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Prevention of Events With Angiotensin-Converting Enzyme Inhibitor Therapy (PEACE)

2014-08-27 04:00:04 | BioPortfolio

Summary

To determine whether the addition of angiotensin converting enzyme (ACE) inhibitor to standard therapy in patients with known coronary artery disease and preserved left ventricular function will prevent cardiovascular mortality and reduce the risk of myocardial infarction.

Description

BACKGROUND:

Individuals with coronary artery disease are at heightened risk for major cardiovascular events. With current advances, a larger segment of our population is manifesting coronary artery disease at a more advanced age. The majority of these individuals have preserved left ventricular function. Prior studies with converting enzyme inhibitor (CEI) therapy in patients with depressed ejection fraction have demonstrated that their long-term administration leads to improved survival and reduced risk of myocardial infarction over and above conventional therapy. There is sufficient rationale and experience to indicate that these benefits will apply to the larger group of individuals with coronary artery disease and preserved left ventricular function and therefore have even broader public health implications. A definitive trial is needed to assess the capacity of CEI therapy to prevent mortality and reduce the risk of myocardial infarction in patients with coronary disease and preserved left ventricular function.

The initiative was proposed by the former Clinical Trials Branch staff and given concept clearance at the May 1994 National Heart, Lung, and Blood Advisory Council. The Request for Proposals was released in October 1994.

DESIGN NARRATIVE:

A multicenter, randomized clinical trial. There are approximately 180 centers in the United States, Canada, Puerto Rico, and Italy. Patients are randomly assigned to treatment groups in which the addition of the angiotensin-converting enzyme (ACE) inhibitor trandolapril is compared to standard therapy. The primary endpoint includes a reduction in the incidence of cardiovascular death, nonfatal myocardial infarction, or the need for coronary revascularization (PTCA or CABG) in coronary artery disease patients with left ventricular ejection fraction of 40 percent or more. Secondary endpoints include the incidence of hospitalization for the management of either unstable angina, congestive heart failure, stroke, or cardiac arrhythmia. Recruitment started in November 1996 and ended in June 2000 with a minimum follow-up of five years.

Study Design

Allocation: Randomized, Control: Placebo Control, Masking: Double-Blind, Primary Purpose: Prevention

Conditions

Cardiovascular Diseases

Intervention

angiotensin-converting enzyme inhibitors

Status

Completed

Source

National Heart, Lung, and Blood Institute (NHLBI)

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T04:00:04-0400

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PubMed Articles [17966 Associated PubMed Articles listed on BioPortfolio]

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Medical and Biotech [MESH] Definitions

A class of cardiovascular drugs indicated for hypertension and congestive heart failure that simultaneously inhibit both NEUTRAL ENDOPEPTIDASE and ANGIOTENSIN CONVERTING ENZYME. They increase the availability of NATRIURETIC PEPTIDES and BRADYKININ and inhibit production of ANGIOTENSIN II.

An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.

A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.

One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.

One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors) used for hypertension. It is a prodrug that is hydrolyzed after absorption to its main metabolite cilazaprilat.

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