COMPLICATIONS - CARDIOVASCULAR

H.R. Chua¹, A. Vathsala^2
1University Medicine Cluster, Division Of Nephrology, National University Health System, Singapore/SINGAPORE, ², NATIONAL UNIVERSITY HOSPITAL, Singapore/SINGAPORE

Body: Introduction Death from cardiovascular disease (CVD) with a functional graft is a major cause of transplant loss, and warrants intensive management in renal transplant recipients (RTX). Inducible myocardial ischemia (IMI) is strongly associated with eventual major cardiovascular events, for which diabetic RTX are at higher risk. However, utility of regular stress myocardial perfusion imaging (MPI) for pre-emptive detection of IMI in asymptomatic diabetic RTX has not been previously evaluated, and its use is not routinely recommended. Methods Of 252 RTX who had undergone transplant between 2000 and 2008, 64 patients with either diabetes mellitus prior to transplant (DM, N=26) or new onset diabetes after transplant (NODAT, N=38), were subjected to routine 2-3 yearly stress MPI at our institution, for detection of asymptomatic IMI. Treadmill, dipyridamole, or dobutamine stress tests were utilized to detect IMI. Traditional CVD risks including dialysis vintage, duration of DM or NODAT, BMI, blood pressure, lipid profiles, and glycemic control were retrospectively analyzed; up till the occurrence of IMI; abnormal coronary angiogram (COROS) with stenosis >70%; major adverse cardiovascular events (MACE), including myocardial infarction, heart failure, coronary revascularization, or angioplasty; graft loss; and death. Results The study population included 59% males, 22% living donor transplants with mean age of 49 (range 20 to 71) years, who had received calcineurin inhibitor-based immunosuppression together with corticosteroids with or without mycophenolate. 16 RTX (25%) had IMI detected at a median interval of 2.5 (range: 0.1 – 7.9) years post transplant. Of these, 10 had NODAT with IMI occurring at median 1.8 (range: 0.2 – 6.3) years after onset of NODAT; the remaining 6 with pre-transplant DM had IMI at 7.5 (range 4.0 – 17.0) years after onset of DM. Incidence of IMI was not significantly different between DM (23%) and NODAT (26%). Among 16 with IMI, 8 had moderate to severe myocardium defects while 4 had depressed ejection fraction (EF) <50% post stress testing. All but 3 with IMI received anti-platelet therapy. 3 RTX (19%) in the IMI group developed MACE at median 0.2 (range 0.1 – 4.0) years post detection of IMI. 1 of 48 RTX (2%) without IMI also developed MACE 1 year following the last normal MPI. Analysis using logistic regression identified depressed post stress EF (p=0.002) and increased myocardium defect size (p=0.019) as significant predictors of MACE and abnormal COROS. Analysis of other traditional CVD risk factors using logistic regression did not reveal significant predictors of subsequent IMI. ConclusionOur study demonstrates a high incidence of IMI of 25% in a diabetic RTX population, in particular a significant occurrence in the sub-group ofpatients with NODAT. Occurrence of MACE in 19% of RTX with IMI despite anti-platelet therapy suggests the need for more aggressive cardiac interventions in this cohort, especially in presence ofdepressed EF or severe myocardium defects post stress testing. These results justify the routine use of regular stress MPI for all asymptomatic diabetic KTR.

Disclosure: All authors have declared no conflicts of interest.