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)

A regimen consisting of chlorthalidone, hydralazine and propranolol would be useful in some hypertensive patients with coronary artery disease or aortic dissection if it could be shown that reflex cardiac stimulation induced by hydralazine is completely neutralized by propranolol. Nine hypertensive patients were treated with chlorthalidone during week 1, chlorthalidone and hydralazine during week 2 and a combination of chlorthalidone, hydralazine and propranolol during week 3. Blood pressure, heart rate, mean velocity of circumferential fiber shortening (VCF) measured echocardiographically and plasma renin activity were measured weekly. This potent three drug regimen reduced mean blood pressure from 142 to 102 mm Hg, and with the third drug, propranolol, heart rate, VCF and plasma renin activity returned to control levels from the greater elevated levels produced by the diuretic drug and hydralazine. In six additional patients VCF (an index of left ventricular contractility) was found to be proportionate to the rate of rise of aortic pressure (dP/dt) or aortic shearing force. This regimen appears safe for use in patients with ischemic heart disease and aortic dissection.
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PMID:Echocardiographic assessment of the effect of an antihypertensive regimen on left ventricular performance. 42 Jan 8

Activation of some neuroendocrine systems is one of the compensatory-adaptation mechanisms in circulatory insufficiency in patients with ischemic heart disease. Evidence of this is that patients with stage I--IIA of the disease are marked by an increase in the activity of the sympatheticoadrenal system (increase in the excretion of free catecholamines) and the renin-angiotensin-aldosterone system, in the glucocorticoid function of the adrenal cortex, in the functional condition of the epiphysis cerebri, and in the blood plasma antidiuretic activity. Participation of these systems in the adaptation processes maintains an adequate level of venous blood return to the heart and inotropic myocardial function.
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PMID:[Adaptive and compensatory mechanisms in chronic circulatory insufficiency in ischemic heart disease]. 43 Sep 56

The activity of the pituitary hormones (ACTH, STH, TTH, FSH, LH), the adrenal hormones (cortisol, aldosterone), the kidney hormone (renin), and the thyroid hormones (thyroxine tri-iodthyronine), the thyroxine binding capacity of blood proteins and the activity of the hormones of the pancreas (insulin) and the sex glands (testosterone, estradiol) were studied in 26 males suffering from ischemic heart disease verified by means of selective coronarography and in 20 healthy males with no atherosclerosis of the coronary arteries of the heart. Patients with ischemic heart disease were found to be marked by increased activity in the blood of ACTH, TTH, cortisol, aldosterone, insulin, and estradiol and reduced concentration of STH, thyroxine, and testosterone. These shifts in the activity of the hypothalamo-hypophyseal system and in its subordinate hormonal systems play an important role in the origin of the atherosclerotic process and assosiated ischemic heart disease.
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PMID:[Hormones in ischemic heart disease with the presence of coronary atherosclerosis]. 73 79

Plasma renin activity (PRA) stimulated by upright posture was measured, in 300 men aged 45-64 years, by a radio-immunoassay of angiotensin I. The subjucts examined were divided into six groups, comparable in mean age, each containing 50 subjects: group 1, normotensives without manifest atherosclerosis; group 2, normotensives with angina pectoris definite; group 3, normotensives with a history of a transmural myocardial infarction; groups 4 to 6, patients with benign essential hypertension, without manifest atherosclerosis in group 4, with angina pectoris in group 5 and with a history of myocardial infarction in group 6. Significant differences in mean PRA were found between corresponding groups of hypertensives and normotensives, the values in hypertensives being lower. The precentage of low renin values was higher in hypertensives with ischaemic heart disease than in other groups. An analysis of 3-year cardiovascular mortality revealed no significant difference in mortality due to ischaemic heart disease between high-renin and low renin sub-groups.
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PMID:Plasma renin activity in men with relation to the presence of ischaemic heart disease. 85 14

Plasma renin activity (PRA) stimulated by upright posture was measured in 300 men aged 45-64 years using a radioimmunoassay of angiotensin-I. The examined subjects were normotensive or patients with benign essential hypertension and were divided into 6 groups according to the absence of manifest atherosclerosis, the presence of definite angina pectoris or a history of myocardial infarction. Each group contained 50 unselected subjects, with a comparable mean age. Significant differences in mean PRA were found between corresponding groups of hypertensives and normotensives, the values in hypertensives being lower. The percentage of low renin values was higher in hypertensives with ischaemic heart disease than in other groups. It is suggested that this finding might be explained by functional disturbances in the kidneys in hypertensives with ischaemic heart disease.
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PMID:Plasma renin activity in patients with ischaemic heart disease. 87 44

Evaluation of the concentration of atrial natriuretic peptide, angiotensin P, renin activity in the blood of the coronary sinus and aorta in 18 patients with IHD and hypertrophy of the left ventricle during development of induced ischemia revealed that in left ventricular hypertrophy secretion of atrial natriuretic peptide by the myocardium is reduced. The level of this reduction depends on the kind of hypertrophy. Dilatation of the left ventricle cavity furthers exhaustion of the secretory function of the ischemic myocardium.
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PMID:[The interrelation of the secretory activity of the myocardium with its hypertrophic characteristics in patients with ischemic heart disease]. 129 16

About 10% of survivors of an acute myocardial infarction will die in the following year. Thereafter the risk declines but reinfarction is still an important cause of mortality and morbidity. The post infarction trials have clearly shown that the best proven agents to mitigate this toll are aspirin, beta adrenoceptor blockers, and verapamil (but not other calcium blockers, except diltiazem for non Q wave infarction). In the context of hypertension treatment these post infarction trials may have important lessons for drug selection and ancillary treatment since the majority of subjects will ultimately die of ischaemic heart disease. Although the newer agents such as ACE and renin inhibitors, newer calcium channel blockers and alpha blockers have many promising properties in terms of risk factor reduction, no convincing mortality data exists; it is needed. This review will deal with the known effects (both good and bad) of antihypertensive agents and will also review other drug strategies relevant to the hypertensive patient. It will also point out large areas of ignorance.
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PMID:The secondary prevention of myocardial infarction by drug treatment; excluding lipid lowering agents. 134 57

In a blind, randomized study, the effects of perindopril, a nonsulfhydryl-containing angiotensin-converting enzyme (ACE) inhibitor, were compared with those of placebo in a closed-chest pig model of myocardial infarction. In anesthetized pigs, myocardial ischemia and reperfusion were induced by inflation and deflation of a catheter balloon in the left anterior descending coronary artery (LAD), respectively. Thirty minutes after induction of ischemia and 15 min before reperfusion, a bolus injection of 0.06 mg/kg perindoprilat (n = 12), the active compound of perindopril, or placebo (n = 12) was administered in the pulmonary artery of these animals. After the acute phase of myocardial infarction, treatment with 12 mg/day perindopril or placebo was continued orally for 2 weeks. During the entire treatment period, 7 of 12 animals died in the placebo group versus 2 of 12 animals in the perindopril group (Fisher's exact test p less than 0.04). This beneficial effect of perindopril on mortality could not be attributed to salvage of myocardial tissue because the increases in creatine phosphokinase and coronary venous purine levels were similar in perindopril- and placebo-treated animals. Neither were there any significant between-treatment differences in the hemodynamic and (neuro)humoral parameters during the acute phase of myocardial infarction. The difference in mortality was observed within 24 h after myocardial infarction. Prevention of acute pump failure and, especially, life-threatening ventricular arrhythmias may explain this improvement in survival by perindopril. Retrospectively, logistic regression analysis showed that, irrespective of treatment, survival was inversely correlated to plasma renin activity (PRA) before induction of ischemia (r = -0.33; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of early angiotensin-converting enzyme inhibition in a pig model of myocardial ischemia and reperfusion. 137 22

1. The transpulmonary pharmacokinetics of the intravenous diacid ACE inhibitor perindoprilat were studied in 10 male patients undergoing diagnostic cardiac catheterisation for the management of ischaemic heart disease. 2. Following successful completion of diagnostic cardiac catheterisation and ventriculography, subjects received a low dose (1 mg) constant rate infusion of perindoprilat over 20 min with co-infusion of the intravenous marker dye indocyanine green (0.5 mg kg-1). Simultaneous transpulmonary blood sampling was conducted for 1 h and subsequent peripheral venous blood samples were collected for 20 h. 3. No acute changes in blood pressure or heart rate were noted despite rapid and marked inhibition of central circulation plasma ACE activity persisting in peripheral venous blood for 20 h. A delayed rise in plasma renin activity was noted. 4. Transpulmonary passage during early accumulation of the drug was seen to incorporate an early delay. Concurrent ICG measurements suggested that this was entirely due to circulatory delay and not to binding of the drug. Thus, despite the suggested high concentration of tissue ACE activity in the pulmonary circulation, transpulmonary passage of perindoprilat was not measurably influenced by binding at this site under the conditions studied.
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PMID:Transpulmonary pharmacokinetics of an ACE inhibitor (perindoprilat) in man. 165 93

The aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic external diameter of the left ventricle by 2.6% (p less than 0.01), but did not lower cardiac output or abolish coronary reserve, since left-ventricular subendocardial blood flow of paced rats increased under dipyridamole (2 mg/kg i.v.) by 56% (p less than 0.01). Systemic neuroendocrine activation and ventricular dilation without enlargement of ventricular mass developed subsequent to chronic tachypacing, but left-ventricular diameter during pacing never exceeded the value of sham rats on sinus rhythm. After 2 weeks, cardiac output was lowered by 14% (p less than 0.001), cardiopulmonary blood volume was elevated by 30% (p less than 0.001), and angiotensinogen mRNA and angiotensin converting enzyme activity in ventricular myocardium were doubled. We conclude that conditions for an enhanced intracardiac angiotensin II-formation developed in tachypacing-induced heart failure, but that enhanced systolic wall stress or myocardial ischemia are not required for this activation of the local cardiac renin-angiotensin system.
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PMID:Enhanced cardiac angiotensinogen gene expression and angiotensin converting enzyme activity in tachypacing-induced heart failure in rats. 165 3


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