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- Open Access
Vasodilator stress cardiovascular magnetic resonance imaging in post-orthotopic heart transplant recipients: evaluation of safety, hemodynamics, and myocardial perfusion
© Narang et al. 2016
- Published: 27 January 2016
- Myocardial Perfusion
- Late Gadolinium Enhancement
- Hemodynamic Response
- Perfusion Abnormality
Long-term survival after orthotopic heart transplant (OHT) is limited by coronary allograft vasculopathy and its associated myocardial perfusion abnormalities. Little is known how post-OHT patients respond to vasodilator stress cardiovascular magnetic resonance imaging (vsCMR). This study aimed (1) to evaluate the safety and hemodynamic response of post-OHT patients undergoing vsCMR with regadenoson and (2) to determine whether these patients have abnormalities in myocardial perfusion detectable by vsCMR.
We studied 50 subjects, including 20 patients post-OHT and 30 controls (10 healthy volunteers and 20 patients with known myocardial infarction [MI]), who underwent vsCMR (1.5T scanner, Achieva, Phillips). Short-axis CMR images of the left ventricle (LV) were obtained during first pass of gadobenate-dimeglumine (0.075 mmol/kg at 4 ml/sec) for approximately 50 consecutive heartbeats. Images were acquired using a hybrid gradient echo/echo planar imaging sequence one minute after administration of regadenoson 0.4 mg and then repeated 15 minutes after reversal with aminophylline (125 mg). Hemodynamic data and side-effects and were recorded in all patients. Time-intensity curves generated from stress and rest perfusion images were used to determine myocardial perfusion reserve index (MPRi), which was calculated as the up-slope ratio of stress to rest (normalized to the LV cavity and rate-pressure-product). For the MI group, MPRi was assessed in a segment remote to the ischemic/infarct territory based on late gadolinium enhancement and invasive coronary angiography. Differences between patient groups were tested using the Mann-Whitney U test.
Post-OHT patients can safely undergo vsCMR imaging and experience a similar hemodynamic response to control patients. MPRi was significant reduced in post-OHT patients when compared to healthy volunteers and patients with known prior MI. Future studies examining the mechanisms of the reduced MPRi in post-OHT patients are warranted.
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