflations, each of 2 min in duration. Gallopamil (0.4 mg) or placebo (0.9% sodium chloride) was administered during the 10-min interval between the two inflations. For determination of myocardial lactate and hypoxanthine release, blood samples were taken simultaneously from the great cardiac vein and the femoral artery before and immediately after each inflation. Electrocardiogram changes were analyzed by measuring ST-segment deviations (80 ms after the J point) and maximal T-wave deviations of the leads I, II, III, and V2, V4, and V6. The most sensitive leads for identification of myocardial ischemia in the LAD area were V2 and V4. If compared to the first balloon inflation, the degree of ST-segment/T-wave changes induced by the second inflation was significantly reduced only in the presence of gallopamil. Furthermore, if compared to placebo, ischemia-induced lactate and hypoxanthine release was decreased in the presence of gallopamil. These results suggest that intracoronary application of gallopamil attenuates myocardial ischemia during PTCA.
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PMID:Intracoronary gallopamil during percutaneous transluminal coronary angioplasty. 128 55

Heart transplantation has become a standard procedure in the treatment for irreversible heart failure. Criteria for both recipients and donors have been extended. One year survival now reaches 81%. In the immediate postoperative course patients are endangered by infection. In the long-term course coronary artery disease of the transplanted heart becomes the most serious problem. Alteration of liver and kidney function due to chronic medication as well as malignancies and hypertension also occur. In case of chronic transplant failure retransplantation may be indicated. Acute cardiac failure before transplantation nowerdays can be treated by mechanical circulatory assist devices.
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PMID:[Heart transplantation--indications and results]. 128 76

The authors present outcomes concerning frequency of appearance and clinical course of aneurysms after acute myocardial infarction. The study population consisted of 730 patients (mean age 54 +/- 9 years) with acute myocardial infarction, including 579 men and 151 women. The diagnosis was based on the following criteria: 1) coronary artery disease history, 2) physical examination, 3) ECG, 4) 2-dimensional echocardiography, 5) biochemical data. Post-infarction aneurysm was revealed in 42 patients (5.8%, 33 men and 9 women); antero-lateral aneurysm--in 36 patients (85.7%), and inferior-posterior aneurysm--in 6 patients (14.3%). Ventricular arrhythmias in the first day of infarction had a high frequency in both groups; with aneurysm--92.9%, without aneurysm--82.2%. The frequency of arrhythmia in 21-st day of infarction decreased similarly in both groups with aneurysm--40.5%, without aneurysm--38.9%. There was no statistically significant difference among both groups. There was no correlation between localisation of aneurysms and degree of contractility disturbances of the heart muscle (dyskinesis, akinesis). Heart failure--class III and IVK (Killip-Kimball classification) occurred in 19.0% of patients with aneurysm and in 10.4% of patients without aneurysm. That was no essential correlation between localisation of aneurysms and advancement of the heart failure.
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PMID:[Aneurysms in acute myocardial infarction (multicenter studies)]. 128 92

1. We studied the effects of chronic calcium antagonist (calcium entry blocker, CEB; nifedipine, verapamil, diltiazem) treatment on beta-adrenoceptor density (assessed by (-)-[125I]-iodocyanopindolol [ICYP] binding) and subtype distribution in right atria from 65 patients without apparent heart failure undergoing elective coronary artery bypass grafting (CAD-patients) and from 13 patients with moderate heart failure (NYHA class III to class III-IV) undergoing mitral valve replacement (MVD-patients). 2. In CAD-patients atrial beta-adrenoceptor density was 79.3 +/- 7.9 fmol ICYP bound mg-1 protein (n = 18), the beta 1:beta 2-adrenoceptor ratio 69:31%. Chronic CEB-treatment did not affect either atrial beta-adrenoceptor density or beta 1:beta 2-adrenoceptor ratio. 3. In contrast, in CAD-patients chronically treated with beta 1-adrenoceptor antagonists (atenolol, bisoprolol, metoprolol) and CEB, atrial beta-adrenoceptor density was significantly increased (108.6 +/- 10.5 fmol ICYP bound mg-1 protein, n = 21); this increase was due to a selective increase in beta 1-adrenoceptors. 4. In MVD-patients atrial beta-adrenoceptor density (55.5 +/- 8.7 fmol ICYP bound mg-1 protein, n = 7) was significantly lower (P less than 0.05) than in CAD-patients; beta 1:beta 2-adrenoceptor ratio, however, was not changed (67:33%). Chronic CEB-treatment of MVD-patients did not prevent the decrease in atrial beta-adrenoceptors. 5. We conclude that chronic CEB-treatment does not affect human right atrial beta-adrenoceptor density, either in patients without apparent heart failure or in patients with moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of effect of chronic calcium antagonist treatment on beta 1- and beta 2-adrenoceptors in right atria from patients with or without heart failure. 131 61

In 100 patients 12 to 60 months after cardiac transplantation, the influence of transplant coronary vasculopathy and of the pretransplantation disease (end-stage heart failure caused by coronary artery disease or dilated cardiomyopathy) on the beta-adrenergic receptor (AR) numbers and beta 1/beta 2-AR ratio of right ventricular biopsies was determined. Patients with coronary vasculopathy (CVP) after cardiac transplantation had lower absolute numbers of beta 1-AR compared with patients without CVP. Since patients with CVP had increased left ventricular (LV) end-diastolic pressure and LV muscle mass, it is suggested that decreased beta 1-AR may be the result of an altered hemodynamic situation of the transplanted heart after development of CVP. Patients with dilated cardiomyopathy (DCM) before cardiac transplantation showed a decrease in total beta-AR and of the beta 1/beta 2-AR ratio as a result of an increase in beta 2-AR and a decrease in beta 1-AR numbers. The decreased beta 1/beta 2-AR ratio in patients with previous DCM may indicate that the beta-AR system of the transplanted heart might be influenced (at least in part) by pathophysiologic factors that are characteristic of the pretransplantation disease ultimately leading to cardiac transplantation and persisting after cardiac transplantation.
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PMID:Changes in cardiac beta 1- and beta 2-adrenoceptor densities after human cardiac transplantation: relation to transplant coronary vasculopathy and pretransplantation disease. 132 8

The paper deals with the course of the illness in a 66 years old male, who had taken an amount of 0.2 mg of medigoxin for an unknown period of time, because of chronic heart failure due to atherosclerotic heart disease and chronic atrial fibrillation. He have had a cholelithiasis also and reduced renal reserve. He was admitted by an emergency admittance because of nausea, vomiting, color vision disturbances: blue colored vision, and with other signs of digitalis toxicity: diffuse abdominal pain, an absolute arrhythmia with a slow ventricular rate, and with a short corrected Q-T interval in an electrocardiogram of 0.315 seconds and with high serum digoxin level reacted 3.8 nmol/L. After stopping of a digitalis treatment, in a period of time of four days, all signs of digitalis toxicity including blue color vision disturbances disappeared. In the paper that rare sign of digitalis toxicity is discussed.
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PMID:[Blue color vision as a sign of digitalis poisoning]. 134 44

Esmolol is a specific beta 1-blocker; it is hydrosoluble, without intrinsic sympathetic activity. Distribution half-life is 2 minutes and elimination half-life 9 minutes. Esmolol is hydrolyzed by the blood esterases. Its indications are all those where inotropism and heart rate must be briefly and specifically diminished using a titration technique: 1) In patients with coronary artery disease, or poor cerebral compliance, just before a strong nociceptive stimulus like intubation, extubation, skin incision, etc. 2) In patients with coronary artery disease, to decrease oxygen consumption by the myocardium. 3) In patients with hypertensive episodes per and post-operatively, especially in vascular surgery and neurosurgery. 4) In cardiac insufficiency due to obstructive cardiomyopathy. 5) In patients with specific cardiac rhythm problems. 6) In all patients where propranolol is indicated bu cannot de administered due to its long duration of action. Esmolol has to be given either as a mini-infusion at a rate of 300-600 micrograms/kg/min for the first 1-2 minutes followed by 200-300 micrograms/Kg/min or as a bolus (just before a nociceptive stimulus) 1-3 mg/kg. When using esmolol, it is important to set limits within which heart rate and blood pressure must remain. Over-dosage can occur easily but can be avoided without difficulty.
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PMID:[Characteristics and clinical use of esmolol]. 135 93

In the last few years several Authors reported positive results using beta-blocking therapy in chronic heart failure. They also observed a group of patients who did not improve after this treatment. The aim of our study was comparing hemodynamic, neurohumoral and heart rate responses to beta-blockers in 2 groups of patients: Group A, patients who improved and Group B, patients who did not improve their clinical conditions after beta-blockade. We studied 26 patients with chronic heart failure of different origin: coronary artery disease and idiopathic dilative cardiomyopathy. They were treated with atenolol 50 mg/die for at least 1 year. Patients were divided into 2 groups: Group A including patients who increased the exercise time and the peak VO2 (> or = 2 ml/min/kg) and Group B, patients who did not increase exercise time and peak VO2 during beta-blockers. In Group A patients we observed a correlation between heart rate and end-diastolic volume by scintigraphy. We did not observe this correlation in Group B patients. The ejection fraction, evaluated by scintigraphy, significantly increased in Group A, while in Group B did not change. In both groups of patients we observed that plasmatic norepinephrine decreased significantly. In our opinion, this reduction is not due to an amelioration of organ clearance, because it was observed even in patients who did not show an increase of cardiac index and of ejection fraction. We suggest that the decrease of plasmatic norepinephrine might be the effect of beta-blockade and that it is not related to clinical response after treatment.
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PMID:[Heart insufficiency treated with beta-blocking agents. Comparison of responders and non-responders]. 135 43

In order to study the occurrence of postbypass hyperamylasemia, 75 patients undergoing cardiopulmonary bypass (CPB) were studied from March 1989 to January 1990. There were 49 males and 26 females. Among them, 27 had congenital heart disease, 30 had valvular disease, and 18 had coronary artery disease. There were 27 patients with at least one elevated serum amylase sample after operation. Thus, the overall incidence of hyperamylasemia was 36%. As compared with the preoperative data (1.3%), there was a statistically significant difference in the occurrence of hyperamylasemia (p less than 0.05). Three patients had overt clinical pancreatitis postoperatively. There was no positive correlation between the serum amylase level and the occurrence of pancreatitis (p greater than 0.05). Forty-two cases had a significant elevation of the amylase creatinine clearance ratio (ACCR) after CPB. However, there was no significant difference between the groups with pulsatile and nonpulsatile CPB (p greater than 0.05). Three patients (4%) died in our series. The causes of death were heart failure in two and fulminant pancreatitis associated with low cardiac output in one. Although our experience in dealing with pancreatitis improved survival, mortality was still high (33.3%) in our series. Nevertheless, there was no apparent correlation between mortality and postbypass hyperamylasemia (p greater than 0.05). Logistic regression analysis was used to analyze the risk factors of the occurrence of hyperamylasemia, and the analysis revealed that patients with coronary artery disease were susceptible to postbypass hyperamylasemia. Our studies indicate that the use of total serum amylase or ACCR to monitor for the occurrence of pancreatitis in postbypass patients is inadequate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperamylasemia following cardiopulmonary bypass. 137 42

Carvedilol is a dual-acting drug designed to produce two complementary effects: beta-blockade and vasodilation. These effects are induced in the same dose range, a prerequisite for utilizing both properties in an appropriate manner. The vasodilation is mediated predominantly by specific alpha 1-adrenoceptor blockade. At markedly higher concentrations, additional vasodilating actions besides alpha 1-blockade can be observed. These effects resemble those of Ca(2+)-antagonistic properties. However, they do not contribute to the acute blood pressure-lowering activity of carvedilol but may be responsible for the increased blood flow to specific organs. At beta-blocking doses, carvedilol reduces the regional and systemic vascular resistance in various experimental models, healthy volunteers, and in patients with cardiovascular diseases such as hypertension, coronary artery disease, and heart failure. The profile of carvedilol thus insures beneficial treatment of hemodynamic disorders characterized by increased sympathetic tone and increased vascular resistance.
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PMID:Vasodilatory action of carvedilol. 137 50


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