UMLS:C0018801 - FACTA Search

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

Ninety patients undergoing coronary bypass surgery were studied prospectively by bedside and subsequent ambulatory electrocardiographic monitoring to investigate the incidence, possible causes, and prevention of atrial fibrillation. Patients with good left ventricular function were divided randomly into a control group or groups treated with digoxin or propranolol. In the control group the incidence of atrial fibrillation was 27% and of significant ventricular extrasystoles 3%. Propranolol reduced the incidence of atrial fibrillation (14.8%), whereas digoxin had no effect and increased the incidence of ventricular extrasystoles. Age, sex, severity of symptoms, cardiomegaly, heart failure, previous myocardial infarction, and number of grafts did not affect the result. The operative myocardial ischaemic time was related to the occurrence of atrial fibrillation. There was also a significant relation between atrial fibrillation and bundle branch block. Atrial fibrillation is common after coronary artery grafting; it may be due to diffuse myocardial ischaemia or hypothermic injury. The incidence may be reduced by beta blockade.
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PMID:Arrhythmias after coronary bypass surgery. 661 Apr 35

We determined the outcome of coronary artery bypass surgery in 500 consecutive patients followed for at least 10 years after operation. There were 446 males (89.2%). Angina pectoris was the major indication for operation. Four hundred six patients (81%) had multivessel coronary artery disease and 348 (69.9%) had good left ventricular function. At 10 years of follow-up, 48% of patients were asymptomatic and 41% were improved. Propranolol was being used by 36% of patients and nitrates by 49%. Of the 355 patients younger than 65 years of age at the time of follow-up, 57% were employed full time and 24% were working part-time. Reoperation was performed in 9% of patients. Analysis of survival by Kaplan-Meier curves indicated that overall 10-year survival rates were 78% for one-vessel disease, 69% for two-vessel disease, 48% for three-vessel disease and 67% for left main coronary artery disease. For patients with good left ventricular function, the 10-year survival rates were 83% for one-vessel disease, 73% for two-vessel disease, 53% for three-vessel disease and 73% for left main disease. For patients with poor left ventricular function, the rates were 56%, 59%, 40% and 54%, respectively. Cox multivariate analysis indicated that preoperative diuretic use, history of heart failure, the number of diseased vessels, and infarct on the preoperative ECG were all good predictors of survival. This study shows that the outcome of coronary artery bypass surgery 10 years operation is highly favorable.
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PMID:Clinical results of coronary bypass in 500 patients at least 10 years after operation. 697 37

A catheter-tip velocity transducer with two high-fidelity pressure manometers was used to evaluate the left ventricular (LV) hemodynamic effects of intravenous propranolol (10 mg). Nine patients without clinical evidence of heart failure were studied. Pulsatile ascending aortic blood flow velocity and pressure and LV pressure were measured continuously during drug administration. Beat-to-beat changes in stroke volume index, stroke work index, LV end-diastolic pressure, maximum blood flow velocity and acceleration, and maximum LV dP/dt were determined. Propranolol produced a decrease in maximum blood flow velocity (from 58 +/- 4.7 to 42 +/- 5.1 cm/sec, p less than 0.002), and acceleration (from 1181 +/- 130 to 847 +/- 117 cm/sec2, p less than 0.002, max dP/dt (from 1361 +/- 70 to 1146 +/- 63 mm Hg/sec, p less than 0.002), stroke volume index (from 47 +/- 3.0 to 38 +/- 3.2 ml/m2, p less than 0.002) and total stroke work index (from 702 +/- 33 to 603 +/- 44 mJ/m2 p less than 0.04), with little change in mean aortic pressure, peak systolic pressure and LV end-diastolic pressure. Depression in myocardial function was detectable within 1 minute after initiation of propranolol and persisted when negative chronotropic effects were eliminated by atrial pacing. The multisensor catheter technique allows rapid and safe detection of changes in cardiovascular function during propranolol administration in conscious man.
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PMID:Use of catheter-tip velocity--pressure transducer to evaluate left ventricular function in man: effects of intravenous propranolol. 736 37

Pulmonary gas exchange was evaluated after 10 mg i.v. propranolol in 12 patients 3-6 months after acute myocardial infarction undergoing haemodynamic examination in our outpatient department. None of them exhibited clinical signs of heart failure or obstructive airways disease. Routine spirometric examination was normal in all patients. Propranolol led to a distinct deterioration of LV function and to a fall in left ventricular filling pressure both at rest and during exercise. At rest, the administration of propranolol resulted only in a significant decrease of total ventilation. During exercise, its administration was followed by a significant decrease of the tidal volume, alveolar ventilation and VA/VE index. Arterial CO2 tension and physiological dead space ventilation increased significantly. Arterial oxygen tension decreased after propranolol insignificantly both at rest and during exercise. No patient reported dyspnoea after propranolol; 8 patients reported a decrease or disappearance of effort dyspnoea. None exhibited clinical signs of bronchospasm.
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PMID:Pulmonary gas exchange after propranolol in patients with ischaemic heart disease. 743 74

In the isolated canine heart-lung preparation modified to measure coronary outflow and myocardial oxygen consumption, an infusion of carbochromen of 1 mg/min produced an increase in coronary outflow of 120.0% and a decrease in myocardial oxygen consumption of 11.0% at a cumulative dose of 28.0 +/- 3.8 mg, resulting in an increase in efficiency of 22.4%. At a total dose of 40 mg, the corresponding figures were +181.0%, -15.0% and +38.0% respectively. No change in heart rate was observed. An infusion of propranolol of 1 mg/min, on the other hand, was characterized by decreases in myocardial contractility and heart rate starting with cumulative doses of 20 mg and 40 mg respectively. At a cumulative dose of 62.9 +/- 3.0 mg a marked degree of myocardial failure occurred (peak failure) characterized by a decrease in cardiac output (-53.3%), dp/dt (-50.8%), heart rate (-18.5%) and myocardial oxygen consumption (-25.5%). In a separate series exposed to the same infusion of propranolol but in which the decrease in heart rate was prevented by pacing, identical changes were observed except that myocardial oxygen consumption decreased only by 7.7%. It may be concluded from this study that carbochromen, in confirmation of reports by other investigators, increases coronary outflow markedly. Carbochromen decreases myocardial oxygen consumption by a direct effect on myocardial metabolism as is evident from the fact that this decrease is not accompanied by changes in any of the parameters which are known to influence myocardial oxygen consumption such as heart rate. Propranolol has no effect on myocardial oxygen consumption unless it is given in a dose which produces myocardial failure and a decrease in heart rate. The decrease in heart rate following propranolol bears a close relationship to the decrease in myocardial oxygen consumption.
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PMID:The cardiodynamic and metabolic effects of carbochromen and propranolol on the isolated dog heart. 745 33

beta-Blockers have been in clinical use for 30 years, and have an accepted role in (among others) the treatment of high blood pressure, the secondary prevention of myocardial infarction and the treatment of arrhythmias. Their place in the treatment of heart failure is currently under investigation. The drugs available in the 1970s and early 1980s were subjected to intense investigation. A new generation of beta-blockers, including some such as carvedilol and bucindolol, with vasodilating properties, is now appearing. As yet these later agents have not been the subject of large clinical trials. Clinical practice involves the treatment of individual patients with defined dosages of particular drugs. It is, therefore, not acceptable to base practice on theories derived from the clinical pharmacology of a particular drug, on the results of small trials or on a meta-analysis of results from a number of trials that were individually inadequate. Clinical practice must follow the results of large-scale trials in defined populations. The major trials in hypertension, myocardial infarction, arrhythmias and heart failure provide the best evidence for the use of individual beta-blockers in each of these clinical situations. In patients with high blood pressure, beta-blockers do not seem to have any particular advantage over other hypotensive agents. In myocardial infarction, relatively late use of a beta-blocker undoubtedly reduces fatality, though the value of early treatment is less clear. beta-Blockers are not powerful antiarrhythmics, but they do appear to prevent sudden death. Their possible role in heart failure is perhaps the most interesting current field of beta-blocker research. There are very few comparative studies of beta-blockers, and it is difficult to make precise recommendations. None of the new generation of beta-blockers has yet been used in a trial that is large enough trial for any of them to be accepted for routine use in preference to older drugs. The use of individual beta-blockers, as with any drug, should follow the results of clinical trials. Propranolol and atenolol have been studied most intensely in hypertension. For secondary prevention of myocardial infarction, the evidence is best for timolol. Sotalol is probably the best antiarrhythmic among the beta-blockers. Whether any individual beta-blocker is best for heart failure remains to be seen.
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PMID:Choosing the right beta-blocker. A guide to selection. 752 29

G proteins serve as transducers between cell surface receptors and intracellular effectors. They consist of three subunits, termed alpha, beta, and gamma. Recently, it has been recognized that the beta gamma subunits play an active role such as activation of beta-adrenergic receptor kinase (beta ARK). The desensitization and down-regulation of beta-adrenergic receptors have been observed in the heart failure. beta ARK is one of the components involved in desensitization of beta-adrenergic receptor and it is reported, recently, that G protein beta gamma subunits bind beta ARK through the pleckstrin homology domain. Therefore, we investigated the effects of beta-adrenergic receptor stimulation on steady-state level of G protein beta subunits (G beta) in the rat heart. The whole rat heart was preliminarily perfused for 10 min by Langendorff's technique at 60 mmHg of hydrostatic pressure with Krebs-Henseleit bicarbonate buffer, and then perfused for 30 min in the same buffer with or without 10 microM isoproterenol (ISO), 0.1mM epinephrine (EPI), 10 microM ISO with 0.1mM propranolol (PROP), or 10 microM ISO with 10 microM CGP20712A (CGP). Immunoblotting using isoform-specific antisera against G protein beta subunits revealed that the rat heart contains at least three G protein beta subunits, beta 1, beta 2 and beta 3 at molecular weight of between 35,000 and 37,000. The level of G beta 3 in the cytosol dramatically decreased in the presence of ISO alone or ISO with CGP. G beta 3 decreased in the presence of EPI as well. Propranolol could block ISO-induced decrease of G beta 3 in the cytosol. In contrast, the levels of G beta 1 and G beta 2 didn't change in the presence of ISO or EPI. On the other hand, in membrane fractions the level of G beta 3 significantly increased in the presence of ISO or EPI. ISO with PROP or ISO with CGP did not change the level of G beta 3 in membrane fractions. The levels of G beta 1 and G beta 2 did not change in the presence of ISO or EPI in membrane fractions. Taken together, beta-adrenoceptor agonist might induce isoform-specific translocation of G beta 3 from the cytosol to the membrane.
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PMID:[Beta-adrenergic receptor-mediated changes in subcellular localization of G protein beta subunits in perfused rat hearts]. 759 Jun

The purpose of this study was to investigate the possible value of continuous administration of propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing chronic endoscopic sclerotherapy. Among 239 patients admitted for acute variceal bleeding, 85 with cirrhosis were randomized to receive sclerotherapy either alone (40) or in combination with propranolol (45). Sclerotherapy was carried out with an intravariceal injection of 5% ethanolamine oleate through a fiberoptic endoscope. The procedure was performed every week, until the esophageal varices at the gastroesophageal junction were too small for any further injections. Varices were reinjected if they recurred. Propranolol was given orally twice a day until heart rate was reduced by 25% in the resting position. The mean follow-up period was 23.2 and 24.2 months for sclerotherapy and the sclerotherapy plus propranolol groups, respectively. During this period a significant (P = 0.001) reduction in the recurrence of esophageal varices was observed in patients treated with the combination of sclerotherapy plus propranolol compared with those treated with sclerotherapy alone. However, the time of rebleeding from any source or from esophageal varices did not differ significantly between the two groups. In the sclerotherapy group 21 patients rebled (35 bleeding episodes) compared with 14 (22 episodes) in the combination therapy group. Patients in the sclerotherapy group were more prone to bleed from gastric varices and congestive gastropathy than patients treated with the combination of sclerotherapy plus propranolol (P = 0.012). Twenty-five patients in the endoscopic sclerotherapy group developed complications attributed to sclerotherapy compared with 23 patients in the sclerotherapy plus propranolol group. Complications directly attributable to propranolol were observed in 11 patients. Three of these patients stopped taking the drug due to heart failure (1) and flapping tremor (2). Eight patients (17.8%) died in the latter group while the corresponding figure in the sclerotherapy group was nine (22.5%). It is concluded that the continuous administration of propranolol may reduce incidences of recurrent upper gastrointestinal hemorrhage from gastric sources in patients with cirrhosis undergoing chronic sclerotherapy.
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PMID:Propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing endoscopic sclerotherapy. A randomized controlled trial. 789 Sep 17

Carvedilol, a new vasodilating beta-adrenoceptor antagonist and a potent antioxidant, produces a high degree of cardioprotection in a variety of experimental models of ischemic cardiac injury. Recent clinical studies in patients with heart failure have demonstrated that carvedilol reduces morbidity and mortality and inhibits cardiac remodeling. The present study was designed to explore whether the protective effects of carvedilol on the ischemic myocardium include inhibition of apoptosis of cardiomyocytes and, if so, to determine its mechanism of action. Anesthetized rabbits were subjected to 30 minutes of coronary artery occlusion followed by 4 hours of reperfusion. Detection of apoptosis of cardiomyocytes was based on the presence of nucleosomal DNA fragments on agarose gels (DNA ladder) and in situ nick end labeling. Carvedilol (1 mg/kg IV), administered 5 minutes before reperfusion, reduced the number of apoptotic myocytes in the ischemic area from 14.7 +/- 0.4% to 3.4 +/- 1.8% (77% reduction, P<.001). Propranolol, administered at equipotent beta-blocking dosage, reduced the number of apoptotic myocytes to 8.9 +/- 2.1% (39% reduction, P<.05). DNA ladders were observed in the hearts of all six vehicle-treated rabbits but only one of six carvedilol-treated rabbits (P<.01). Immunocytochemical analysis of rabbit hearts demonstrated an upregulation of Fas protein in ischemic cardiomyocytes, and treatment with carvedilol reduced both the intensity of staining as well as the area stained. Myocardial ischemia/reperfusion led to a rapid activation of stress-activated protein kinase (SAPK) in the ischemic area but not in nonischemic regions. SAPK activity was increased from 2.1 +/- 0.3 mU/mg (basal) to 8.9 +/- 0.8 mU/mg after 30 minutes of ischemia followed by 20 minutes of reperfusion. Carvedilol inhibited the activation of SAPK by 53.4 +/- 6.5% (P<.05). Under the same conditions, propranolol (1 mg/kg) had no effect on SAPK activation. Taken together, these results suggest that carvedilol prevents myocardial ischemia/reperfusion-induced apoptosis in cardiomyocytes possibly by downregulation of the SAPK signaling pathway, by inhibition of Fas receptor expression, and by beta-adrenergic blockade. The former two actions represent novel and important mechanisms that may contribute to the cardioprotective effects of carvedilol.
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PMID:Possible involvement of stress-activated protein kinase signaling pathway and Fas receptor expression in prevention of ischemia/reperfusion-induced cardiomyocyte apoptosis by carvedilol. 946 87

1. Chronic treatment with beta-adrenergic blocking agents can improve survival in patients with heart failure. The mechanisms underlying the beneficial effects and whether these effects are generalizable to ischaemic heart failure are unresolved. 2. We performed echocardiographic-Doppler examinations in rats (n=28) 1 and 6 weeks after myocardial infarction (MI) or sham surgery. Rats were randomized to no treatment or propranolol (500 mg/l in drinking water) after the first echocardiogram. Isometric contractions and intracellular Ca transients were recorded simultaneously in noninfarcted left ventricular (LV) papillary muscles. 3. Untreated MI rats had significant LV dilatation (10.6+/-0.4* vs 8.9+/(-0.3) mm, MI vs control), impaired systolic function (fractional shortening=11+/-2* vs 38+/-2%), and a restrictive LV diastolic filling pattern. MI rats receiving propranolol had similar LV chamber sizes (10.6+/(-0.5) mm) and systolic function (13+/(-2%). The propranolol treated animals had higher LV end-diastolic pressures (27+/-2* vs 20+/(-3 mmHg) and a more restricted LV diastolic filling pattern (increased ratio of early to late filling velocities and more rapid E wave deceleration rate). Contractility of papillary muscles from untreated MI rats was depressed (1.6+/(-0.3) vs 2.4+/(0.5 g mm(-2). In addition, Ca transients were prolonged and the inotropic response to isoproterenol was blunted. Propranolol treatment did not improve force development (1.6+/(-0.3 g mm(-2) or the duration of Ca transients during isoproterenol stimulation. 4. Chronic propranolol treatment in rats with postinfarction heart failure did not improve LV remodeling or systolic function. LV diastolic pressures and filling patterns were worsened by propranolol. Treatment also did not produce appreciable improvement in contractility, intracellular Ca regulation or beta-adrenergic responsiveness in the noninfarcted myocardium.
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PMID:Effects of propranolol treatment on left ventricular function and intracellular calcium regulation in rats with postinfarction heart failure. 1045 25

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