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Angiotensin-Converting Enzyme Inhibitors and Change in Aortic Valve Calcium
Kevin D. O’Brien, MD;
Jeffrey L. Probstfield, MD;
Michael T. Caulfield, MD;
Khurram Nasir, MD, MPH;
Junichiro Takasu, MD;
David M. Shavelle, MD;
Audrey H. Wu, MD, MPH;
Xue-Qiao Zhao, MD;
Matthew J. Budoff, MD
Arch Intern Med. 2005;165:858-862.
Background Calcium accumulation in the aortic valve is a hallmark of aortic sclerosis and aortic stenosis. Because lipoproteins, angiotensin-converting enzyme, and angiotensin II colocalize with calcium in aortic valve lesions, we hypothesized an association between angiotensin-converting enzyme inhibitor (ACEI) use and lowered aortic valve calcium (AVC) accumulation, as measured by electron beam computed tomography.
Methods Rates of change in volumetric AVC scores were determined retrospectively for 123 patients who had undergone 2 serial electron beam computed tomographic scans. The mean (±SD) interscan interval was 2.5 (±1.7) years; 80 patients did not receive ACEIs and 43 received ACEIs. The relationship of ACEI use to median rates of AVC score change (both unadjusted and adjusted for baseline AVC scores and coronary heart disease risk factors) was determined. We also examined the relationship of ACEI use to the likelihood of and adjusted odds ratio for definite progression (AVC change >2 times the median interscan variability).
Results Unadjusted and adjusted median rates of AVC score change were significantly higher in the no-ACEI group than in the ACEI group (adjusted median AVC changes [95% confidence interval]: relative, 28.7%/y [18.9%-38.5%/y] vs 11.0%/y [–1.9% to 24.0%/y], P = .04; absolute: 25.1/y [19.7-30.5/y] vs 12.2/y [4.5-19.9/y], P = .02). The adjusted odds ratio (95% confidence interval) for definite AVC progression was significantly lower for patients who received ACEIs (0.29 [0.11-0.75], P = .01).
Conclusions This retrospective study finds a significant association between ACEI use and a lower rate of AVC accumulation. The results support the need for prospective, randomized trials of ACEIs in calcific aortic valve disease.
Author Affiliations: Division of Cardiology, Department of Medicine, University of Washington, Seattle (Drs O’Brien, Probstfield, Caulfield, Shavelle, Wu, and Zhao); and the Departments of Medicine, Johns Hopkins Medical Institutions, Baltimore, Md (Dr Nasir); and Harbor-UCLA Medical Center, Torrance, Calif (Drs Takasu and Budoff). Drs Caulfield, Shavelle, and Wu are now with the Departments of Medicine, Massachusetts General Hospital, Boston, Harbor-UCLA Medical Center, and University of Michigan, Ann Arbor, respectively.
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