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)

Twenty-one subjects who suffered a recent medium sized anterior myocardial infarction conditioning a mild congestive heart failure were randomly allocated to treatment with captopril (25 mg b.i.d., 10 pts) or placebo (11 pts). After 2 months of therapy the group on the active treatment showed a significant increase of apexcardiographic protodiastolic filling period duration reflecting a clear cut decrease of mean pulmonary capillary wedge pressure (from 14 +/- 2 to 7 +/- 3 mm Hg) while patients on placebo did not show any difference in respect to baseline. Neither treatment significantly modified the PEP/LVET ratio despite a significant increase of left ventricular ejection fraction in patients receiving captopril (from 37 +/- 4% to 43 +/- 5%). Cardiac response to ACE-inhibitors can thus be noninvasively monitored by apexcardiography.
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PMID:Mechanocardiographic effects of ACE-inhibitors. 207 1

Administration of potent vasodepressor agents such as the angiotensin converting enzyme inhibitor, captopril, may precipitate myocardial ischemic events in patients with coronary artery disease, particularly if this treatment is preceded by a discontinuation of beta-blocking drugs such as propranolol. In one case studied, a patient experienced three episodes of angina pectoris under these conditions; in another, acute anterior myocardial infarction was suspect.
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PMID:Ischemic cardiovascular complications concurrent with administration of captopril. A clinical note. 624 3

Prevention of post-infarction ventricular remodeling is an important therapeutic aim since left ventricular dilatation is one of the most important prognostic post-infarction determinants. Early reperfusion and chronic treatment with ACE-inhibitors are able to limit remodeling by means of two distinct mechanisms. Early reperfusion limits the extent of the infarcted area by salvaging a part of the myocardial area at risk of necrosis. ACE-inhibition, on the other hand, by reducing afterload, facilitates cardiac ejection and therefore tends to reduce left ventricular volume. Remodeling could be limited also by drugs which, like L-carnitine, act, as has been demonstrated by experimental studies, on the use of energy substrates both in the area at risk of necrosis and in the area subjected to a greater wall stress because of remodeling and which will progressively dilate over time. The CEDIM study is a double-blind, randomized, placebo-controlled, multicentre trial which has involved 36 Heart Divisions. The CEDIM study aims at evaluating the effects of L-carnitine on left ventricular function, as assessed by echocardiography, in patients with acute anterior myocardial infarction.
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PMID:[Prevention of post-infarction remodelling with L-carnitine: multicenter study CEDIM (L-Carnitine digital echocardiography myocardial infarction)]. 763 89

The study was designed to examine the safety and efficacy of acute interventional use of captopril on left ventricular volumes, ventricular arrhythmias and neurohormones during thrombolysis in patients with a first anterior myocardial infarction, within 6 h of onset of symptoms. Left ventricular dysfunction and prognosis after myocardial infarction can be improved by angiotensin converting enzyme inhibition started after the ischaemic phase. Experimental evidence suggests that intervention during thrombolysis may lead to even further benefit. In a randomized, double-blind placebo-controlled trial, 298 patients with a first anterior myocardial infarction, eligible for thrombolytic therapy were treated with captopril 6.25 mg or placebo, started immediately upon streptokinase infusion and titrated to 25 mg t.i.d.. The efficacy of captopril by an intention-to-treat-analysis to reduce left ventricular volumes, ventricular arrhythmias, neurohumoral activation and enzymatic infarct size was measured. During dose titration, mean blood pressure and heart rate were similar in both groups. However, hypotension after the first dose was reported in 18 patients on placebo and 31 patients on captopril (P < 0.05). At discharge, 80% of patients were on study medication. Left ventricular volumes were significantly increased in both groups at 3 months, but they tended to be lower in the captopril group; however, the differences were not statistically significant. The incidence of accelerated idioventricular rhythm and non-sustained ventricular tachycardia in captopril patients was lower than in placebo patients (P < 0.05), parallelled by transiently lower norepinephrine levels (P < 0.05) upon thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute intervention with captopril during thrombolysis in patients with first anterior myocardial infarction. Results from the Captopril and Thrombolysis Study (CATS). 792 10

The rationale, design, organization and outcome definitions of the Survival of Myocardial Infarction Long-term Evaluation (SMILE) study are described in detail. The recruitment of a total of 1500 patients (750 per treatment group) has been planned for this multicenter, double-blind, randomized, placebo-controlled study to investigate the effects of oral treatment with zofenopril calcium (7.5-30 mg twice a day) on the combined short-term total mortality and occurrence of severe refractory congestive heart failure in patients with acute anterior myocardial infarction (AMI). Secondary end-points of the study include recurrent myocardial infarction, angina, progression of congestive heart failure as well as long-term mortality. Patients are initially treated in hospital within 24 hours from the onset of symptoms of AMI and their active follow-up continued for 6 weeks. In addition, the patients will be passively followed for a total of 12 months from the index AMI to assess their vital status and the occurrence of congestive heart failure. The study data will be analyzed on an intention to treat basis. An international independent Policy and Safety Monitoring Board is acting as the overall supervisory body and is responsible for the ethical conduction of the trial. A Scientific Committee is responsible for the scientific aspects of the trial and for the regular review of the progress of the study. We assume that the rationale and design of the SMILE trial will provide reliable information on the ability of ACE-inhibitors to reduce the occurrence of major cardiovascular events in patients with acute myocardial infarction.
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PMID:[The SMILE study: the rationale, design, organization and definition of the objectives. Survival of Myocardial Infarction Long-term Evaluation]. 816 79

Large-scale trials of angiotensin converting enzyme (ACE) inhibitors after acute myocardial infarction (AMI) suggest that the benefits are greatest in patients with left ventricular (LV) dysfunction. However, early evaluation of LV function in all patients after AMI by current methods can be difficult due to a lack of resources and skilled personnel. Thus a clinical algorithm that could be used at the bedside to reliably identify patients with a left ventricular ejection fraction (LVEF) < or = 40% would be helpful as an occasional alternative to echocardiography. We have devised such an algorithm based on the presence of one of: (i) clinical signs of heart failure; (ii) an index Q-wave anterior myocardial infarction; (iii) lack of thrombolytic therapy when there is a history of two or more previous myocardial infarctions and a CK rise > 1000 U/l. We tested this new algorithm prospectively in the coronary care units of two hospitals (one UK and one USA). In the UK centre, the sensitivity and specificity of the algorithm at identifying patients with a LVEF < or = 40% were 82% and 72%, respectively. In the US centre, the sensitivity of the algorithm was 91% and the specificity 78% at identifying patients with LV dysfunction. We have validated a simple clinical algorithm which can be used at the bedside for identifying patients who would benefit from an ACE inhibitor after AMI.
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PMID:Diagnosing left ventricular dysfunction after myocardial infarction: the Dundee algorithm. 947 48

Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. For vascular endothelium, hepatocyte growth factor (HGF) is one of the most potent and specific growth factors, which acts protectively against endothelial dysfunction. HGF production is downregulated by angiotensin II (Ang II) in vitro. We hypothesized that HGF production is impaired as the result of increased Ang II in patients with congestive heart failure, and that if so, the impaired production should be restored with angiotensin-converting enzyme inhibitors (ACE-I). We studied 16 patients with congestive heart failure caused by previous anterior myocardial infarction in whom left ventricular ejection fraction was 35+/-8% (mean+/-SD). Before and approximately 4 weeks after the treatment with ACE-I, blood samples were collected to measure the levels of HGF, Ang II, and brain natriuretic peptide as a biochemical marker for severity of heart failure. We also studied 5 control subjects, in whom heparin increased HGF production to 48+/-5-fold. However, in patients with heart failure, HGF response to heparin was significantly attenuated (24+/-5-fold, P<0.05 vs control). Therapy with ACE-I decreased the levels of Ang II and brain natriuretic peptide and restored HGF production in response to heparin by 43+/-7-fold, comparable to the control response. In conclusion, impaired HGF production was restored after the treatment with ACE-I probably by the mechanism of Ang II suppression. This novel effect of ACE-I may contribute to the clinical improvement in patients with heart failure and thereby may have an important therapeutic implication.
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PMID:Angiotensin-converting enzyme inhibition restores hepatocyte growth factor production in patients with congestive heart failure. 1037 19

The effect of beta-blockade on left ventricular (LV) remodeling, when added to angiotensin-converting enzyme inhibition (ACEI) after anterior myocardial infarction (MI), is incompletely understood. On day 2 after coronary ligation-induced anteroapical infarction, 17 sheep were randomized to ramipril (ACEI, n = 8) or ramipril and metoprolol (ACEI-beta, n = 9). Magnetic resonance imaging was performed before and 8 wk after MI to measure changes in LV end-diastolic, end-systolic, and stroke volume indexes, LV mass index, ejection fraction (EF), and regional percent intramyocardial circumferential shortening. (123)I-labeled m-iodobenzylguanidine (MIBG) and fluorescent microspheres before and after adenosine were infused before death at 8 wk post-MI for quantitation of sympathetic innervation, blood flow, and blood flow reserve in adjacent and remote noninfarcted regions. Infarct size, regional blood flow, blood flow reserve, and the increase in LV mass and LV end-diastolic and end-systolic volume indexes were similar between groups. However, EF fell less over the 8-wk study period in the ACEI-beta group (-13 +/- 11 vs. -22 +/- 4% in ACEI, P < 0.05). The ratio of adjacent to remote region (123)I-MIBG uptake was greater in ACEI-beta animals than in the ACEI group (0.93 +/- 0.06 vs. 0.86 +/- 0.07, P < 0.04). When added to ACE inhibition after transmural anteroapical MI, beta-blockade improves EF and adjacent regional sympathetic innervation but does not alter LV size.
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PMID:Beta-blockade improves adjacent regional sympathetic innervation during postinfarction remodeling. 1051 78

The objective of the present study was to analyse the potential synergistic influence of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene (I/D ACE) and the A1166C polymorphism of the angiotensin-II type 1 receptor gene polymorphisms (A1166C AT1R) on the left ventricular size and performance. Three hundred sixty and one consecutive, Caucasian patients with angiographically confirmed coronary artery disease (CAD) were enrolled into the study. Left ventricular diameter, mass and function were evaluated by echocardiography. Screening for the I/D ACE and A1166C AT1R genotypes was performed by polymerase chain reaction of genomic DNA, followed by restriction enzyme digestion and agarose gel electrophoresis. The I/D ACE and A1166C AT1R genotypes separately were not significantly associated with the left ventricular size and function parameters in CAD patients. However, trends towards decreased left ventricular ejection fraction (LVEF) as well as increased left ventricular end-diastolic diameter (LVEDD) and left ventricular mass index (LVMI) were observed when patients with genotype DD+CC/AC and DD+CC were compared to patients homozygous only in one locus (DD or CC). Significant increase in LVEDD and LVMI was observed only in patients with a history of anterior myocardial infarction with combined genotype DD+CC/AC or DD+CC. This study does not support the role of the ACE I/D and AT1R A1166C polymorphisms in the determination of the left ventricular size and performance in patients with significant coronary atherosclerosis. However, it indicates that the influence of polymorphisms may be present in specific patient populations.
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PMID:Left ventricular size, mass and function in relation to angiotensin-converting enzyme gene and angiotensin-II type 1 receptor gene polymorphisms in patients with coronary artery disease. 1274 97