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)

Restenosis remains the principal limitation of coronary angioplasty; its main mechanisms are neointimal hyperplasia and vascular remodeling. The endothelium destroyed at angioplasty will progressively recover the denuded zone. However, dysfunction of this neo-endothelium persists for quite a period and may participate in restenosis by influencing these two components (hyperplasia and remodeling). Several therapeutic strategies are under evaluation to try and accelerate the regeneration of the endothelium and make it functional more rapidly. Increasing available nitric oxide (NO) decreases the hyperplasia and improves endothelial function. Growth factors accelerate the endothelial regeneration and improves its function: the effect on hyperplasia depends on the growth factor used. The angiotensin converting enzyme inhibitors decrease hyperplasia by improving endothelial function. These therapeutic strategies merit evaluation in the clinical setting.
Arch Mal Coeur Vaiss 1997 Nov
PMID:[Endothelial dysfunction in cardiovascular diseases: therapeutic implications after coronary angioplasty]. 951 12

The international, prospective, randomized HOT study was aimed at determining the influence of a targeted BP reduction on cardiovascular morbidity and mortality. Patients were randomly allocated to 3 DBP targets (< 80, < 85, < 90 mmHg). In addition, the impact of a coprescription of aspirin was studied. The BP target had to be reached within 3 months, according to a well-defined strategy : felodipine 5 mg o.d. as a 1st intention drug, 1, 2 or 3 additional drugs, if necessary, on the following steps. BP measurements were made, using an oscillometric automatic device (Hestia). From April 1992 to October 1994, 18,790 patients with an age range 50-80 years, coming from 26 countries, entered the study. The data collected on the 36th month were in agreement with those obtained on the 12th and the 24th months. Baseline DBP was reduced by 21, 23 and 25 mmHg in the 90, 85 and 80 mmHg target groups, respectively. The rate of patients whose DBP reached the target, obviously increased from the 3rd to the 12th month: from 43 to 56%, 60 to 70%, 74 to 83% in the 90, 85 and 80 mmHg, target groups, respectively. From the 2nd to the 3rd year, BP control was further improved, with a slightly higher rate of controlled patients in the elderly (age > 60 y), especially in the 80 mmHg target group. From inclusion to the 3rd month, one-drug treated patients decreased, whereas 2- or 3-drug treated patients increased. Felodipine-treated patients decreased on the 36th month, but remained over 80%. From the 6th to the 36th month, additional prescription of a betablocker or an ACE-inhibitor increased from 36 to 39%, and from 23 to 28%, respectively; moreover, the side-effects rate decreased from 10.5 to 3.6%, with a special decline in ankle edema from 4 to 1%. In conclusion, the BP reduction observed on the 36th month was of the same extent as that observed in the first months. It seems obviously possible to reach a targeted DBP and to maintain it over time, along with a good acceptability of the treatment. Targeted DBP could be more easily achieved in elderly patients, possibly due to a better drug compliance.
Arch Mal Coeur Vaiss 1998 Aug
PMID:[The Hypertension Optimal Treatment Study: efficacy and tolerability on the 36th month]. 974 62

The authors report the case of a 30 year old man with a left ventricular aneurysm who was seropositive to HIV 1 and HIV 2. The patient was stage IVC 1 (AIDS related complex) by the "Center for Disease Control" classification. The clinical presentation was pyrexia, loss of weight, micropolyadenopathy and cardiac failure. The electrocardiogramme showed low voltage in the peripheral leads with a QS morphology in S2, S3 and aVF and abrasion, of the R wave in the precordial leads. Doppler echocardiography demonstrated a large left ventricular aneurysm with a wide neck. Despite treatment with a diuretic, angiotensin converting enzyme inhibitor and anticoagulants, the patient died suddenly. Autopsy confirmed the wide necked left ventricular aneurysm. This would appear to be the first report of this form of cardiac disease during HIV infection. However, a simple coincidence of the two pathologies cannot be excluded.
Arch Mal Coeur Vaiss 1998 Apr
PMID:[Left ventricular aneurysm in human immunodeficiency virus infection: a case report]. 974 29

Plasma noradrenaline is little used in evaluating the prognosis of cardiac failure because of the theoretical necessity of interrupting treatment for a few days before blood sampling. The present study reevaluated the prognostic value of this parameter with blood sampling performed during treatment and then 48 hours after withdrawal of treatment in 192 patients with chronic stable cardiac failure at an advanced stage (64% of patients in Classes III or IV with an average ejection fraction of 28.5 +/- 13.5%). During follow-up (average 43 months) there were 51 deaths and 17 transplants. None of the patients were lost to follow-up. Univariate analysis of 52 variable observers during the initial phase of evaluation found in decreasing order of predictive value for death plasma noradrenaline levels before and after withdrawal of treatment for 48 hours. Serum sodium, age, systolic mean and diastolic pulmonary artery pressures. In multivariate analysis: noradrenaline with or without withdrawal of treatment, hyponatraemia and systolic pulmonary artery pressure. Actuarial survival curves distinguished the following parameters: noradrenaline levels became predictive at concentrations of over 210 pg/mL and there was a significant difference in survival with respect to 4 levels of serum noradrenaline (with or without treatment) > 300 pg/mL, 300 to 600 pg/mL and > 900 pg/mL. This serum noradrenaline measured without withdrawal of treatment (especially angiotensin converting enzyme inhibitors) is a powerful predictor of mortality, carrying a progressively poorer prognosis as the concentration increases.
Arch Mal Coeur Vaiss 1998 Feb
PMID:[Plasma noradrenaline and the prognosis of chronic cardiac failure: a multicenter study]. 974 45

Temporal and spectral analysis of heart rate variability over 24 hours (HRV) was undertaken in 89 patients with primary dilated cardiomyopathy (DCM) confirmed by left ventriculography with normal coronary angiography and compared with 60 control subjects. The left ventricular ejection fraction was 35 +/- 12% in the DCM patients (71 men and 18 women: age 51 +/- 11 years). Clinical signs of cardiac failure were observed in 66% of patients, requiring medication in 62% of patients (diuretics: 47%, digitalis: 45% and ACE inhibitors: 33%). The HRV was significantly lower in the DCM patients than in the control group, even in the absence of clinical signs of cardiac failure. The global HRV was correlated to left ventricular fractional shortening (r = 0.5, p < 0.001) and peak oxygen consumption on exercise (r = 0.56, p < 0.01), but was independent of the degree of left ventricular dilatation, pulmonary capillary pressure and cardiac index. It was not significantly different in cases of sustained or non-sustained ventricular tachycardia on Holter ECG or in cases with late ventricular potentials on signal averaging of the surface ECG. During follow-up of 51 +/- 35 months, patients with decreased HRV on the global indices and those reflecting sympathetic activity had a much higher risk of cardiovascular death and of cardiac transplantation (p < 0.01). The authors conclude that HRV is decreased in DCM. This is mainly related to the degree of left ventricular dysfunction and is independent of the ventricular arrhythmogenic substrate. The HRV may also identify subgroups of patients with DCM at high risk of cardiovascular death or of haemodynamic decompensation requiring cardiac transplantation.
Arch Mal Coeur Vaiss 1998 Feb
PMID:[Temporal and spectral analysis of heart rate variability in primary dilate cardiomyopathy: evaluation by case control study]. 974 48

Circulating endothelin-1, a very strong peptide vasoconstrictor first discovered in 1988, is raised in cardiac failure. This increase contributes to the deleterious effects of cardiac failure. Although specific anti-endothelin drugs are under development in this condition, the effects of more commonly used drugs on circulating endothelin-1 levels are not well known. The aim of this study was to evaluate the effects of ACE inhibitor therapy on plasma endothelin-1 levels in cardiac failure. The plasma endothelin-1 levels were measured in 24 patients (stages III and IV of the NYHA classification), before and after treatment with angiotensin converting enzyme inhibitor (Captopril: test doses, then 75 mg/day). A control group of 10 paired patients was used to shake off the effects of bed rest and hospital salt-free diet. The initial endothelin-1 levels were high but equivalent in the control and study groups: 9.13 +/- 1.87 fmol/mL vs 8.98 +/- 1.92 fmol/mL. Plasma endothelin-1 decreased significantly in the study group 72 hours after beginning ACE inhibitor therapy (7.44 +/- 1.95, p < 0.02) but remained higher than normal (p < 0.01), whereas the values in the control group remained the same. This study demonstrates a decreases in plasma endothelin-1 levels 72 hours after onset of ACE inhibitor therapy in patients with stable severe cardiac failure. This results, already suggested by many experimental studies and certain ancillary clinical trials, could explain some of the beneficial effects of ACE inhibitors in this condition.
Arch Mal Coeur Vaiss 1998 Jan
PMID:[Rapid decrease of serum endothelin-1 levels after treatment with ACE inhibitors in chronic cardiac failure]. 974 64

A review of the results of randomised trials of the use of betablockers in acute myocardial infarction shows by techniques of meta-analysis that their prescription in the early hours of the acute event leads to a reduction in short-term mortality: the reduction of risk is 12% as compared with groups which are not given betablockers. In addition to its impact on mortality, early betablocker therapy is associated with a reduction in the risk of recurrence of myocardial infarction and a proven antalgic effect. However, in patients receiving thrombolysis, the beneficial effect on mortality and recurrence of infarction of intravenous betablockers seems less evident. In daily clinical practice, the prescription of betablockers in the first days of infarction has significantly increased over the last ten years. In the USIK trial carried out in France in November 1995, nearly two thirds of patients received betablocker therapy. In the same study, the prescription of betablockers is associated with a reduction in mortality independent of the classical risk factors and the prescription of angiotensin converting enzyme inhibitors. These results confirm the value of this therapeutic class in the acute phase of myocardial infarction.
Arch Mal Coeur Vaiss 1998 Apr
PMID:[Betablocker therapy in acute myocardial infarction]. 974 76

Eight randomised clinical trials of angiotensin converting enzyme (ACE) inhibitors versus placebo in myocardial infarction have been published in three years, including over 100,000 patients. High risk myocardial infarction carries a poor prognosis with a 25% death rate at 42 months in SAVE, 23% at 15 months in AIRE and 42% at 37 months in TRACE. This form of myocardial infarction benefits the most from treatment with ACE inhibitors: the relative reductions in risk for the previously mentioned trials were 19%, 27% and 22% respectively, and the absolute reductions in risk of death were 4% at 42 months, 6% at 15 months and 8% at 37 months, respectively. Studies including all forms of myocardial infarction involve populations at lower risk. The effects of ACE inhibitors on mortality are then less obvious: from 7.7% to 7.2% at 5 weeks in ISIS-4, from 7.1% to 6.3% at 6 weeks in GISSI-3, from 9.6% to 9.0% at 4 weeks in CCS-1, corresponding to relative reductions in the risk of death of 7%, 12% and 3% respectively and absolute reductions of the risk of death of 0.5% at 5 weeks, 0.8% at 6 weeks and 0.6% at 4 weeks, respectively. Who should be treated? All patients for 4 to 6 weeks or only high risk patients. When should treatment be started? Some investigators institute treatment from the first day but others think it prudent to wait until the second day. For how long? Four to 6 weeks would be sufficient to counteract ventricular remodelling while the benefits are sustained in the long term. But treatment should be continued long term in high risk patients. Which molecule, which dose and how many times, should it be taken per day? The logical answer is molecules with proven efficacy at the dose given in the clinical trials respecting the number of times indicated per day.
Arch Mal Coeur Vaiss 1998 Apr
PMID:[Treatment with angiotension converting enzyme inhibitors]. 974 77

The initial phase of the epidemiological USIK study has recensed data concerning 2,563 patients admitted to hospital for acute myocardial infarction. The second phase of this study has documented the 1 year survival of 2,152 patients (84%). The population comprised 1,533 men and 619 women with a mean age of 67 years. Severe left ventricular dysfunction (LVEF < 35%) was observed in 18% of patients and clinical signs of cardiac failure were present in 35% of patients in the first 5 days of infarction. The mortality was 8.2% at 5 days, 13.2% at 28 days and 19.5% at one year. In multivariate analysis, the principal predictive factor of mortality at 1 year was age (RR = 1.06, p = 0.0001): the mortality increased by 6% per year of age. In survivors 5 days after the onset of infarction, the 1 year prognosis was significantly correlated with age (RR = 1.05, p = 0.0001) and with cardiac failure (LVEF: RR = 1.57, p = 0.0001) and Killip class (RR = 1.66, p = 0.0001). The prescription of an ACE inhibitor or a betablocker in the first 5 days of infarction was associated with a reduction in 1 year mortality of 27% (p = 0.04) and 37% (p = 0.01) respectively. In conclusion, this study has determined the features of patients admitted to the Intensive Care Unit for acute myocardial infarction in France and to identify the factors influencing 1 year survival.
Arch Mal Coeur Vaiss 1998 Sep
PMID:[Epidemiology of myocardial infarction in France. One-year survival in the Usik study]. 980 68

The aim of this study was to identify the similitudes and the differences in the epidemiology and prevention of myocardial infarction and cerebrovascular accidents by analysis of trials of primary and secondary prevention of myocardial infarction and cerebrovascular accidents. The principal risk factors common to both pathologies are hypertension, smoking and increased LDL-cholesterol. However, the statistical significance with respect to causality differs from one pathology to the other. Similarly, the impact of preventive measures is not the same: the treatment of hypertension is more important in the prevention of cerebrovascular accidents than myocardial infarction; the situation is the other way around with respect to the treatment of hypercholesterolaemia. Of the therapeutic interventions, aspirin is effective in all stages of coronary artery disease but does not prevent cerebrovascular accidents in patients without documented atherosclerosis. Thrombolysis carries a much higher benefit/risk ratio in the treatment of myocardial infarction than in that of cerebral infarction. The so-called cardioprotective drugs, such as the betablockers and angiotensin converting enzyme inhibitors, have only been used to any extent in the secondary prevention of myocardial infarction. These differences reflect the fact that cerebrovascular accident covers a range of diseases much more diverse than does myocardial infarction, and also that the brain is much more exposed to haemorrhage whereas cardiac haematoma is highly unusual. Finally, cerebral atherosclerosis is a later event than coronary atherosclerosis and this has epidemiological implications which are difficult to assess. In conclusion, the prevention of myocardial infarction and of cerebrovascular accidents may proceed theoretically by a common pathway but in practice, it is very different.
Arch Mal Coeur Vaiss 1998 Oct
PMID:[Heart and brain: are the risk factors the same? Are the results of primary and secondary trials comparable?]. 983 81


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