January 1, 2003Open Access
View Full PaperMechanisms of cardiovascular risk reduction with ramipril: insights from HOPE and HOPE substudies
Key Result
Ramipril has potent, dose-dependent, and largely blood pressure-independent effects on atherosclerosis progression, plaque stabilization, myocardial structure and function, and glucose metabolism.
Structured PICO
What are the mechanisms of cardiovascular risk reduction with ramipril in the HOPE trial?
I
Intervention
Ramipril
Ramipril provides cardiovascular protection through mechanisms including atherosclerosis progression, plaque stabilization, and improved glucose metabolism, independent of blood pressure lowering.
Abstract
Angiotensin converting enzyme (ACE) inhibitors decrease angiotensin formation, prevent breakdown of bradykinin, and may also act on other peptides of the renin-angiotensin system. Thus, these agents have many effects that can potentially protect the coronary and peripheral vascularature. Which of these "theoretical" mechanisms account for the clinical benefit observed in The Heart Outcomes Prevention Evaluation (HOPE) trial? While the answer to this question is complex and cannot be fully answered, several potential mechanisms have been explored within HOPE and its substudies. These studies demonstrate that ramipril has potent effects on atherosclerosis progression and plaque stabilization as well as on myocardial structure and function. Ramipril also improves glucose metabolism. These effects are dose-dependent but largely blood pressure independent.