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)

Hospital mortality from acute myocardial infarction has decreased in the last two decades. Left ventricular dysfunction therefore have been mainly due to ischemia. After extensive myocardial infarction, there are processes of adaptation (remodeling) which result in altered geometry of the left ventricle. The effects of this on neurohormonal systems (organ regulation), on the changed ratio of myocyte mass and collagen content owing to reactive and reparative fibrosis (organ texture) and on the molecular and cellular mechanisms (organ structure) are of crucial importance. Depending on the structural changes, the myocardial contractility decreases. This is associated with an activation of the circulating renin-angiotensin-aldosterone system (RAAS). The fundamental knowledge available has led to the therapeutic use of ACE inhibitors in the post-infarct period. This treatment enabled a sustained reduction of mortality in several large-scale randomized studies. The effect of early administration in patients with clinical signs of heart failure and/or left ventricular dysfunction was very much greater compared to unselected controls. Only 17 and 13 patients had to be treated after selection in order to save one life in the AIRE and TREACE Study respectively (NNT: number needed to treat), whereas e.g. in the ISIS-4 study 200 unselected patients had to be treated. In clinical practice, however, this life-saving therapy is only used in every second patient requiring treatment. With consideration of an individual form of treatment (anterior infarction, large infarct area, reinfarction, clinical signs of heart failure as well as arterial hypertension and diabetes mellitus), a greater acceptance of evidence-based guidelines is thus desirable. Treatment with a high dose may be expected to be of additional benefit.
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PMID:[Left ventricular remodeling: pathophysiological mechanisms and therapeutic recommendations]. 1065 89

The causes of chronic heart failure at the end of the 20th century are quite different from those 30 or 50 years ago. The last data from the Framingham study indicate that ischaemic heart disease and/or hypertension are the main cause in as many as 90% patients. The prevalence of chronic heart failure in European countries, 0.4-2%, implies 40-200,000 patients in the Czech Republic. Pharmacological treatment during the last 15 years revealed clearly that the drugs of choice which prolong life are inhibitors of the angiotensin converting enzyme (ACE-I) which are combined with other drugs as needed by the patient. A combination of five drug groups (ACE-I, digitalis, diuretics, beta-blockers, and spironolactone) are nowadays the basic treatment. In the 4S study (Scandinavian Simvastatin Survival Study--4,444 patients with ischaemic heart disease followed up for 5.4 years) 412 (9.2%) developed chronic heart failure requiring treatment, i.e. 228 (10.3%) in the placebo group and 184 (8.3%) patients in the group treated with simvastatin (p < 0.015). In the group of patients with signs of heart failure 73 of 228 died the placebo group and 47 of 184 in the simvastatin group (reduction of the relative risk by 19%, p = 0.014), to save one life (NNT) it was necessary to treat 15 patients for a period of 5 years. From the aspect of the number of patients it was necessary to treat six times as many patients without heart failure than with heart failure to save one life in five years. Hypolipidaemic treatment should be an obvious part of treatment of heart failure due to ischaemic heart disease. Hyperlipoproteinaemia is described in 60-80% patients after transplantation of the heart. Treatment involves diet, reduction or discontinuation of corticoids, maintenance of cyclosporin at the lowest effective level and treatment wit statins.
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PMID:[Lipids and chronic heart failure]. 1134 43