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 is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.
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PMID:[Ventricular "remodeling" after myocardial infarction]. 191 Mar 27

We present a case in which a patient took an overdose of captopril (Capoten) and alprazolam (Xanax) in a suicide attempt. The patient presented with hypotension (systolic blood pressure of 80 mm Hg) and drowsiness. The hypotension initially responded to administration of intravenous fluids and dopamine; however, it recurred twice at 18.5 and 24.5 hours after ingestion. These episodes again responded to administration of fluids and dopamine. A plasma captopril level of 27,391.1 nmol/L (5982 ng/mL) was documented, as well as a depressed level of angiotensin converting enzyme. Captopril is an angiotensin converting enzyme inhibitor used in the management of hypertension and ventricular failure; to our knowledge, this is the first case of an acute captopril overdose reported in the English-language literature. The role of captopril in inducing hypotension is discussed herein.
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PMID:Captopril overdose resulting in hypotension. 328 10

Within a period of three months indications and diagnostic as well as therapeutic consequences of all echocardiographic studies were investigated in a middle-size hospital. 174 of a total of 188 examinations were usable. Most examinations were performed in order to detect or to verify left-ventricular failure or coronary heart disease. The diagnostic and therapeutic consequences were enormous; more than 90% of all pathological findings were listed as diagnoses in the final medical report. In terms of valvular heart disease, pericardial effusion and left-ventricular failure the echocardiographic study was most essential for diagnosis. In contrast most normal findings were seen with suspicion of coronary heart disease. Changes in medication or new prescription of oral anticoagulation, ACE inhibitors and beta-adrenergic antagonists were significantly related to the therapeutic recommendations of the echocardiographic studies. The recommendations concerning antibiotic prophylaxis of endocarditis or further diagnostic investigation were respected with few exceptions. Obviously little conclusion could be drawn from a normal echocardiographic study; a well-established indication is essential for the benefit of echocardiography.
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PMID:[Indications for, diagnostic conclusions and therapeutic consequences of echocardiography. Studies in a medium-sized hospital]. 772 53

When a large multicenter research trial is abruptly terminated, it is usually a consequence of significant adverse events. In contrast, when the Randomized Aldactone Evaluation Study (RALES) mortality trial was discontinued 18 months early, it was because of the prominent salutary effect of spironolactone, added to standard multidrug therapy consisting of an angiotensin converting enzyme (ACE) inhibitor and loop diuretic (with or without digoxin), in reducing the incidence of death and hospitalization in patients with severe congestive heart failure (CHF). Therapies directed toward suppression of neurohormonal activation have contributed to significant reductions in morbidity and mortality. ACE inhibitors, in particular, have had the largest impact on adverse outcome measures in CHF. Yet despite combined therapy with an ACE inhibitor and loop diuretic, patients on these agents still have an unacceptably high incidence of progressive ventricular failure and death. In the years that followed its discovery in 1954, aldosterone was considered a target for therapy in CHF because of its role in sodium retention. It is now clear that chronic elevations in plasma aldosterone are responsible for many other adverse effects (Fig. 1), including enhanced potassium and magnesium excretion, myocardial fibrosis, inhibition of catecholamine reuptake, endothelial cell and baroreceptor dysfunction, and ventricular arrhythmias. Blockade of aldosterone action is a desirable pharmacologic approach to treating both the underlying pathophysiology of CHF and its clinical consequences. Spironolactone promotes magnesium and potassium retention, increases uptake of myocardial norepinephrine, attenuates formation of myocardial fibrosis, and decreases mortality associated with both progressive ventricular dysfunction and malignant ventricular arrhythmias. Despite the encouraging results seen in the recent RALES mortality trial, a diagnosis of CHF still carries 30% to 40% mortality at 2 years. We need to continue the trend of evaluating newer therapies directed at the pathophysiologic mechanisms of this syndrome, with a goal toward delaying and eventually reversing long-term consequences.
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PMID:Spironolactone in congestive heart failure. 1099 20