Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study is aimed at checking whether treatment with glutathione (GL) and captopril (CA) before thrombolysis can further improve the protective effects of ACE-inhibitors in cases with anterior acute myocardial infarction (AMI). Ninety-eight double blind randomized patients (86 men and 12 women) showing symptoms of AMI anterior and undergoing thrombolytic treatment were admitted to our study and subdivided into 4 groups. Group A (25 pts) received thrombolytic treatment only, Group B (23 pts) received 3 g GL intravenously 15 min before thrombolysis and for 2 h thereafter, Group C (26 pts) received 6.25 mg CA orally 15 min before starting thrombolytic treatment, Group D (24 pts) received 3 g GL intravenously before thrombolysis and for 2 h thereafter, and captopril as well like group C. On the third day after AMI onset groups A and B received CA also. In all groups, the doses of CA were gradually increased according to blood pressure values. The following features were considered: a) the occurrence of early (within the first 2 h after thrombolysis) ventricular hyperkinetic arrhythmias; b) CK peak; c) the normalization time of CK peak (NT); d) the occurrence of late ventricular hyperkinetic arrhythmias (VHA) in the predischarge Holter test (Lown's class 2); e) ejection fraction (EF) being measured in 60 pts undergoing haemodynamic test. The results were an follows: Group A: VHA early 13/25, CK peak 1982 +/- 282; NT 71 +/- 2 h; Late VHA 8/25; EF 53.5 +/- 2.5% (16 pts). Group B: VHA early 11/23; CK peak 1917 +/- 242 U/l; NT 69 +/- 3 h; late VHA 7/23; EF 54.5 +/- 5.4% (14 pts). Group C: VHA early 4/26; CK peak 1671 +/- 266 U/l; NT 58 +/- 3 h; late VHA 5/26; EF 55.5 +/- 3% (16 pts). Group D: VHA early 3/24; CK peak 1463 +/- 201; NT 56 +/- 4 h; late VHA 5/24; EF 57.6 +/- 4% (14 pts).
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PMID:Captopril and glutathione before thrombolysis in acute myocardial infarction: a pilot study. 129 90

For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.
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PMID:Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction. 130 Dec 46

Twelve healthy male volunteers were given adrenaline infusions, 0.05 microgram/kg body weight/min over 120 minutes in order to achieve serum adrenaline concentrations comparable with those seen in acute myocardial infarction. The infusions were given on four occasions, at intervals of at least 4 weeks. Before the infusions the subjects were given, in random order, 14 days of pretreatment with placebo, hydrochlorothiazide 50 mg once daily, amiloride 10 mg once daily, or lisinopril 20 mg once daily. The adrenaline infusion induced a drop in serum potassium of the same magnitude in all four groups, with the lowest absolute value after hydrochlorothiazide because of the lowest pre-adrenaline level. The infusion-induced decreases in serum calcium and magnesium were of the same magnitude in all groups, with the absolute calcium being least low in the hydrochlorothiazide group because of the highest preinfusion value. Preinfusion serum urate was highest after hydrochlorothiazide and fell during the adrenaline infusion in all groups, although not significantly. Blood glucose increased during the adrenaline infusion in all groups, but significantly more after hydrochlorothiazide and amiloride than after lisinopril. Heart rate increased during the adrenaline infusion in all groups but least after lisinopril. QTc preinfusion was longer after hydrochlorothiazide than after amiloride and placebo, but the infusion-induced prolongation of QTc was of the same magnitude in all pretreatment groups. Since our results were obtained in short-term experiments in normal subjects, their clinical relevance is questionable, but they support the view that ACE inhibitors may have certain metabolic advantages over diuretics.
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PMID:Effects of hydrochlorothiazide, amiloride, and lisinopril on the metabolic response to adrenaline infusions in normal subjects. 132 62

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

Restoration of coronary blood flow in the ischemic myocardium is absolutely needed to prevent irreversible cellular damage but on the other hand may have potentially hazardous consequences. Since thrombolysis during myocardial infarction is designed to salvage a maximal number of myocardial cells threatened by ischemia, a concommitant intervention which reduces cellular damage due to reperfusion will improve the net result of such procedure. The adjunctive use of ACE-inhibitors with thrombolytic therapy early during acute myocardial infarction offers theoretic advantages. This article summarizes the results indicating that ACE-inhibitors do play an important role in cardioprotection in the acute phase of myocardial ischemia followed by reperfusion. Probably, their effect on bradykinin breakdown is at least partly responsible for this effect.
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PMID:Early ACE-inhibition in myocardial infarction. Possible role of bradykinin. 146 86

We treated 48 patients with intravenous enalaprilat within 24 hours from the onset of acute myocardial infarction. Concomitant therapy included thrombolytic treatment (29), intravenous metoprolol (34), intravenous nitroglycerin (16) and intravenous furosemide (15). The first 40 patients included had systolic blood pressure at baseline greater than or equal to 110 mmHg. Intravenous bolus injections of 0.2-1.2 mg (mean 1.0 mg) enalaprilat in one hour were given to 20 patients and an intravenous infusion of 1 mg over two hours was administered to another 20 patients, as well as to a separate group of 8 patients with systolic blood pressure between 100-109 mmHg at baseline. The infusion was stopped in five cases when the systolic blood pressure fell below 100 and 90 mmHg, respectively, in the two infusion groups. No hypotensive reactions were symptomatic. Blood pressure decreased from a mean of 134/82, 131/79 and 106/72 mmHg to a minimum of 117/71, 118/73 and 97/63 mmHg, respectively, in the three groups. Almost complete suppression of plasma angiotensin converting enzyme activity was achieved within 30 minutes. No significant changes were found in plasma levels of angiotensin II, renin activity or atrial natriuretic peptide between baseline and 24 hours. Treatment was continued with oral enalapril 2.5-10 mg/day, which was generally well tolerated. We conclude that intravenous and oral enalapril added to conventional therapy in the early phase of acute myocardial infarction is well tolerated in selected patients, but should be carefully titrated.
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PMID:Enalaprilat in acute myocardial infarction: tolerability and effects on the renin-angiotensin system. 165 99

A serial measurements of plasma renin activity (PRA), serum angiotensin converting enzyme activity (ACE), concentrations of plasma angiotensin II (AII) and plasma aldosterone (Ald) in 38 consecutive patients with acute myocardial infarction (AMI) or suspected AMI showed that PRA, AII and Ald levels increased in patients with AMI, especially within first week after onset, and were significantly higher in those cases with severe complications. ACE kept in normal range in all subjects. After small dose captopril therapy, ACE and Ald decreased significantly, PRA and AII increased in 6 patients with AMI. Small dose captopril could cause remarkable blood pressure reduction, but no effect on heart rate. The results suggested that renin-angiotensin-aldosterone system was activated during AMI, especially in cases with severe complications. Captopril could inhibit this system partially.
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PMID:[The changes in renin-angiotensin-aldosterone system in acute myocardial infarction and the effects of converting enzyme inhibitor-captopril]. 166 33

'Primary cardioprotection' has, arguably, already been shown with thiazide diuretics and probably with beta-blockers. The proven safety and efficacy of these established drugs override any theoretical or experimental considerations in favour of ACE inhibitors. It is unfortunate that, as yet, the number of hypotheses generated in support of ACE inhibitors has not been matched by large scale clinical trials employing these drugs. The first report of the clinical use of an ACE inhibitor was in 1984; it is high time comparative studies with conventional, and proven, agents were undertaken. With regard to 'secondary cardioprotection', there is overwhelming evidence in favour of the use of beta-blockers in patients with myocardial ischaemia. Indeed, we would argue that ACE inhibitors should be used with caution in such patients to avoid impairment of coronary infusion. In the patient with acute myocardial infarction, intravenous nitrates are cheap, easy to use, safe and seem to be effective (in preventing early remodelling and reducing mortality). In the subacute phase, beta-blockers improve prognosis and, according to the currently available evidence in humans, nitrates are as effective as captopril in altering late remodelling; as in the acute situation, nitrates are cheaper, simpler to use and have a track record of long-term safety. ACE inhibitors improve symptoms, exercise capacity and prognosis in chronic heart failure. In this condition, they have been a major therapeutic advance and, on the available evidence, are to be initially preferred to other vasodilators though they should be given in addition to diuretics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unique cardioprotective potential of angiotensin converting enzyme inhibitors: a hypothesis still to be tested on humans. 166 67

An acute myocardial infarction, particularly one that is large and transmural, can produce expansion and alterations in the topography of both the infarcted and non-infarcted regions or the ventricle. This remodelling can importantly affect the function of the ventricle and the prognosis. Side-to-side slippage of myocytes in the myocardium occurring in association with ventricular dilatation is responsible for wall thinning. The increased internal load that is sustained through the cardiac cycle is thought to promote further stress, dilatation and hypertrophy of the non-infarcted area. The collagen network has been showed to be high responsible for the remodelling of the interstitium and therefore for the scar formation involved in the expansion. The process for ventricular enlargement can be influenced by infarct size, healing end ventricular wall stresses. The process of scarification can be interfered with during the acute infarct period by the administration of glucorticosteroids and non-steroidal anti-inflammatory agents, which results in thinner infarct and further expansion. A most effective way to prevent or minimize the increase in ventricular size is to limit the initial insult. Acute thrombolytic reperfusion therapy may work in this way. Finally early and long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions of the left ventricle, reducing progressive enlargement with a prolongation in survival.
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PMID:[Left ventricular remodelling]. 184

Acute myocardial ischemia results from an increased cardiac workload in presence of a critical coronary stenosis (demand ischemia), coronary occlusion (supply ischemia) or a combination of both. It is complicated by cardiac arrhythmias and deterioration of function of ischemic myocardium and results in an increased load and dilatation of non-ischemic myocardium. Cardiac protection in acute myocardial ischemia can be related to preservation of coronary blood flow, function of ischemic and non-ischemic myocardium or prevention of cardiac arrhythmias. In control animals and humans, ACE-inhibitors have no major effect on coronary blood flow. Myocardial ischemia raises plasma-renin-activity, angiotensin I-conversion by passage through coronary circulation, and plasma-angiotensin-II-concentrations. ACE-inhibitors and angiotensin-II-receptor blockers increase coronary blood flow during myocardial ischemia. Other mechanisms (bradykinin potentiation) may be involved. We found a potentiation of the coronary dilatory effect of the neuropeptide neurotensin (which is probably mediated by prostaglandins) by ACE-inhibitor. ACE-inhibitor may delay infarct development in animal experiments and improve function of ischemic myocardium. The importance of early dilatation of non-ischemic myocardium is unknown and it is unclear whether it may be prevented by an ACE-inhibitor as was shown for late dilatation. Studies on the effect of ACE-inhibitors in exercise-induced angina pectoris are controversial. An antiischemic and coronary dilatory effect has been shown by invasive studies in patients. A preliminary study in unstable angina pectoris was positive. Beneficial hemodynamic and antiarrhythmic effects (as well as excessive hypotension, however) have been shown in patients with acute myocardial infarction.
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PMID:[Possibilities of ACE inhibitor therapy in acute myocardial ischemia]. 186 31


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