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)

111 patients below 70 years old, with the first acute myocardial infarctions, 6 hours since the pain occurred--have been treated with streptokinase i.v. In 102 patients we obtained full curve of CK-MB activity. Early peak of CK-MB activity < 15 hours after onset of symptoms we have observed in 59 patients, and late peak of CK-MB activity > 15 hours in 43 patients. There was not any significant statistics differences between early and late groups in frequency of: early ventricular fibrillation (< 48 hours), complex ventricular arrhythmia (in 21 day), heart failure and in-hospital mortality. 1 patient died in hospital in early group and in late group also died 1 patient. The follow-up period was from 10 to 48 months (av. 26 +/- 13). 100 patients left the hospital and the full informations we have obtained in 97 cases. No one died in that time. In the group with early peak CK-MB activity we observed more often the unstable angina and the new myocardial infarction (21%) than in the group with late peak of CK-MB activity (15%), but these differences were nonsignificant. In conclusion our results don't confirm that the early peak of CK-MB activity is the positive risk factor of unstable angina and the new myocardial infarction.
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PMID:[Prognostic value of an early peak CK-MB in plasma of patients treated with streptokinase for acute myocardial infarction]. 130 May 54

To study the relative roles of creatine kinase (CK) and adenylate systems in cardiac energy turnover, the effect of CK inhibitor, iodoacetamide- (IAA, 0.5 mM), and 2-deoxyglucose-(DOG, 2 mM) induced) 65% depletion of adenine nucleotides at slightly decreased CK flux was determined in isolated rat heart. Both substances did not substantially affect contractile parameters of the isovolumic heart. However, an augmentation of cardiac work induced by isoproterenol addition was feeble and transient in IAA-treated hearts while the response of DOG-treated hearts was well preserved. The cardiac failure after IAA treatment was associated with irreversible fall in myocardial ATP content as evidenced by 31P-NMR technique. Furthermore, these hearts were unable to perform cardiac pump function due to insufficient cardiac filling and distensibility. The DOG-treated hearts exhibited 50% reduction in the pump function and were able to increase their work in elevated resistance. The results suggest that CK pathway is extremely important for both full cardiac relaxation and maximal contractile function.
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PMID:[Functional significance of 2 pathways of energy transport in cardiomyocytes]. 140 43

The effects of clinically used cardioactive agents in furazolidone-induced cardiomyopathy in the turkey poult have been recently reported, and note-worthy differences in cardioprotective efficacy of adrenergic effectors, calcium channel blockers, and cardiac glycosides have been noted in animal and human studies of heart failure. We therefore investigated the effects of chronic oral administration of cardioactive agents on ventricular tissue from normal turkey poults, and we determined whether these agents altered cardiac function, energetics, or transmembrane signaling pathways in a manner that might contribute to the varying degrees of cardioprotection and therapeutic efficacy reported previously. Creatine content was significantly higher in propranolol- and atenolol-treated animals. There was also higher lactate dehydrogenase and creatine kinase activities, reflecting an overall increase in energy reserve. Treatment with the calcium channel antagonists verapamil and nifedipine produced a significant increase in adenylyl cyclase activity and beta-adrenergic receptor density. Nifedipine treatment resulted in upregulation of both beta-adrenergic receptors and dihydropyridine receptors. This finding was associated with enhanced peak twitch force at all extracellular Ca2+ concentrations. We demonstrate for the first time that clinically used pharmacological agents (nifedipine and propranolol) result in alteration in two transmembrane signaling pathways, with associated alterations in physiological performance. Moreover, agents without cardioprotective effect in furazolidone-induced cardiomyopathy did not induce alterations in transmembrane signaling or energetics in normal hearts.
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PMID:Chronic administration of cardiovascular drugs: altered energetics and transmembrane signaling. 144 9

The purpose of this study is to evaluate the efficiency of energy metabolism in the myocardium by means of the activities of creatine kinase (CK) and CK isoenzyme following age-related change in the heart and experimental heart failure. Wistar strain male rats aged from 3 weeks to 57 weeks after birth were used. The main experimental results obtained are as follows. (1) There were differences in the compositions of CK isoenzyme of the ventricular, atrial, and papillar muscles. No apparent variation, however, was noted among the basal portions of the left and right ventricular muscles, free wall of the left ventricle, and apex. (2) Compositions of CK isoenzyme analyzed from the ventricle and atrium were clearly different. The level of CK-B subunit activity of the ventricular muscle was highest level in the 5-week-old rat, and subsequently dropped significantly in the 24-week-old rat. Thereafter, the level gradually increased with aging. Dramatic change in the energy metabolism in the myocardium occurred in rats more than 3 weeks old. (3) Decrease in activity of m-CK but increase in activity of succinate dehydrogenase analyzed from the ventricular muscle of experimental heart failure induced by monocrotaline was recognized. From these results, the author assumed that the trend of the composition of CK isoenzyme is one of the indices in the determination of the regulation of energy metabolism of the myocardium.
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PMID:[Evaluation of energy metabolism on the myocardium analyzing of creatine kinase isoenzymes in rats]. 151 14

To determine whether cardiac hypertrophy secondary to chronic renovascular hypertension is associated with altered in vivo myocardial metabolism, phosphorus-31 nuclear magnetic resonance saturation transfer techniques were used to study creatine kinase (CK) kinetics in six chronically hypertensive dogs with moderate cardiac hypertrophy and eight control dogs. The forward rate constant of CK and the flux of phosphocreatine to adenosine triphosphate were determined in both groups of dogs before and during norepinephrine administration (1 microgram/kg per min), used to increase heart rate x systolic blood pressure (rate-pressure product), cardiac output and oxygen consumption. Baseline and norepinephrine-induced changes in rate-pressure product, cardiac output and oxygen consumption were similar in both groups of dogs, as were baseline forward rate constant and flux of phosphocreatine to adenosine triphosphate. However, the norepinephrine-induced changes in forward rate constant and flux were significantly less in hypertensive than in control dogs (p less than 0.05) even though changes in hemodynamic and functional variables were similar in both groups. These data demonstrate that moderate myocardial hypertrophy is associated with altered CK kinetics, which do not appear to affect the heart's ability for global mechanical recruitment at this stage in the hypertensive process. It is possible that the changes in myocardial enzyme kinetics may contribute to diastolic dysfunction previously reported in this model and may be a precursor for ultimate development of heart failure if hypertension is maintained for prolonged periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Creatinine kinase kinetics studied by phosphorus-31 nuclear magnetic resonance in a canine model of chronic hypertension-induced cardiac hypertrophy. 153 Aug 55

In recent years, captopril has attracted considerable clinical attention as an agent for use in treating heart failure. We administered 15 mg/kg of captopril or 1.5 mg/kg of enalapril to 5-week-old J-2-N cardiomyopathic hamsters for 10 or 15 weeks, and investigated the roles of the renin-angiotensin-aldosterone and kallikrein-kinin systems in the onset and progress of cardiomyopathy. In the untreated group, serum creatine kinase levels increased in accordance with the progression of cardiomyopathy, but this increase was markedly inhibited by the administration of captopril. The rise in serum aldolase levels was similarly inhibited. Serum malondialdehyde levels were significantly reduced by the administration of captopril. ECG findings and the ventricular myosin isoenzyme pattern were also markedly improved by captopril. The improvement in all these parameters was less with enalapril. These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril.
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PMID:The effects of angiotensin converting enzyme inhibitors and the role of the renin-angiotensin-aldosterone system in J-2-N cardiomyopathic hamsters. 153 90

Myositis and myocarditis have been reported in progressive systemic sclerosis, and these patients have had favorable therapeutic responses to intravenous pulse methylprednisolone. Thus far, premortem biopsy documentation of myocarditis and myocardial fibrosis has not been reported in such patients. We report the case of a patient with subacute congestive heart failure six months after she developed Raynaud's phenomenon. Clinical examination was typical of scleroderma but there was no proximal muscle weakness. She had elevated creatine kinase and MB-creatine kinase and laboratory evidence of hypothyroidism. Echocardiogram demonstrated four-chamber dilatation and severe left ventricular dysfunction. Cardiac catheterization revealed normal epicardial coronary arteries and severely decreased cardiac index. A skin biopsy specimen of the forearm was consistent with diffuse systemic sclerosis, and an endomyocardial biopsy specimen demonstrated mild fibrosis and lymphocytic infiltrate. Her heart failure initially improved with digoxin, furosemide, and enalapril. She also received L-thyroxine and intravenous methylprednisolone. The heart failure progressed over the next six weeks and she died. Patients with scleroderma and new-onset heart failure may have acute myocarditis.
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PMID:Acute myocarditis in fulminant systemic sclerosis. 154 Nov 69

To develop improved prognostic algorithms for routine bedside use in acute myocardial infarction (AMI), the prognostic value concerning 2- and 12-month mortality of an early (within 72 hours after AMI) resting echocardiogram was defined in 201 consecutive patients. The relation between (1) the clinical variables (age, sex, prior and repeat AMI, arrhythmias, cardiac arrest, early [less than 72 hours after AMI] and late heart failure, early and maximal in-hospital Killip class, and maximal creatine kinase-MB isoenzyme), (2) early myocardial performance by echocardiography, and (3) mortality was characterized by Kaplan-Meier survival curves and receiver-operating characteristic curves based on Cox regression model. Only age and clinical heart failure in terms of the maximal in-hospital Killip class had independent predictive value of death (p less than 0.05) when an early echocardiographic estimate of left ventricular ejection fraction (LVEF) was included in the multivariate statistical models. The following 2 optimized algorithms for admission and predischarge calculation of risk of mortality at 2 and 12 months were developed based on the Cox model, using combinations of age, maximal Killip class and early echocardiographic LVEF: mortality at 2 months = 1 - exp - [0.051 x exp [0.044 x (age -60) - (0.117 x (LVEF - 40)]]; and mortality at 1 year = 1 - exp - [0.101 x exp [0.408 x (maxKillip - 1) - (0.061 x (LVEF - 40)]]. Discriminative power for prediction of mortality of the predischarge algorithm in an independent population of 195 patients 5 days after AMI compared favorably with that obtained in the original population, confirming the validity of the proposed method of prognostication.
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PMID:Echocardiographic algorithms for admission and predischarge prediction of mortality in acute myocardial infarction. 159 66

Although alcohol has long been known to induce cardiac depression and cardiomyopathy, it is not known whether drug therapy or pharmacologic manipulation can be used to prevent or reverse these toxicities. With this in mind, high levels (15 mM) of magnesium (Mg) were investigated for their potential antialcohol effects on perfused rat hearts. A high concentration of ethanol (135 mM) was used to induce rapid cardiac failure as assessed by hemodynamic and metabolic parameters. During ethanol perfusion in normal 1.2 mM [Mg2+]o physiologic salt solution, coronary flow decreased immediately, and all of the hemodynamic parameters studied (except for heart rate) were depressed significantly. After 10 min of 135 mM ethanol perfusion, only 60% of the hearts kept beating; at 15 min, only 42% of the hearts continued to beat. Myocardial metabolism under such conditions as assessed by examination of coronary effluent concentrations of lactic acid (LA), lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) was rapidly and severely compromised. Although 15 mM MgSO4 alone did not alter coronary flow and systolic pressure under the conditions studied, it did decrease cardiac output, heart rate and total pressure developed. However, when 15 mM MgSO4 was given 10 min before ethanol, and continued during ethanol perfusion, the usual depression in all assessed cardiac hemodynamic parameters (except heart rate) caused by ethanol was not observed. During 15 min of high [Mg2+]o perfusion, coronary flow recovered from 19.1 +/- 6.8% (ethanol alone) to 68.1 +/- 9.9% of control values (p < 0.01); cardiac output recovered from 10.4 +/- 4.6% (ethanol alone) to 43.6 +/- 7.5% of control (p < 0.01); stroke volume went from 12.9 +/- 5.8% (ethanol alone) to 97.1 +/- 14.5% of control (p < 0.01); systolic pressure from 55.3 +/- 3.6% (ethanol alone) to 88.8 +/- 4.0% of control (p < 0.01), and total pressure developed from 23.9 +/- 7.8% (ethanol alone) to 35.0 +/- 4.5% of control (p < 0.05). Assessment of the metabolic biochemical parameters supported these changes in hemodynamic improvement. For example, LA, LDH and CPK all went from elevated values towards normal levels. There were similar hemodynamic and metabolic responses to high [Mg2+]o given during ethanol perfusion to that given before ethanol perfusion. The hemodynamic and metabolic beneficial effects between groups pretreated or treated with high [Mg2+]o exhibited no significant differences. These results suggest that high [Mg2+]o (15 mM) given either before or during ethanol-induced cardiotoxicity is effective in attenuating both functional and metabolic damage caused by high ethanol perfusion in the rat heart.
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PMID:Beneficial effects of high magnesium on alcohol-induced cardiac failure. 166 23

We examined the acute phase reaction in myocardial infarction after thrombolytic treatment by streptokinase or tissue plasminogen activator. The magnitude of the acute phase reaction as determined by measurements of serum C-reactive protein and amyloid-A protein did not correlate with infarct size (determined by serial measurements of creatine kinase-MB) in this patient population. On the other hand, the development of acute cardiac failure was more closely associated with the magnitude of the acute phase reaction than with infarct size. The peak serum values of C-reactive protein in patients with and without acute cardiac failure were 128 mg/l (95% confidence intervals 85-170) and 60 mg/l (30-89); P less than 0.01 and concentration time integrals 578 mg/l x days (368-787) and 205 mg/l x days (62-350); P less than 0.01. The corresponding creatine kinase-MB values were 310 U/l (191-429) and 207 U/l (125-289) not significant; and 319 U/l x days (201-437) and 204 U/l x days (124-286) not significant; respectively. Patients requiring medication for cardiac failure on discharge from hospital had higher C-reactive protein and serum amyloid A protein values than those who did not, although the difference did not quite reach statistical significance. The infarct sizes were similar whether the patients needed medication for cardiac failure at discharge or not. Subjectively felt morbidity due to myocardial infarction was linearly associated with serum C-reactive protein peak values (P less than 0.05) and concentration time integrals (P less than 0.05), but not with infarct size. We conclude that thrombolytic treatment of myocardial infarction may reduce hospital inpatient morbidity independently of the limitation of infarct size. This diminished morbidity seems to be associated with modest or low acute phase reaction.
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PMID:Acute phase reaction, infarct size and in-hospital morbidity in myocardial infarction patients treated with streptokinase or recombinant tissue type plasminogen activator. 175 22


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