Open AccessIschemic Cardiomyopathy is Associated With Coronary Plaque Progression and Higher Event Rate in Patients After Cardiac Transplantation
Author(s) -
Guddeti Raviteja R.,
Matsuo Yoshiki,
Matsuzawa Yasushi,
Aoki Tatsuo,
Len Ryan J.,
Lerman Lilach O.,
Kushwaha Sudhir S.,
Lerman Amir
Publication year - 2014
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.114.001091
Subject(s) - medicine , cardiology , hazard ratio , intravascular ultrasound , ischemic cardiomyopathy , heart transplantation , heart failure , myocardial infarction , coronary artery disease , transplantation , cardiomyopathy , ejection fraction , confidence interval
Background Cardiac allograft vasculopathy is the leading cause of graft failure and death in heart transplant ( HT x) recipients; however, the association between the etiology of heart failure (ischemic cardiomyopathy [ ICM ] or non‐ ICM ) that led to HT x and progression of c ardiac allograft vasculopathy , and adverse events after HT x has not been explored. Methods and Results We retrospectively included 165 HT x patients, who were followed‐up with at least 2 virtual histology–intravascular ultrasound examinations after HT x, 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 HT x (hazard ratio 2.02; 95% CI 1.01 to 4.00; P =0.048). Conclusion Our study demonstrates that ischemic etiology of cardiomyopathy prior to HT x may be independently associated with plaque progression and higher event rate after HT x.