Circulation. 2001;104:1615-1621
doi: 10.1161/hc3901.096700
doi: 10.1161/hc3901.096700
(Circulation. 2001;104:1615.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Reduction of Cardiovascular Risk by Regression of Electrocardiographic Markers of Left Ventricular Hypertrophy by the Angiotensin-Converting Enzyme Inhibitor Ramipril
Division of Cardiology, Department of Medicine, University of Iowa College of Medicine, Iowa City, and Galesburg Cottage Hospital, Galesburg, Ill (J.M.); the Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK (P.S.); the Division of Cardiology, McMaster University, Hamilton, Canada (E.L., Q.Y., J.P., J.B., S.Y.); the Department of Medicine, Dalhouse University, Halifax, Nova Scotia, Canada (D.J.); the Department of Medicine, Memorial University of Newfoundland, St John’s, Newfoundland, Canada (B.S.); and the Departments of Medicine and Epidemiology, Washington University, Seattle (J.P.).
Correspondence to James Mathew, MD, 695 North Kellogg St, Galesburg, IL 61401. E-mail manthi{at}galesburg.net Post publication correspondence to Canadian Cardiovascular Project Office, 237 Barton St E, Hamilton, Ontario, Canada L8L 2X2.
Background— Electrocardiographic markers of left ventricular hypertrophy (LVH) predict poor prognosis. We determined whether the ACE inhibitor ramipril prevents the development and causes regression of ECG-LVH and whether these changes are associated with improved prognosis independent of blood pressure reduction.
Methods and Results— In the Heart Outcomes Prevention Evaluation (HOPE) study, patients at high risk were randomly assigned to ramipril or placebo and followed for 4.5years. ECGs were recorded at baseline and at study end. We compared prevention/regression and development/persistence of ECG-LVH in the two groups and related these changes to outcomes. At baseline, 676 patients had LVH (321 in the ramipril group and 355 in the placebo group) and 7605 patients did not have LVH (3814 in the ramipril group and 3791 in the placebo group). By study end, 336 patients in the ramipril group (8.1%) compared with 406 in the placebo group (9.8%) had development/persistence of LVH; in contrast, 3799 patients in the ramipril group (91.9%) compared with 3740 in the placebo group (90.2%) had regression/prevention of LVH (P=0.007). The effect of ramipril on LVH was independent of blood pressure changes. Patients who had regression/prevention of LVH had a lower risk of the predefined primary outcome (cardiovascular death, myocardial infarction, or stroke) compared with those who had development/persistence of LVH (12.3% versus 15.8%, P=0.006) and of congestive heart failure (9.3% versus 15.4%, P<0.0001).
Conclusions— The ACE inhibitor ramipril decreases the development and causes regression of ECG-LVH independent of blood pressure reduction, and these changes are associated with reduced risk of death, myocardial infarction, stroke, and congestive heart failure.
Key Words: hypertrophy • angiotensin • myocardium • cardiovascular diseases • risk factors • prevention
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G. Y.H. Lip Regression of Left Ventricular Hypertrophy and Improved Prognosis: Some HOPE Now...or Hype? Circulation, October 2, 2001; 104(14): 1582 - 1584. [Full Text] [PDF]
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