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)

The TRACE (TRAndolapril Cardiac Evaluation) study was designed to determine whether long-term treatment with an ACE inhibitor is beneficial in patients with early post-myocardial infarction cardiac failure. A total 6,676 consecutive patients with 7,001 myocardial infarctions were included; 2,606 patients had echocardiographic signes of left ventricular dysfunction (ejection fraction < 35%), 3 to 7 days after myocardial infarction; 1,749 patients were randomised and given either oral trandolapril (876 patients) or placebo (873 patients). Follow-up ranged from 24 to 50 months. Three hundred and four patients (34.7%) in the trandolapril group died, compared with 369 (42.3%) in the placebo group (p = 0.001). The relative risk of death in the trandolapril group compared with the placebo group was 0.78. Trandolapril was also associated with a statistically significantly lower risk of cardiovascular death and of sudden death. Progression to severe cardiac failure was also less frequent in the treatment group. On the other hand, the risk of recurrent myocardial infarction was not significantly reduced. In conclusion, long-term treatment with trandolapril in patients with early post-infarction left ventricular dysfunction significantly reduced the risk of cardiovascular mortality, sudden death and progression to severe cardiac failure.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Trandolapril in patients with left ventricular insufficiency after myocardial infarction]. 894 15

Most clinical trials of angiotensin converting enzyme inhibitors after myocardial infarction have shown an improved outcome with reduction of morbidity and mortality. In comparable groups of patients, the results are concordant with a decrease in mortality which is all the more significant and early in severe infarction with serious haemodynamic consequences. The clinician has a new arm in his therapeutic arsenal either for use in the acute phase of all cases of myocardial infarction but for only a short period of 4 to 6 weeks after which the treatment is withdrawn when the anatomical sequellae are more moderate, or for use in selected cases for longer periods (patients with severe infarction with cardiac failure and/or severe left ventricular dysfunction). The second attitude has the advantage of treating a selected population which will derive greater benefits. In all cases, treatment should be started orally at low doses, and the dose must be increased rapidly do attain the target dosage under close clinical and biological surveillance. When the classical contraindications are respected, ACE inhibitors seem to be well tolerated even at the relatively high dosages recommended after myocardial infarction. Hypotension and, more rarely, renal failure, are the two most common complications leading to withdrawal of treatment, but neither of these side effects was associated with increased mortality in any of the clinical trials. The mechanisms by which ACE inhibitors exert these beneficial effects after myocardial infarction are not only their haemodynamic effects and their role in ventricular remodelling, but also probably by a vascular protective action which, if confirmed, would further increase the indications of this therapeutic class in cardiovascular diseases.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Treatment by angiotensin converting enzyme inhibitors after myocardial infarction. What did the clinical trials teach us?]. 894 16

The betablockers are the most important drugs in the secondary prevention after myocardial infarction. Several studies have shown that, in patients without a contraindication to these drugs, betablockers reduce the mortality and recurrence of infarction by about 25%. The best results observed in the subgroup of patients with criteria of severity (previous myocardial infarction or cardiac failure, left ventricular dysfunction, arrhythmias, residual ischaemia, occluded artery or triple vessel disease) has been shown in the APSI and BHAT studies where the reduction in mortality was almost 50% in the subgroup of patients with cardiac failure. The duration of treatment and the role of betablockers with respect to ACE inhibitors are not as clearcut in 1996.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Secondary prevention after myocardial infarction; role of beta blockaders]. 894 18

Diuretics were used in most of the major trials that demonstrated that lowering the blood pressure reduced cardiovascular morbidity and mortality. Nevertheless in the second half of the eighties, there were misgivings about the widespread use of thiazide diuretics, driven in part by the relative failure of the large trials to reduce myocardial infarction-to the extent predicted by large scale epidemiological studies. There was much attention on metabolic side effects of thiazide diuretics including dyslipidaemia, glucose intolerance, hypokalaemia, hyperuricaemia, and then microalbuminuria particularly in diabetic subjects. These issues were current when JNC (IV) (1988) and the WHO-ISH guidelines (1989) were being written. Three major clinical trials SHEP, STOP and MRC published in the early nineties established that thiazide diuretics alone, or in combination with beta blockers, did reduce cardiovascular morbidity and mortality in elderly subjects with hypertension. All guidelines published since 1993 include diuretics among the first line drugs. Possibly the most important factor in the restoration of diuretics has been the use of progressively lower doses that minimise the metabolic side effects. Diuretics are effective as monotherapy in the treatment of mild essential hypertension and of isolated systolic hypertension in elderly subjects. They are very useful in combination with beta blockers or with ACE inhibitors. They should be avoided in patients with gout and should not be used as first line drugs in patients with diabetes. They should only be used with caution in young obese subjects with dyslipidaemia and increased risk of coronary artery disease, facing many decades of treatment for hypertension. However there is no doubt that diuretics are effective, cheap and have a central role in the control of hypertension in all communities around the world.
Arch Mal Coeur Vaiss 1996 Sep
PMID:[Role of diuretics in the treatment of hypertension: from large controlled trials to international guidelines]. 895 12

Although there is undoubtedly a link between ventricular dysfunction and heart failure the interrelationship is complex. Most patients with left ventricular dysfunction die before progression to heart failure. Heart failure is not preceded by a period of chronic left ventricular dysfunction for the large number of patients who develop heart failure soon after a myocardial infarction. Atrial fibrillation and myocardial ischaemia/infarction need to be considered as mechanisms of progression as well as left ventricular remodelling. ACE inhibitors and beta-blockers, but not diuretics or digoxin, may alter progression to and of heart failure. Potential adverse effects of aspirin on prognosis in patients with heart failure and coronary artery disease are cause for considerable concern.
Arch Mal Coeur Vaiss 1996 Nov
PMID:From left ventricular dysfunction to heart failure. 909 98

Terminal cardiac failure, despite the gain obtained by angiotensin converting enzyme inhibitors, continues to carry a high annual mortality. Cardiac transplantation, with a 1 year survival of about 80% (a result which is sustained at 5 years), constitutes the treatment of choice for these patients. However, in view of the contraindications to transplantation and the cruel lack of donors organs, many cases of terminal cardiac failure are unable to benefit from transplantation. What are the pharmacological means available for these patients? This is a real therapeutic challenge. The essential objective in the management of these patients with a poor short-term prognosis is the reduction of mortality. However, this aim is not easily attained, at least in the short or medium-term in the present state of our knowledge. Other objectives can therefore by legitimately considered in the management of patients with cardiac failure in the terminal phase: the most important ones are to improve symptomatology and the quality of life. Terminal cardiac failure is a complex syndrome implicating a number of non-cardiac abnormalities. They may not only participate in the symptomatology and high mortality, but also make therapeutic management a delicate operation. Nevertheless, the abnormalities of cardiovascular function remain the cardinal problem. The treatment which we use aims to correct them. The authors propose a review of the possibilities available with reference to data in the medical literature.
Arch Mal Coeur Vaiss 1996 Nov
PMID:[Terminal heart failure; therapeutic strategies. Drug therapy in cases of absence of possibility of heart transplantation: dobutamine therapy, aspects of compassion?]. 909 23

The lack of consensus concerning the diagnostic criteria of cardiac failure explains the relative paucity of epidermiological data. Most of the available information comes from American health registers and the Framingham study: in the United States, there are more than 3 million people with cardiac failure (over 1% of the population) and over 400,000 new patients each year. Cardiac failure is the main cause of death in 40,000 deaths and an associated cause in a further 250,000 deaths. In the Framingham study (1948-1988) the mean survival time after diagnosis is 1.7 year in men and 3.2 years in women, corresponding to 1 and 5 year survival rates of 57% and 25% in men and 64% and 38% in women. These figures are worse than those of the large scale therapeutic trials of the last 10 years and represent survival of the most severe cases. Although not strictly epidemiological data, analysis of the large scale trials allows evaluation of the clinical features and survival of patients under optimal medical treatment (ACE inhibitors associated with other treatments): these results are important to bear in mind when considering alternative therapies (transplantation, mechanical assist devices), the accessibility of which may be limited for reasons of availability or cost. In terms of public health, it is important that accurate epidemiological data concerning cardiac failure. In particular severe cardiac failure, is made available in France.
Arch Mal Coeur Vaiss 1996 Nov
PMID:[Epidemiology of cardiac failure and current prognosis of the most seriously ill patients]. 909 35

The association of sarcoidosis and chylothorax is rare. A patient aged 64 presented with mediastinal sarcoidosis. Two years after the diagnosis he developed a right chylothorax. The computed tomographic examination showed a retraction of the right hemithorax associated with large mediastinal nodes, without signs of interstitial lung disease. Pulmonary function tests revealed a restrictive ventilatory defect with a Forced Vital Capacity (FVC) of 53% and a Forced Expired Volume in one second (FEV1) of 54% from the predicted values; the FEV1/FVC ratio was 78%. Steroid therapy was started at 1 mg per kilogram per day for three months then progressively decreased to 15 mg per day. Inspite of the steroid therapy there was as well biological evidence of continued disease activity (bronchoalveolar lavage lymphocytosis and increased serum angiotensin converting enzyme), as persistence of pleural effusion and mediastinal adenopathy; the contraction of the right hemithorax increased. Restrictive ventilatory defect worsened with a FVC of 44% and an FEV1 of 47% of the predicted values. The presence of a significant contraction of the hemithorax and of a severe restrictive ventilatory defect suggested the existence both of pleural fibrosis and of a compression of the main lymphatic pathways responsible for the chylothorax.
Rev Mal Respir 1997 Sep
PMID:[Chylothorax and sarcoidosis]. 941 15

Intracoronary injection of acetylcholine leads to coronary vasodilatation in normal subjects and vasoconstriction in hypertensive subjects, suggesting an abnormality of endothelial function in hypertension. In order to study the response to physiological stimulation which induces endothelium-dependent vasodilatation, the effects of sympathetic stimulation (cold pressor test) and of the increase in flow velocity in the left anterior descending artery were analysed in 10 control and 26 hypertensive subjects. All had angiographically normal coronary arteries and normal lipid profiles. None of the subjects were smokers or diabetic. During the cold test (12 patients), the flow velocity increased by 47 +/- 26% (p < 0.05) in controls and by 68 +/- 48% (p < 0.01) in the hypertensives. Dilatation of the coronary arteries was observed in controls (+12.0 +/- 4.5%, p < 0.001) and constriction in the hypertensives (-10.3 +/- 8.5%, p < 0.001). Injection of papaverine in the distal left anterior descending artery (14 patients) induced proximal dilatation in controls (+17.0 +/- 10.6%, p < 0.001) and was ineffective in hypertensives (-0.4 +/- 1.5%), whereas the flow velocity increased by 521 +/- 129% and 406 +/- 120% (p < 0.001) respectively. Intracoronary injection of 2 mg of isosorbide dinitrate induced comparable dilatation in control subjects (+30.0 +/- 12.9%, p < 0.001) and in the 26 hypertensives (+22.8 +/- 6.5%, p < 0.001). In 10 hypertensive patients, intravenous injection of an angiotensin converting enzyme inhibitor, perindoprilat, immediately re-established the vasodilatory response to these two stimuli. The authors conclude that the coronary responses to physiological stimuli (sympathetic stimulation, increase in flow velocity) are altered in hypertensive subjects with angiographically normal coronary arteries with no other risk factors. Normal vasomotion may be restored by an angiotensin converting enzyme inhibitor.
Arch Mal Coeur Vaiss 1997 Nov
PMID:[Coronary endothelial dysfunction in hypertension]. 951 10

From the vascular point of view, cardiac failure is characterised by increased systemic resistances secondary to an increased concentration of a number of vasoconstrictor substances and also to decreased endothelium dependent vasodilatation. Endothelial dysfunction has been described both in man and in animal models, but its causes are not well understood. Such dysfunction could be due to a decrease in the production of nitric oxide, a decrease in its vasodilator effect due to an increased degradation or an increased vasoconstrictor tone. Recent data suggests an improvement or prevention of this endothelial dysfunction observed in cardiac failure by physical training and by chronic treatment with an angiotensin converting enzyme inhibitor. The improvement or preservation of endothelial function induced by exercise or ACE inhibitor could explain some of the benefits of these treatments in terms of tissue perfusion and haemodynamic conditions.
Arch Mal Coeur Vaiss 1997 Nov
PMID:[Endothelial dysfunction in cardial failure: potential mechanisms]. 951 11


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