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Ischemic Cardiomyopathy is Associated With Coronary Plaque Progression and Higher Event Rate in Patients After Cardiac Transplantation

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      Cardiac allograft vasculopathy is the leading cause of graft failure and death in heart transplant (HTx) recipients; however, the association between the etiology of heart failure (ischemic cardiomyopathy [ICM] or non‐ICM) that led to HTx and progression of cardiac allograft vasculopathy, and adverse events after HTx has not been explored.

      Methods and Results

      We retrospectively included 165 HTx patients, who were followed‐up with at least 2 virtual histology–intravascular ultrasound examinations after HTx, and grouped them as ICM (n=46) or non‐ICM (n=119). Coronary artery plaque volume was analyzed using virtual histology–intravascular ultrasound, and cardiovascular event data—a composite of myocardial infarction, hospitalization for heart failure and arrhythmia, revascularization, retransplantation, and death including cardiovascular death—were collected from the medical records of all study subjects. ICM patients had significantly higher plaque volume at both first ( P=0.040) and follow‐up ( P=0.015) intravascular ultrasound examinations. After multivariate adjustment for traditional coronary risk factors, ICM was significantly associated with plaque progression (odds ratio 3.10; CI 1.17 to 9.36; P=0.023). Ten‐year cardiovascular event‐free survival was 50% in ICM patients compared with 84% in non‐ICM patients (log‐rank test P=0.003). In multivariate Cox proportional hazard analysis, ICM was significantly associated with a higher event rate after HTx (hazard ratio 2.02; 95% CI 1.01 to 4.00; P=0.048).


      Our study demonstrates that ischemic etiology of cardiomyopathy prior to HTx may be independently associated with plaque progression and higher event rate after HTx.

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      Most cited references 42

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            Author and article information

            [1 ]Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN (R.R.G., Y.M., Y.M., T.A., S.S.K., A.L.)
            [2 ]Division of Biomedical Statistics and Informatics, Mayo College of Medicine, Rochester, MN (R.J.L.)
            [3 ]Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN (L.O.L.)
            Author notes
            Correspondence to: Amir Lerman, MD, Division of Cardiovascular Diseases and Department of Internal Medicine, Mayo College of Medicine, 200 First Street SW, Rochester, MN 55905. E‐mail: lerman.amir@
            J Am Heart Assoc
            J Am Heart Assoc
            Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
            Blackwell Publishing Ltd
            August 2014
            5 August 2014
            : 3
            : 4
            25095871 4310404 jah3634 10.1161/JAHA.114.001091
            © 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

            This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

            Original Research
            Preventive Cardiology


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