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)

To identify the role of the myocardial beta-adrenergic pathway in congestive heart failure, we examined beta-adrenergic-receptor density, adenylate cyclase and creatine kinase activities, muscle contraction in vitro, and myocardial contractile protein levels in the left ventricles of failing and normally functioning hearts from cardiac-transplant recipients or prospective donors. Eleven failing left ventricles had a 50 to 56 per cent reduction in beta-receptor density, a 45 per cent reduction in maximal isoproterenol-mediated adenylate cyclase stimulation, and a 54 to 73 per cent reduction in maximal isoproterenol-stimulated muscle contraction, as compared with six normally functioning ventricles (P less than 0.05 for each comparison). In contrast, cytoplasmic creatine kinase activity, adenylate cyclase activities stimulated by fluoride ion and by histamine, histamine-stimulated muscle contraction, and levels of contractile protein were not different in the two groups (P less than 0.05). We conclude that in failing human hearts a decrease in beta-receptor density leads to subsensitivity of the beta-adrenergic pathway and decreased beta-agonist-stimulated muscle contraction. Regulation of beta-adrenergic receptors may be an important variable in cardiac failure.
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PMID:Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. 628 49

Using equilibrium radionuclide ventriculography, the authors investigated left ventricular ejection fraction in 10 healthy men and in 57 men who had undergone their first transmural myocardial infarction (MI) 4 to 7 months earlier, were below 65 years of age and did not present signs of heart failure at the time of examination. Resting ejection fraction in healthy men amounted to 63 +/- 5%, in patients with uncomplicated MI to 54 +/- 7%, and in patients with clinical manifestations of heart failure in the acute phase to 37 +/- 8%. Patients with anteroseptal MI showed a negative correlation between the ejection fraction, on the one hand, and the sum of Q wave voltages in the precordial ECG map and the maximum value of serum creatine kinase in the acute phase of MI, on the other hand. The ejection fraction correlated with the degree of pulmonary hypertension during exercise. At work load of 50 W the ejection fraction measured in 31 patients was not significantly different shortly before discharge from hospital and 6 months after the onset of MI.
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PMID:Equilibrium radionuclide ventriculography in men after transmural myocardial infarction. 632 97

The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A randomized trial of intravenous and intracoronary streptokinase in patients with acute myocardial infarction. 638 54

Various methods have been proposed and tried to limit the extent of myocardial damage at the time of infarction. We chose to assess the usefulness of intravenous magnesium in this regard because of its important role in myocardial metabolism and function and the suggestion of its deficiency in ischemic hearts. A double-blind randomized trial was carried out and results analyzed in 76 patients. At the end of the infusion period the mean serum Mg++ level for the treated group was 3.6 versus 1.9 mg/dl for the control group. The estimated size of infarction (as measured by MB-CK release) was not significantly smaller overall in the treated group (37.4 +/- 4.3 vs. 45.6 +/- 4.6 MB-CK g/Eq), but was significantly smaller in the treated subgroup without heart failure (31.6 +/- 5.8 vs. 44.7 +/- 4.8 MB-CK g/Eq). A trend toward less ventricular ectopy was seen in the group treated with magnesium. There was significantly less lidocaine used for the treatment of ventricular dysrhythmias in this group. Magnesium supplementation in patients undergoing acute coronary events is promising and deserves further study.
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PMID:Magnesium therapy in acute myocardial infarction--a double-blind study. 639 46

The study was made in order to determine the relationship between myocardial infarct size and the incidence of cardiac arrhythmias during acute myocardial infarction (AMI). In 317 consecutively admitted patients infarct size was estimated from serial serum CK-MB measurements. The ECG was continuously monitored during 18 days in hospital, and all electrocardiographic recordings were analysed daily. All patients were followed up one year after discharge. The median infarct size was larger among the 220 patients with arrhythmias than among the 97 patients without (814 Ul-1 vs 419 Ul-1, P less than 0.0001). There was a significant relationship between the estimated infarct size and the following arrhythmias: ventricular ectopic beats, sinus tachycardia, and atrioventricular block, whereas supraventricular ectopic beats showed no such relation. Patients with heart failure, however, had a high incidence of ventricular arrhythmias regardless of the size of their infarcts. The follow-up study demonstrated that the ventricular arrhythmias positively correlated with infarct size were also associated with significantly increased one-year mortality among hospital survivors. Thus, the present study indicates that not only pump failure, but also cardiac arrhythmias are connected with the negative influence of infarct size on prognosis.
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PMID:Myocardial infarct size: correlation with cardiac arrhythmias and sudden death. 647 89

Three metabolic adaptive or compensatory mechanisms of heart failure were discussed: Adaptation of energy production and of energy availability in the myocardial cell. With increased myocardial oxygen demands this is achieved by a progressive displacement of the mass action ratio of the creatine phosphokinase reaction, so that pronounced changes in the creatine phosphate-ratio, related to myocardial oxygen consumption, are accompanied by only small changes in adenosine-5'-triphosphate adenosine-5'-diphosphate and hence in free energy of the adenine-nucleotide system. Adjustment of the oxygen availability by adaptation of the hemoglobin dissociation curve due to an increase in the erythrocyte content of 2, 3-diphosphoglycerate. This is accompanied by a swelling of erythrocytes as a consequence of an increase in the Gibbs-Donnan potential. In patients with congestive heart failure 2,3-diphosphoglycerate-synthesis is augmented due to respiratory alkalosis and increased concentrations of deoxygenated hemoglobin. Increase in the sympathetic drive of the heart due to increased net discharge of the neurotransmitter caused by reduced neuronal reuptake of norepinephrine. The diminished myocardial norepinephrine content in heart failure is due to the diminished neuronal uptake and to insufficient de novo catecholamine synthesis in the heart. Rather than tyrosine-hydroxylase the transformation of dopamine to norepinephrine seems to be the rate limiting step for catecholamine synthesis in heart failure.
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PMID:Metabolic aspects of compensatory mechanisms in cardiac failure. 651 Jun 22

An increasing proportion of patients hospitalized with myocardial infarction have previously undergone coronary artery bypass surgery. To define this subgroup, 77 patients with acute infarction occurring 2 or more months (mean 52.8) after bypass surgery were compared with 77 control patients with infarction. Baseline characteristics of the groups were similar except that post-bypass patients were more often men (p = 0.02) and more likely to have had a previous infarction (37 versus 21, p = 0.008). Infarct size was smaller in the post-bypass group as assessed by peak creatine kinase (CK), peak CK-MB, maximal number of electrocardiographic leads with ST elevation, maximal summed ST elevation and QRS score measured 7 to 10 days after admission (p less than 0.001 for each variable). Five control patients but none of the post-bypass patients died in the hospital (p = 0.06). Serious complications (death, acute heart failure, ventricular fibrillation, second or third degree atrioventricular block) occurred in 24 control patients but in only 5 post-bypass patients (p less than 0.001). Angiography was performed after infarction in 45 of the 77 post-bypass patients. Occlusion of both a native coronary artery and its graft was found in 24 of the 45; these patients had had higher peak CK levels (p = 0.008) than the other 21 patients who had angiography. The probable causes of infarction in these 21 were disease progression in nonbypassed arteries or graft occlusion with arterial stenosis, or vice versa, and disease progression distal to a patent graft.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial infarction in patients with previous coronary artery bypass surgery. 660 47

From 1978 to 1981, 818 consecutive patients with acute myocardial infarction were admitted, 112 (13.7%) of whom required artificial ventilation because of complications. Their mean age (62) corresponded to the mean age of all acute myocardial infarction patients (63). 28 (25%) survived the hospitalization and were followed after discharge. 2 were lost to follow-up. After a mean follow-up period of 26 months, 8 patients had died and 18 were still alive, none of them free of symptoms. There was no difference of age, duration of respirator therapy and maximal creatine kinase activity between survivors (group A) and nonsurvivors (group B). In 50% of patients cardiac failure leading to endotracheal intubation was triggered or made worse by arrhythmias. The remaining 50% of patients showed pure pump failure. Again in these two subsets, cardiac failure was significantly less marked in group A than in group B according to the hemodynamic findings. In conclusion, inpatient mortality in patients with acute myocardial infarction requiring artificial ventilation was high (75%) and hemodynamic findings were significantly worse in those not surviving. Patients discharged from the hospital also had a reduced life expectancy (less than 50% after 3 years).
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PMID:[Prognosis in complications of acute myocardial infarction requiring artificial respiration]. 662 39

Early recanalization of infarct-related coronary arteries has been attempted in 40 patients with acute myocardial infarction (AMI) and angiographically proven total occlusion by brief high dose intravenous streptokinase infusion (IVSK). In 24 patients (60%) recanalization was achieved after 48 +/- 14 min of IVSK at an infusion rate of 30,000 to 40,000 IU/min (group A), in 16 patients there was a late (greater than 2 h) or no recanalization (group B). The total dose of SK was 1.7 +/- 0.48 Mio IU in group A and 1.74 +/- 0.41 Mio IU in group B, the time from the onset of symptoms to peak myocardial enzyme of creatine phosphokinase (CKMB) 11 +/- 3 h in group A and 22 +/- 6 h in group B (p less than 0.001). Biplane left ventricular ejection fraction increased from 55 +/- 9% at the time of acute angiography to 58 +/- 10% after 14 to 24 days in group A (p less than 0.1) and decreased from 49 +/- 11 to 41 +/- 11% in group B (p less than 0.005). There were four reocclusions in group A, two could be reopened by i.v. urokinase (1 Mio IU over 30 min). During a follow-up period of 18 +/- 8 months one patient in group A died from an early ventricular rupture 2 hours after recanalization, and one patient in group B from heart failure 7 months after IVSK. There was no serious bleeding or other complication related to IVSK. We conclude that IVSK is an effective and safe means of early recanalization of coronary thrombosis in AMI, and feasible in the majority of patients with AMI.
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PMID:High dose intravenous streptokinase in acute myocardial infarction. 662 71

Results of dibunol use in 31 patients with progressive myocardial infarction (MI) are presented. The effect of the drug was studied by precardial charting and serial determination of creatine phosphokinase activity, integral rheography and phase analysis of the cardial systole. It was established that in the acute phase of MI, dibunol significantly reduced the ischemic damage to the myocardium and limited the focus of necrosis. Prolonged total intake of the drug throughout the acute period of MI stimulated cardiac activity without a statistically significant improvement in the contractile capacity of the myocardium, however. Patients treated with dibunol in the acute period of MI tended to show a lower frequency of pain recurrences and a decrease in such parameters as the development of heart failure, and/or rhythm disturbances and the mortality rate.
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PMID:[1st attempt at using the antioxidant dibunol in the acute stage of a myocardial infarct]. 670 Jan 25


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