CARDIAC ALLOGRAFT VASCULOPATHY ASSESSED BY INTRAVASCULAR ULTRASONOGRAPHY AND NONIMMUNOLOGICAL RISK-FACTORS

The genesis of cardiac allograft vasculopathy has been linked to nonim munologic endothelial injury. Studies evaluating the role of nonimmuno logic risk factors have thus far been limited to angiographic assessme nt. Intravascular ultrasound can detect cardiac allograft vasculopathy before it becomes angiographically evident. To assess the influence o f nonimmunologic risk factors in the development of cardiac allograft vasculopathy, we studied 101 consecutive cardiac transplant recipients who underwent intracoronary ultrasound imaging during routine, annual coronary angiography. Based on the severity of intimal thickening, pa tients were divided into 2 groups: group 1 = minimal, mild, or moderat e intimal thickness; and group 2 = severe intimal thickness. Cardiac t ransplant recipients with severe intimal thickness had higher levels o f total cholesterol (267 +/- 70 vs 227 +/- 41 mg/dl, p = 0.0008), low density lipoprotein cholesterol (187 +/- 47 vs 139 +/- 31 mg/dl, p = 0 .0001), and triglycerides (237 +/- 75 vs 182 +/- 88 mg/dl, p = 0.0001) , a higher percentage of weight gain (12 +/- 4% vs 8 +/- 5%, p = 0.000 1), a larger body mass index (30 +/- 4 vs 25 +/- 3, p = 0.0001), and o lder donor age (27 +/- 5 vs 23 +/- 7 year p = 0.005) than recipients w ith mild or moderate intimal thickness. Multiple regression analysis e stablished that total cholesterol, (low-density lipoprotein cholestero l, triglyceride levels, obesity indexes, donor age, and years followin g cardiac transplantation (p <0.01) were independent predictors of the severity of intimal thickening and thus the severity of cardiac allog raft vasculopathy. Hyperlipidemia, significant weight gain, and advanc ed donor age are predictors of the severity of intimal thickness by in travascular ultrasound. These findings may identify a group of cardiac transplant recipients in whom early intervention aimed at modificatio n of hyperlipidemia and weight loss may be beneficial in preventing or delaying the development of cardiac allograft vasculopathy.