Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten healthy (aged 28 to 39) and ten heart failure NYHA II (aged 19 to 49) male subjects were prospectively studied under no drugs, under furosemide (40 mg/day), under captopril (150 mg/day) and under their association. Arterial compliance (ml/mmHg) was measured in all subjects at rest and supine. Heart failure etiology was dilated cardiomyopathy or ischemic heart disease without significant regurgitation. Arterial compliance was significantly higher in healthy than in heart failure patients in all studied conditions (p less than 0.001) (healthy = 2.2 + 0.29 vs. heart failure = 0.79 + 0.14). Neither single drug nor their association induced any change in healthy subjects. Arterial compliance progressively increased in heart failure with furosemide, captopril, and their association (no drug = 0.79 + 0.14; furosemide = 0.87 + 0.15; captopril = 0.94 + 0.15 and furosemide + captopril = 0.99 + 0.14). Captopril induced a higher increment than furosemide (p less than 0.001) and their association even a higher increment (p less than 0.001) than any single drug. Thus captopril and/or furosemide increased arterial compliance in heart failure but not in healthy subjects, possibly through changes in arterial wall edema and smooth muscle contraction.
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PMID:Effect of drugs on a noninvasive index of arterial compliance in healthy and heart failure patients. 174 91

The Captopril Prevention Project (CAPPP) is a prospective, randomized, multi-centre intervention trial designed to investigate whether antihypertensive treatment with the angiotensin converting enzyme (ACE) inhibitor captopril may reduce cardiovascular mortality and morbidity more than a therapeutic regimen which does not include an ACE inhibitor. Secondary objectives are to compare total mortality, the development or deterioration of ischaemic heart disease, left ventricular failure, atrial fibrillation, diabetes mellitus and possible differences in renal function in the two groups. Male and female patients with essential hypertension, aged 25-66 years, will be randomly allocated to antihypertensive treatment which will comprise either the use of the ACE inhibitor captopril or will exclude all types of ACE inhibitors. Some 275 hypertension centres and health care centres in Sweden and Finland will take part in this multi-centre trial. A total of 7000 patients will be recruited and studied for an average period of 5 years, the assumption being that a 20% difference in cardiovascular mortality between the two groups can be detected with a power of 80% at the 5% significance level (two-sided test).
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PMID:The Captopril Prevention Project: a prospective intervention trial of angiotensin converting enzyme inhibition in the treatment of hypertension. The CAPPP Group. 198 Dec 18

Captopril (C), isosorbide dinitrate (ID), and nifedipine (N) were evaluated for antianginal effects (AAE) in 12 patients with ischemic heart disease. The effects were assessed by treadmill exercise tests performed before and repeatedly 1, 2, 3, and 6 hours after the single dose of a drug or placebo. C, ID, and N were given in doses of 50, 10, and 20 mg, respectively. The drugs were equally effective in lowering systolic blood pressure at rest. Unlike ID and N, C failed to affect the duration of exercise testing until an anginal episode occurred and the magnitude of ST-segment depression at the same exercise intensity. ID and N caused a significant increase in the duration of exercise and a decrease in ST-segment depression during exercise 1-3 h later. An individual analysis has shown that C, ID, and N produced an antianginal effect only in 2, 9, and 10 patients, respectively. Thus, C is unable to show a substantial antianginal effect.
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PMID:[Does captopril produce an antianginal effect in patients with stable exercise-induced angina pectoris?]. 204 Dec 79

The possibility of a coexistence of coronary arteriolar constriction mediated by the renin-angiotensin system and myocardial ischemia was evaluated. Left anterior descending coronary artery was cannulated and perfused at normal (mean aortic), intermediate (50 mm Hg), and low (30-40 mm Hg) pressure in analogy to a progressive coronary stenosis. Lactate production was present at low coronary pressure indicating myocardial ischemia. In control animals (n = 18), mean coronary conductance was higher (p less than 0.005) at intermediate than at high coronary pressure consistent with autoregulation at coronary flow. Coronary conductance was lower (p less than 0.05) at low than at intermediate coronary pressure, indicating coronary constriction during myocardial ischemia. Adenosine (20 micrograms/kg per min i.c., n = 6) resulted in higher coronary conductance, suggesting coronary vasodilator reserve even at low coronary pressure. Indomethacin (5 mg/kg i.v., n = 12) resulted in low coronary conductance; however, the increase at intermediate (autoregulation) and the decrease (constriction) at low pressure was maintained. Plasma renin activity increased, and saralasin (0.1 microgram/kg per min i.c.) and captopril (0.25 mg/kg i.v.) acted as coronary vasodilators in various models of myocardial ischemia. Captopril limited myocardial infarct size at 6 hours of coronary occlusion, diminished flow repayment and prevented lactate production after 30 s of coronary occlusion, and abolished the deterioration of myocardial function during myocardial ischemia induced by coronary hypoperfusion and atrial pacing. Thus, myocardial ischemia does not generally represent a state of maximal coronary dilatation. The renin-angiotensin system is activated by myocardial ischemia and may exert a coronary constrictive tone. Captopril was beneficial in experimental myocardial ischemia.
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PMID:Coronary vasoconstriction in experimental myocardial ischemia. 244 Dec 6

Many studies in recent years have dealt with the use of angiotensin converting enzyme (ACE) inhibitors for the treatment of ischemic heart disease. The renin-angiotensin system is widely distributed in plasma and peripheral tissues and is activated following certain conditions including myocardial ischemia. The effects of ACE inhibitors on the ischemic heart are apparently many and achieved through a blockade of plasma and tissue ACE as well as through their property of scavenging free radicals. Captopril seem to exert a beneficial effect in preventing heart failure after myocardial infarction probably by restoring the contractile function of infarcted myocardium. An antianginal effect of ACE inhibitors has been demonstrated in patients with coronary artery disease along with a potentiation of isosorbide dinitrate coronary vasodilator capacity. The antiarrhythmic efficacy, clearly evident in animal models, deserves further investigations in humans. The above listed effects of ACE inhibitors and the suppressive action demonstrated for captopril on platelet aggregation could represent a very useful tool for the future treatment of patients with coronary artery disease.
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PMID:Potential use of ACE inhibitors after acute myocardial infarction. 248 42

Recent intervention trials failed to show a significant decrease in mortality of ischemic heart disease in hypertensive patients given pharmacological treatment. These results led to a reassessment of cardiovascular risks of antihypertensive drugs per se and particularly diuretics. Captopril and Enalapril, antihypertensive drugs acting as converting enzyme inhibitors, might have some theoretical advantage over other antihypertensive drugs. The chronic ACE inhibitors therapy does not compromise glucose, lipid and urate and it seems not to be persistent in long-term administration.
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PMID:[Effect of angiotensin converting enzyme inhibitors on lipid, purine and glucose metabolism]. 254 May 15

The authors used Captopril (Tensiomin, Egis Pharmaceuticals, Budapest) therapy in seven patients suffering from chronic heart failure of ischaemic etiology. As controls, seven patients with dilated cardiomyopathy were involved in the study. All 14 patients received digitalis, diuretic, and isosorbide dinitrate therapy but their condition aggrevated in spite of the therapy. The above-mentioned therapy was completed with daily 3 x 12.5-mg or 3 x 25-mg oral Captopril doses. Significant improvement proved by chest X-ray, echocardiography, and clinical data was observed in four of the ischaemic heart disease patients and three of the dilated cardiomyopathic patients. In other two patients each the improvement was temporary, after 6 weeks of therapy deterioration of the disease was observed. Notable change was not observed in response to Captopril in one ischaemic and two primary cardiomyopathic patients. Tensiomin may be considered as one of the drugs of primary importance in the treatment of chronic congestive heart failure.
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PMID:Captopril (Tensiomin) in the treatment of chronic heart failure of ischaemic heart disease patients. 269 19

The purpose of this retrospective study was to consider impaired renal function in patients with severe congestive heart failure after converting enzyme inhibition and to emphasize the characteristics of this population. The study concerned 26 patients (pts), 72.5 +/- 8.1 years old, with a severe congestive heart failure (NYHA Class IV). Before treatment serum creatinine was slightly increased and the introduction of angiotensin converting enzyme inhibitor (ACEI) - Captopril 58.9 +/- 17.3 mg/j or enalapril 9.2 +/- 4.4 mg - impaired renal function from 132.0 +/- 50.7 mumol/l to 183.5 +/- 139.3 mumol/l (n = 26; p less than 0.05). Patients were separated in 3 groups: in group I; 15 pts, serum creatinine remained unchanged under ACEI in despite of the significant decrease of blood pressure (BP); from 140.7 +/- 24.0/82.5 +/- 13.4 to 120.3 +/- 12.8/71.8 +/- 8.7 mmHg (p less than 0.01). The cause of heart failure was an ischemic heart disease (IHD) in 15 patients (chi 2 test, p less than 0.05), a dilated cardiomyopathy in 4 pts and an aortic or mitral valvular regurgitation in 2 pts. In contrast renal function was significantly impaired in group II; serum creatinine increased from 120.8 +/- 25.2 to 189.0 +/- 80.7 mumol/l under ACEI. BP remained unchanged 136.9 +/- 29.0/78.1 +/- 4.9 and 118.7 +/- 13.6/75.6 +/- 7.6 mmHg respectively before and after treatment. There was 4 pts with dilated cardiomyopathy, 4 pts with mitral or aortic valvular regurgitation and only one with IHD. The introduction of an ACEI in two pts--group III--with severe tricuspid regurgitation induced an acute and reversal renal failure (serum creatinine at 600 mumol/l).
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PMID:[Renal insufficiency and treatment of persistent cardiac insufficiency with converting enzyme inhibitor]. 273 17

The protective effect of angiotensin-converting enzyme inhibitors (ACEI) on myocardial ischemia and reperfusion damage was estimated in rat hearts, both in vivo and in vitro. Enalapril 2.5 mg/kg ip pretreatment at 24 and 5 h before coronary occlusion, significantly blunted the rise of CPK (445 +/- 151 vs 649 +/- 244 mu/ml, P less than 0.05) and improved electrocardiogram (ECG) 8 h after coronary occlusion. In global ischemia and reperfusion ex vivo, enalapril improved contractility (0.9 +/- 0.2 vs 0.3 +/- 0.3 g, P less than 0.05) and coronary flow (15.6 +/- 3.3 vs 11.9 +/- 3.1 ml/min/g, P less than 0.05), shortened significantly the duration of reperfusion arrhythmia (3.1 +/- 2.7 vs 9.7 +/- 8.1 min, P less than 0.05). In Langendorffs heart, captopril remarkably preserved force of contraction (2.1 +/- 0.4 vs 1.4 +/- 0.4 g, P less than 0.01) and coronary flow (2.7 +/- 0.5 vs 3.6 +/- 0.9 ml/min/g, P less than 0.05) in segmental infarction deteriorated by angiotensin I. Captopril 10(-5) M infusion reduced the release of CPK (435 +/- 112 vs 640 +/- 123 mu/min coronary flow, P less than 0.05). This action was almost completely abolished by pretreating and infusing with indomethacin. As a positive control, prostacyclin 5 X 10(-7) M infusion further reduced the release of CPK to 330 +/- 77 mu/min. It is concluded that angiotensin-converting enzyme inhibitor can protect both myocardial ischemia and reperfusion damage in rat hearts. The mechanism of protection was ascribed to reduced production of angiotensin II by ACE inhibition and increased prostacyclin release in the myocardium.
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PMID:Protective effects of captopril and enalapril on myocardial ischemia and reperfusion damage of rat. 282 45

The authors have compared the short-term effect of two captopril (ACE inhibitor) preparations namely the Lopirin (SQUIBB) and Tensiomin (EGIS) and dihydralazine as well as placebo in 15 patients with severe heart failure (NYHA III-IV, class). In case of 8 patients with NYHA IV, functional class the short-term effect of the combined therapy of dihydralazine and Lopirin and dihydralazine and Tensiomin as well dihydralazine and placebo have been compared. The underlying disease was dilated cardiomyopathy (DCM) and ischaemic heart disease (IHD). At the end of the treatment with different drugs and placebo the clinical signs of heart failure (complaints and physical status) and the echo and mechanocardiographic parameters of left ventricular function were assessed. The parameters, apart from the clinical signs, have been evaluated in double blind fashion. Compared to placebo all the three drugs i.e. dihydralazine, Lopirin as well as Tensiomin have decreased significantly the NYHA classes, influenced favorably the non-invasive parameters of left ventricular function and decreased blood pressure. As to the dihydralazine, it improved the left ventricular ejection function and the clinical state of the patients with DCM in a higher degree than the two ACE inhibitors did. The effect of Tensiomin and Lopirin was the same in every respect. Both have influenced more favourable the complaints and physical state of patients with IHD than dihydralazine has. The left ventricular filling pressure, the double product (heart rate x wall tension) indicating the myocardial oxygen demand were more reduced in their effect than in that of dihydralazine. Unlike dihydralazine both decreased the heart rate. Administering one of the two ACE inhibitors to the dihydralazine beneficial additive effects have been experienced; the NYHA classes, the heart rate, the left ventricular wall tension and the double product diminished. The authors, on the bases of the results, consider Tensiomin and Lopirin as equivalent in their effect. In their opinion the administration of these drugs mean a new, efficient way of therapy, first of all in cases of heart failure caused by IHD. In the most severe cases they suggest a trial with the combined dihydralazine-ACE inhibitor therapy.
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PMID:Comparative study on the short-term effects of angiotensin converting enzyme inhibitors (Lopirin, SQUIBB and Tensiomin), and dihydralazine in chronic cardiac failure. 307 6


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