Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In acute as well as in chronic ischemic heart disease, congestive heart failure indicates a poor prognosis. Treatment after acute myocardial infarction should differentiate between specific subsets. In cardiogenic shock due to extensive ischemic damage, acute revascularization by PTCA or CABG improves the otherwise poor outcome substantially. In congestive heart failure, pre- and afterload reduction by nitrates should be combined with dopamine if systolic blood pressure is below 100 mmHG or dobutamine if an inotropic substance is necessary despite systolic blood pressure greater than 100 mmHg. Amrinone is a potent alternative which combines positive inotropic and vasodilating properties. In chronic ischemic heart disease, congestive heart failure is a clearly defined indication for complete revascularization, if possible. As to drug treatment, progression of the disease characterized by a cardiomyopathy of overload as well as neurohormonal and peripheral maladaptation should be stopped in parallel with symptom relief. Therefore, ACE-Inhibitors are combined very early with diuretic treatment, and digitalis should be added in refractory patients.
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PMID:[The treatment of heart insufficiency in coronary heart disease]. 192 14

It is known that angiotensin converting enzyme (ACE) inhibitors not only prevent the formation of angiotensin II, but also potentiate the activity of bradykinin. We investigated the effects of the ACE-inhibitor ramipril in two models of cardiac ischemia. In anesthetized dogs with a coronary occlusion of 6-h duration, both ramiprilat and bradykinin significantly reduced infarct-size. This effect was prevented by the co-administration of the bradykinin antagonist HOE 140. In rats with a coronary occlusion of 6-weeks duration, ramipril administration significantly reduced infarct-size and prevented the development of left ventricular hypertrophy. Thus, ramipril showed a cardioprotective activity in models of acute as well as of chronic myocardial ischemia. These effects are probably mediated by the potentiation of bradykinin.
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PMID:[Reduction of infarct size and remodeling after ramipril]. 785 82

Restriction of physical activities (which does not exclude participation in tailored rehabilitation programmes), limitation of water and sodium intake, diuretics and digitalis (at least in the presence of atrial fibrillation) have long been used in the therapy of symptomatic congestive heart failure. Nowadays, the value of inhibiting the sympathetic and renin-angiotensin-aldosterone response to cardiac output lowering is well established; ideally, this requires concomitant administration of an ACE-inhibitor, a beta-blocker and spironolactone. All treatable causes of myocardial dysfunction should be adequately corrected (including chronic myocardial ischemia). When needed, patients should also be protected against lethal ventricular arrhythmias, and thrombo-embolic complications.
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PMID:[Pharma-clinics. How I treat...symptomatic heart failure]. 1049 87

In a series of articles the authors analyze literature data concerning controlled studies in which cardio-, cerebro-, and vasoprotective effects of angiotensin converting enzyme inhibitors (ACEI) have been assessed. In the second communication they discuss the results of three recently completed major randomized placebo controlled trials assessing effect of ACEI on the risk of cardiovascular events in patients with chronic ischemic heart disease (IHD) and preserved left ventricular systolic function. In PROGRESS and PEACE trials ACEI perindopril and trandolapril as monotherapy turned out incapable to prevent development of myocardial infarctions and strokes in patients with cardiovascular diseases without left ventricular systolic dysfunction. In EUROPA positive results were achieved at the account of special selection of patients, post hoc replacement of end points, and the use of high dose of perindopril (8 mg/day). Therefore results of this trial can not be applied to majority of patients with IHD. Biochemical studies have shown that ACEI are unable to suppress angiotensin II formation in human heart and vessels and thus in principle are not capable to cause cardio- and vasoprotective effects independent of their antihypertensive action. The fact is that contrary to rats in human heart and vessels angiotensin converting enzyme is responsible for just a portion (2-20% and 40%, respectively), of entire angiotensin II production. The remaining part of angiotensin II is formed under influence of chymase, activity of which is not altered during treatment with ACEI.
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PMID:[Antiatherogenic effects of angiotensin converting enzyme inhibitors from the point of view of evidence based medicine]. 1826 Aug 63

In patients with arterial hypertension and/or high cardiovascular risk, including patients with diabetes, chronic ischemic heart disease and kidney disease, the risk of heart failure decreases with blood pressure reduction and the use of drugs that inhibit the renin-angiotensin system (RAS) [angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs)]. The heart failure incidence seen in ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (TRANSCEND) is in line with this observation. In ONTARGET, telmisartan and ramipril were equally effective in heart failure prevention and with the same blood pressure reduction. The low event rate, including the low incidence of heart failure in TRANSCEND with the greater use of diuretics in the placebo arm, may help to explain the absence of significant differences between telmisartan and placebo.
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PMID:The question of heart failure in ONTARGET and TRANSCEND: implications for clinical practice. 1949 21