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Cardiac allograft vasculopathy (CAV) is a unique form of accelerated atherosclerosis and remains the leading cause of late morbidity and mortality in heart transplant patients accounting for 30% mortality at 5 years (Miller et al., 1993), (Taylor et al., 2007). Although the pathogenesis of CAV is not fully elucidated, it seems to result from a complex interplay between immunologic and nonimmunologic factors, with consequent repetitive vascular injury and a localized sustained inflammatory response (Costanzo et al., 1998), (Julius et al., 2000). CAV affects large epicardial vessels and the microcirculation which results in a progressive luminal narrowing (Gao et al., 1990) and reduces myocardial blood flow (Kushwaha et al., 1998). CAV may be present in intramyocardial vessels even if epicardial disease is not evident (Clausell et al., 1995). Autopsy findings have demonstrated the presence of CAV in nearly all specimens at two years and changes are seen as early as 6 weeks after cardiac transplant (Baldwin et al., 1987), (St. Goar et al., 1992). Early CAV is clinically silent, and ischemia is usually not evident until the disease is far advanced (Ciliberto et al., 1993), (Collings et al., 1994, (Mairesse et al., 1995), (Smart et al., 1991), (Stark et al., 1991) and graft failure tends to develop as a late manifestation of the disease. Therefore, identification of the asymptomatic patient at early stages of the disease is an important strategy for the prevention of irreversible detrimental effects on the graft.

IVUS in the Assessment of Coronary Allograft Vasculopathy