Renal transplant patients have impaired myocardial perfusion independent of the degree of left ventricular hypertrophy: a CMR study

Abstract

Background: Cardiovascular (CV) disease remains one of the commonest causes of death in the first five years after renal transplantation, often in patients with no known cardiac disease. Cardiovascular magnetic resonance (CMR) imaging enables concurrent assessment of myocardial function, perfusion and irreversible injury. We hypothesized that myocardial perfusion reserve would be impaired in asymptomatic post-renal transplant patients when compared with hypertensive controls, independent of the degree of left ventricular hypertrophy (LVH). Methods: Twenty-five asymptomatic renal transplant patients (RT) (3 months to 5 years post-transplant) with no known history of ischemic heart disease and 17 hypertensive controls (HT) without renal disease underwent CMR scanning at 1.5 T. Myocardial function, late enhancement, and first-pass perfusion at rest and stress was performed. Myocardial Perfusion Reserve Index (MPRI) was calculated as the ratio of hyperemic to resting myocardial blood flow by dividing the myocardial perfusion at stress by rest perfusion (corrected to rate pressure product). Statistical analyses were performed using mixed effects modeling. Results: Baseline clinical characteristics, left and right ventricular ejection fraction and volumes were similar for both RT and HT control groups. LV mass index was similar in the RT and HT groups (LV mass index 63±12 g/m2 RT vs 62±11 g/m2 HT, p>NS). Global MPRI was significantly lower in the RT group compared to the HT group (1.36±0.52 vs 2.06±0.59, P=0.0004). MPRI in all three coronary artery territories were significantly lower in the RT group (see table 1). One patient in the RT group had late Gadolinium enhancement suggesting occult sub-endocardial infarction. View this table: MPRI in Coronary Artery Territories Conclusions: Post renal transplant patients have global reductions in myocardial perfusion compared to hypertensive controls, independent of the degree of LVH. This may reflect both severe coronary microvascular disease and/or undiagnosed epicardial coronary artery disease, and may in part explain the poorer cardiac outlook in these patients.