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CLINICAL RESEARCH: HEART FAILURE

Influence of Pre-Existing Donor Atherosclerosis on the Development of Cardiac Allograft Vasculopathy and Outcomes in Heart Transplant Recipients

Haiyan Li, MD^_*, Koji Tanaka, MD, Hitoshi Anzai, MD, Brandy Oeser, MPH, Dominic Lai, BA, Jon A. Kobashigawa, MD and Jonathan M. Tobis, MD^,_*

^_* Department of Cardiology, Peking University Third Hospital, Beijing, China
Department of Medicine, Division of Cardiology, University of California Los Angeles, David Geffen School of Medicine, Los Angeles, California.

Manuscript received November 23, 2005; revised manuscript received January 10, 2006, accepted January 16, 2006.

^_* Reprint requests and correspondence: Dr. Jonathan M. Tobis, Division of Cardiology, UCLA Medical Center, 10833 Le Conte Avenue, BL-394 CHS, Los Angeles, California 90095. (Email: jtobis{at}mednet.ucla.edu).

OBJECTIVES: This study sought to evaluate the influence of donor lesions on the development of cardiac allograft vasculopathy and outcomes in heart transplant recipients.

BACKGROUND: After orthotopic heart transplantation (OHT), coronary artery narrowing occurs as a combination of pre-existing donor lesions and new lesions that develop as a result of cardiac allograft vasculopathy.

METHODS: Intravascular ultrasound (IVUS) studies were performed in 301 recipients at 1.3 ± 0.6 months and again at 12.2 ± 0.8 months after OHT. Additional IVUS studies were performed in 90 patients at two and three years of follow-up. Sites at baseline with maximum intimal thickness 0.5 mm were defined as pre-existing donor lesions. The angiographic diagnosis of transplant coronary artery disease (TCAD) was defined as a new 50% diameter narrowing of a major epicardial vessel.

RESULTS: Donor lesions were present in 30% of the hearts. By IVUS, sites with donor lesions did not have a greater increase in intimal area compared with sites without donor lesions. Angiographically, the incidence of TCAD up to three years after transplantation was higher in recipients with donor lesions than in recipients without donor lesions (25% vs. 4%, p < 0.001). However, the three-year mortality rate was similar between recipients with or without donor lesions (4.5% vs. 5.2%, p = 1.0).

CONCLUSIONS: Pre-existing donor lesions do not act as a nidus for accelerating the progression of intimal hyperplasia. However, patients with donor lesions have a higher incidence of angiographic TCAD. Donor lesions do not affect the long-term survival of patients with OHT up to three years.

Abbreviations and Acronyms   EEM = external elastic membrane   IVUS = intravascular ultrasound   MIT = maximum intimal thickness   OHT = orthotropic heart transplantation   TCAD = transplant coronary artery disease

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