Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the cardioselective beta-blocker, metoprolol, were evaluated under double-blind conditions in eighteen patients with angina pectoris. During an introductory run-in period of eight weeks, a placebo was given single-blindly. Thereafter two double-blind crossover periods each of four weeks followed, either 20 mg metroprolol or placebo being given t.i.d. Metoprolol gave a significant reduction in the number of anginal attacks and in nitroglycerin consumption. The patients' subjective assessments of their daily angina pectoris symptoms also showed a significant improvement compared with the placebo. At the end of each period, a standardized exercise test was performed. In comparison with placebo, metoprolol gave a significant increase of total work performed until the appearance of 1 mm ST-segment depression and until the end of exercise. The heart rate was significantly reduced at rest and during exercise. The blood pressure was significantly reduced only during exercise. None of the patients reported any severe unwanted effects. The complaints reported were mild to moderate, and the frequency during metoprolol treatment was even lower than during placebo treatment. No signs or symptoms of cardiac failure were seen in any of these patients on any occasion. It is concluded that 20 mg metoprolol t.i.d. is of benefit in the treatment of angina pectoris but further benefit might be obtained with higher doses.
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PMID:Effects of the cardioselective beta-blocker metoprolol in angina pectoris. A subacute study with exercise tests. 0 92

Eighteen patients with angina pectoris, who had previously participated in a cross-over study with 20 mg metoprolol t.i.d. and placebo, have been included in this study. During an introductory six-month open tolerability study, all patients were treated with 50 mg metoprolol t.i.d. and during a subsequent cross-over study, the efficacy of this dose was compared with that of placebo under double-blind conditions. An exercise was performed at the end of each cross-over period. Metoprolol, in a dose of 50 mg t.i.d., gave a significant improvement compared with placebo in respect of the number of anginal attacks, nitroglycerin consumption and daily subjective assessment of the patients' anginal symptoms. Metoprolol also gave a significant increase in exercise capacity, both until the appearance of 1 mm ST segment depression and until the end of exercise. Heart rate and blood pressure were reduced both at rest and during exercise. No severe unwanted effects were observed during this study ranging over eight months, and none of the patients had any signs or symptoms of cardiac failure or pulmonary dysfunction on any occasion. Unwanted effects reported were mild to moderate, and the frequency was the same as during placebo treatment. No abnormal laboratory findings were observed and the relative heart volume was not significantly changed. Administration of 50 mg metoprolol t.i.d. seems to be of greater benefit than 20 mg metoprolol t.i.d., previously investigated in these patients.
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PMID:Effects of metoprolol in angina pectoris. A subacute study with exercise tests and a long-term tolerability study. 0

A wide variety of drugs may be associated with serious cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiac disorders is the most extensively documented, especially the arrhythmias due to digitalis glycosides. Various arrhythmias are also caused by toxic levels of many antiarrhythmic agents including quinidine, procainamide and phenytotin. Myocardial depression and heart failure are serious side-effects of beta-adrenoceptor blocking agents and myocardial ischaemia due to sympathominetic amines may result from both direct and indirect mechanisms. The many toxic reactions in the cardiovascular system due to non-cardiac drugs are less widely known and for the most part less clearly understood. Many remain controversial at the current time; for example, the diathesis toward thromboembolism in women taking oral contraceptives. Potential cardiac toxicity due to drugs used in the rapidly expanding sphere of anti-neoplastic chemotherapy is exemplified by the cardiomyopathy-like toxicities of doxorubicin and daunorubicin. Many of the psychotherapeutic drugs including phenothiazine antipsychotics and tricyclic antidepressants have arrhythmogenic potential.
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PMID:Drug-induced cardiovascular diseases. 1 29

In 95 patients treated by electroimpulse techniques for their cardiac fibrillation the incidence and diagnostic importance of postextrasystolic depression of the sinus rhythm were studied. Two groups of patients were singled out for a comparative study of the value of different prognostic criteria of the stability of the restored sinus rhythm: group 1--53 patients with unsatisfactory results of treatment (the sinus rhythm was preserved for not more than 1 month), and group 2--21 patients with good late results (the sinus rhythm persisted for over 6 months). A study of the distribution of the incidence of different prognostic signs in either of these groups showed that their prognostic value may be presented in the following succession: presence of intraventricular conductivity, severity of cardiac insufficiency, frequent postconversion extrasystoles, history of cardiac fibrillation of over 3 years, presence of a postextrasystolic depression of the sinus rhythm.
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PMID:[Postextrasystolic depression of sinus rhythm during electroimpulse therapy of auricular fibrillation]. 6 42

75 patients aged under 70 years who had survived acute myocardial infarction complicated by both significant arrhythmias and cardiac failure were followed-up for 1 year in an attempt to identify features which suggest the likelihood of late death or reinfarction. Patients were carefully instructed in the identification and importance of possible prodromal symptoms and the availability of a mobile intensivecare ambulance service and a 24 h hospital control centre. Horizontal ST-segment depression or anginal pain on an exercise test done within 6 weeks of infarction was a useful predictor of late death. Routine twice weekly E.C.G. recordings taken by telephone transmitter at rest and after mild exertion resulted in the identification of significant arrhythmias in only 7 patients. 13 patients (17%) died, 5 of them instantaneously. 4 of the 13 patients and 22 of the 62 survivors reported "prodromal symptoms". Unreported prodromal symptoms were elicited retrospectively in 14 of the 62 survivors and from the relatives of 4 of the 13 patients who died. Thus, 35% of prodromal symptoms were not reported despite intensive patient education and counselling. The incidence of "prodromal symptoms" was no higher in patients who died than in those who did not die.
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PMID:Predictors of reinfarction and sudden death in a high-risk group of acute myocardial infarction survivors. 8 97

The purpose of the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.
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PMID:Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results. 12 66

We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.
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PMID:Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit. 13 11

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.
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PMID:Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. 13 86

The Ca2+-activated myosin ATPase and the amino acid compositions of actin and myosin were determined for preparations from chronically failing dog hearts. Hypertrophy and congestive heart failure were produced by combined tricuspid valve insufficiency and pulmonary artery stenosis. Control, shamoperated, and noncardiac circulatory failure (inferior vena cava constriction) dogs also were studied. All hearts were divided into right ventricle, septum and left ventricle and each sample was individually analyzed. Calcium-activated ATPase decreased in the failing hearts and showed a distinct gradient of depression from right to left ventricles. There were no changes in ATPase activity among the other groups. The amino acid composition of actin was the same regardless of origin. The amino acid composition of myosin was unaltered except that cystine/2 residues were markedly decreased in failing heart myosin. The same gradient of depression was present as was found for Ca2+-activated myosin ATPase. This study suggests that protein metabolism is abnormal and that altered proteins are produced in hypertrophy and congestive heart failure. It appears that these changes do not affect all proteins, since actin was normal by the parameters studied. It is clear that the stressed ventricle is the most severely involved, but the entire heart is altered to some degree. Thus, we conclude that altered protein metabolism may be an important primary factor in the genesis of heart failure.
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PMID:The amino acid composition of actin and myosin and Ca2+-activated myosin adenosine triphosphatase in chronic canine congestive heart failure. 13 12

The effects of gramnegative endotoxin-induced myocardial failure in the pentobarbital-anesthetized dog were examined by monitoring its influence on cardiac myofibrillar ATPase activity. Myofibrils were isolated from endo- and epicardial portions of the left ventricular wall. ATPase activities were determined in animals treated with 4 mg/kg endotoxin and monitored 5 h, in animals monitored for 5 h without endotoxin (controls), and in animals implanted with a unilateral femoral shunt and given endotoxin. No differences were seen in the activities between the endo- and epicardial portions of any preparation. Activity was significantly depressed in endotoxemic animals. Increasing venous return by 313 +/- 71 ml/min significantly increased coronary flow by reducing coronary vascular resistance and prevented any observed depression of myofibrillar ATPase activity. In in vitro studies, adding endotoxin directly to a myofibril preparation did not modify normal activity. It appears that the mechanical and myofibrillar dysfunctions are due to the action of endotoxin at sites not associated with the actomyosin ATPase, but may be due to the production of an intermediary agent in concert with a decreased venous return.
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PMID:Endotoxin and myocardial failure: role of the myofibril and venous return. 15 Jul 99


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