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)

Cardiac failure remains a serious complication of myocardial infarction. In addition to therapeutic interventions to limit the infarct size, it would seem possible to influence the progressive changes in geometry and size of the left ventricle, known as remodeling. Experimental and clinical studies have shown beneficial effects of angiotensin converting enzyme inhibitors and the SAVE trial evaluated the prognostic consequences of this therapy, reporting a significant reduction in mortality after 10 months' treatment. Many questions remain which require further research in this field, mainly concerning the optimal time of introduction the treatment, the importance of the chemical molecule used, the most appropriate dosage and the influence of associated drug therapy. ACE inhibitors are now part of the therapeutic arsenal of myocardial infarction but their prescription should be strictly reserved for the population concerned by these trials, that is to say patients with a recent, extensive infarct with left ventricular dysfunction but without clinical signs of cardiac failure.
Arch Mal Coeur Vaiss 1992 Nov
PMID:[Prevention of postinfarction cardiac insufficiency: role of angiotensin converting enzyme inhibitors]. 130 44

Elevated serum angiotensin I-converting enzyme activity may occur in diabetic subjects. This may signal alteration of vascular endothelium. To study the effect of acute glucose change on serum Angiotensin Converting Enzyme (ACE), we performed an oral glucose tolerance test in 17 obese subjects (7M/10F), (Body Mass Index, (BMI): 31 +/- 1 kg/m2), aged 48 +/- 3 years. We measured serum ACE activity (Lieberman's method), active renin (RIA Pasteur kit), and aldosterone (RIA, Cis-International kit), before and 2 hours after oral glucose intake (75 g), and plasma glucose and insulin every 30 min. After oral glucose tolerance test, subjects were classified as 6 Non Insulin-Dependent Diabetic (NIDD), 8 Glucose intolerant (GI), and 3 NormoGlycaemic (NG) subjects. Active renin did not vary after glucose loading (14 +/- 2 vs 15 +/- 2 pg/ml) nor aldosterone (104 +/- 14 vs 133 +/- 18 pg/ml), while ACE activity rose significantly (229 +/- 25 vs 277 +/- 28 IU/l; p = 0.02). Serum ACE activity were different in the 3 groups before glucose loading (NIDD: 266 +/- 37, GI: 252 +/- 32, NG: 90 +/- 21 IU/l; Kruskal-Wallis H = 7.03; p = 0.03), but not after 2 hours (NIDD: 297 +/- 42, GI: 275 +/- 36, NG: 204 +/- 113 IU/l; ns).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Increase of angiotensin converting enzyme activity during oral load of glucose]. 133 58

A biological cancer marker is a molecule, synthetized from a neoplastic tissue, which is present in the tumor and can be detected in measurable amounts in circulating blood. The natural history, prognosis, heterogeneity of each tumor and the histology of bronchial cancers clearly show the difficulty to establish the role of markers in the management of these tumors, especially for the initial assessment of extension. The analysis of the literature shows that studies on this subject are rare. The use of an isolate marker is not sufficient for a positive diagnosis of non-small-cell bronchial cancer. The use of several markers produces better results. However, no model is accurate enough to formally influence the diagnosis of operability. No isolate or associated marker allows differentiating between small-cell and non-small-cell bronchial cancers. The most interesting two markers finally seem to be ACE and CA 125. All other markers must not be used as a routine during the assessment of non-small-cell bronchial cancers. However, these markers are still important for therapeutic follow-up. Even though they are not predictive of chemosensitivity, and even though their decrease is not regarded as an objective criterion of response, their variations are linked with the response to chemotherapy, and their persistent normalization after surgery is compatible with apparent complete remission. The ACE and CA 125 assays can therefore be used as a reference, in case of initial positive findings, for the subsequent follow-up of the patient.
Rev Mal Respir 1992
PMID:[The role of tumor markers in the pre-therapeutic staging of non-small cell bronchial cancer]. 133 77

The effect of enoximone was assessed by a randomised double blind trial versus placebo. The clinical status of the patients was evaluated by the NYHA classification and quality of life score. Inotropic state was estimated from the maximum acceleration of aortic and pulmonary blood flow recorded by Doppler echocardiography. Thirty patients with severe cardiac failure, aged 66.4 +/- 14 years, symptomatic despite maximal therapy associating diuretics, digitalis, nitrate derivatives and angiotensin converting enzyme inhibitors, were included. Fifteen patients were given enoximone 100 mg three times a day orally (Group E) and the other 15 were given a placebo (Group P). The NYHA class and quality of life scores were assessed at D0, D4 and D31. Doppler echocardiography and Holter recordings were performed on D0 and D31. The two groups were comparable at D0. Ten patients abandoned the trial, 3 from Group E (including 1 death) and 7 from Group P (including 3 deaths). At D4, 13 patients from Group E and 8 from Group P were clinically improved (p < 0.05). At D31, the clinical state was stable or improved in 10 of the 12 patients in Group E and 6 of the 8 patients in Group P (NS). No secondary effects were severe enough to warrant the withdrawal of treatment: the frequency of ventricular extrasystoles was comparable in the two groups at D0 and D31. At D31 the maximal aortic acceleration had increased by 20% compared with D0 (p < 0.05) and the maximal pulmonary acceleration by 31% (p < 0.05) in Group E. The same parameters showed no significant change in Group P (-6% and +5% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Jul
PMID:[Double-blind clinical and echocardiographic study of oral enoximone versus placebo in severe cardiac insufficiency]. 144 35

Left ventricular remodeling describes a number of geometric and structural changes that the left ventricle undergoes after myocardial infarction. Briefly, it comprises expansion of the infarct and dilatation of the healthy left ventricular segments. Its severity is related to the infarct size. These changes in ventricular geometry, in particular the dilatation, influence the long-term incidence of cardiac failure, the main secondary complication of myocardial infarction. Up to now, therapeutic interventions have been oriented to reducing the infarct size with the aim of avoiding or delaying the occurrence of left ventricular dysfunction. Nowadays, it seems possible to influence the natural process of post-infarction. Left ventricular remodeling independently of efforts to reduce infarct size. There is evidence that this process may be limited pharmacologically with angiotensin converting enzyme inhibitors. In animal studies, these agents limit remodeling and improve survival after myocardial infarction, but for the moment, despite confirmed benefits on left ventricular modeling, it is not possible to extrapolate these results in terms of clinical mortality.
Arch Mal Coeur Vaiss 1992 May
PMID:[Left ventricular remodeling after myocardial infarction]. 153 Apr 20

Nitrate derivatives are venous vasodilators which are effective in reducing the symptoms of pulmonary congestion. The beneficial action on exercise capacity was recently demonstrated in the Veterans II Study in association with Hydralazine and has also been suggested by other trials. The reduction in mortality from cardiac failure was demonstrated in the Veterans I Study in association with Hydralazine compared to conventional digitalo-diuretic therapy but seems less important than that obtained by angiotensin converting enzyme inhibitors. The phenomenon of tolerance seems to be related to the use of high doses in continuous therapy and may be countered by discontinuous use of the drug during the 24 hour period. Tolerance seems to be related to neuro-hormonal factors and perhaps to depletion of SH groups. Simultaneous use of nitrates and ACE inhibitors seems to be an interesting therapeutic concept.
Arch Mal Coeur Vaiss 1992 Apr
PMID:[Nitrate derivatives and cardiac insufficiency]. 153 Apr 25

The atrial natriuretic factor (ANF) is secreted by the atria in mild and moderate cardiac failure but, during the evolution of the cardiac failure, the ventricles are also recruited and secrete ANF. In order to investigate the relation between plasma ANF and Doppler echocardiographic parameters of severe cardiac failure, the concentrations were measured simultaneously in 20 patients with NYHA Class III and IV cardiac failure (10 due to ischaemic and 10 due to primary dilated cardiomyopathy) despite optimal medical treatment including an angiotensin converting enzyme inhibitor. Overall, there was a weak negative correlation between the plasma ANF concentrations and the decrease in right ventricular surface area (r = -0.58, p less than 0.005, n = 20 patients). This relation was highly significant in ischaemic cardiomyopathy (r = -0.81, p less than 0.002, n = 10 patients) and not significant in primary dilated cardiomyopathy (r = -0.29, NS, n = 10 patients). No relationship was observed between plasma ANF and other echocardiographic parameters (atrial surface area, right and left ventricular dimensions, left ventricular ejection fraction and mass) or with Doppler aortic indices (acceleration, maximum and mean velocities, aortic velocity-time integrals). However, plasma ANF was related to the velocity of mitral regurgitant jets (r = -0.70, p less than 0.01) which is dependent on left ventricular pump function. These results show that plasma ANF concentrations are only related to right ventricular systolic function and the velocity of mitral regurgitation in patients with severe cardiac failure.
Arch Mal Coeur Vaiss 1992 Jan
PMID:[Correlations between plasma concentrations of atrial natriuretic factor and right ventricular function in patients with severe cardiac failure]. 153 2

In a prospective study the level of carcinoembryonic antigen (ACE) were simultaneously measured in plasma and bronchoalveolar lavage liquid (LBA), in fifteen patients suffering from bronchopulmonary cancer and fifteen patients suffering from non-malignant pulmonary disease. In these two groups the level of ACE in LBA liquid (cancer 8,990 +/- 4,050 ng/ml; controls 2,510 +/- 1,060 ng/ml) were clearly more elevated than the corresponding plasma levels (cancer 1,931 +/- 1,760 ng/ml; controls 8.2 +/- 2 ng/ml) and the plasma levels of ACE were more elevated in the cancer group; in the same group the ACE levels in the LBA liquid were more elevated in the tumour group (4,770 +/- 2,180 ng/ml versus 808 +/- 300 ng/ml). This study has also shown the elevated levels of ACE in the LBA liquid in patients suffering from chronic bronchial inflammation (2,510 +/- 1,060 ng/ml) and during the course of acute bacterial pneumonia. The contribution of the ACE level in LBA liquid in relation to the plasma levels in the diagnosis of bronchopulmonary cancer would thus appear to have no clinical value, but the exact relationships between the phenomenon of chronic bronchial inflammation and metaplasia of the bronchial epithelium merit further study.
Rev Mal Respir 1992
PMID:[Significance of the level of carcinoembryonic antigen in the alveolar lavage fluid in cancerous and non-cancerous bronchopulmonary pathology]. 156 30

In the kidney, angiotensin I-converting enzyme (ACE) is present in the vascular endothelial cells and in the brush border of epithelial cells of the proximal tubule. In spite of this well-known distribution of ACE, little is known of its regulation. In order to elucidate the possible mechanisms of control for brush border ACE, the effects of dexamethasone (DM), (40 micrograms s.c. per day, for 7 days) and triiodothyronine (T3) 0.5 mg/kg s.c. per day, for 10 days) were investigated in male Wistar rats. Plasma and brush border ACE activities were measured by fluorimetry in the presence of an artificial substrate Cbz-Phe-His-Leu and brush border ACE was characterized with a binding assay using 3H-ramiprilat, a specific radiolabelled ACE inhibitor. DM elicited a significant decrease in plasma ACE activity (from 0.46 +/- 0.03 to 0.28 +/- 0.02 nmol His-Leu/min/mg protein) but did not alter enzyme activity in the brush border: 47.12 +/- 5.12 nmol His-Leu/min/mg protein (control, n = 6) and 47.78 +/- 5.63 (DM, n = 6). Administering T3 produced a marked increase in the brush border ACE activity (from 42.87 +/- 4.9 to 81.41 +/- 11.7 nmol His-Leu/min/mg protein). Similarly, the maximum number of 3H-ramiprilat-binding sites increased in the brush border, indicating a good correlation between ACE activity and the quantity of 3H-ramiprilat bound. Thus, the variation in tissue ACE activity corresponded to a change in the enzyme concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1991 Aug
PMID:[Changing factors of the activity of angiotensin converting enzyme of renal brush border in rats]. 165 46

Experimental myocardial infarction is a model of cardiac overload due to amputation of part of the cardiac muscle. The development of cardiac failure depends on the size of the infarct and the time factor. This model of overload is associated with changes of the phenotype of the remaining healthy muscle and with peripheral vascular modifications partially dependent of the activation of pressor and/or deactivation of dilator systems. These changes are proportional to the size of the infarction at a given time after induction of the model. The degree of right ventricular hypertrophy and the decrease in blood pressure reflect the severity of infarction and the deterioration of the remaining myocardial function, affecting the haemodynamics both before and after the left ventricle. The increases in the 1/3 forms of isomyosins, the amount of subendocardial collagen, the biosynthesis, stocking and secretion of ANF are related to the infarct size and degree of overload. Similarly, the concentration of cyclic GMP is proportional to the infarct size. These parameters reflect ventricular overload, the increase of stress and energy deprivation of the remaining healthy muscle. The activation of peripheral pressor systems is also dependent on the infarct size reflects the effect of cardiac pump dysfunction on the kidney, liver, brain and endothelium. Large infarcts are associated with increased circulating renin and renal concentrations, with a decrease in angiotensinogen levels related to its consumption by the renin and to reduced hepatic synthesis and also with increased secretion and biosynthesis of vasopressin by the hypothalamus. In this model, Perindopril is beneficial by decreasing the cardiac load. It reduces the blood pressure, causes regression of bi-auricular and right ventricular hypertrophy. Changes in myosin isoenzyme configuration regress and subendocardial fibrosis and ANF concentrations are normalised. The effects of ACE inhibitors in this context, though very beneficial, are limited by the impossibility of normalising cardiac load and stress when the initial amputation of cardiac contractile mass exceeds 40%.
Arch Mal Coeur Vaiss 1991 Dec
PMID:[Experimental myocardial infarction in the rat. Effect of perindopril]. 166 27


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