Prognostic utility of longitudinal quantification of PET myocardial blood flow early post heart transplantation
- PDF / 1,319,582 Bytes
- 12 Pages / 593.972 x 792 pts Page_size
- 52 Downloads / 232 Views
Cardiology, University of Ottawa Heart Institute, Ottawa, ON, Canada ´ s-graduac ´ i, Brazil ˆ ncias Cardiovasculares, Universidade Federal Fluminense, Nitero ˜o em Cie Po ¸a Cardiac Sciences Department, King Saud University, Riyadh, Saudi Arabia
Received Apr 18, 2020; accepted Jul 19, 2020 doi:10.1007/s12350-020-02342-7
Background. Myocardial blood flow (MBF) quantification by Rubidium-82 positron emission tomography (PET) has shown promise for cardiac allograft vasculopathy (CAV) surveillance and risk stratification post heart transplantation. The objective was to determine the prognostic value of serial PET performed early post transplantation. Methods and Result. Heart transplant (HT) recipients at the University of Ottawa Heart Institute with 2 PET examinations (PET1 = baseline, PET2 = follow-up) within 6 years of transplant were included in the study. Evaluation of PET flow quantification included stress MBF, coronary vascular resistance (CVR), and myocardial flow reserve (MFR). The primary composite outcome was all-cause death, re-transplant, myocardial infarction, revascularization, allograft dysfunction, cardiac allograft vasculopathy (CAV), or heart failure hospitalization. A total of 121 patients were evaluated (79% male, mean age 56 ± 11 years) with consecutive scans performed at mean 1.4 ± 0.7 and 2.6 ± 1.0 years post HT for PET1 and PET2, respectively. Over a mean follow-up of 3.0 (IQR 1.8, 4.6) years, 26 (22%) patients developed the primary outcome: 1 death, 11 new or progressive angiographic CAV, 2 percutaneous coronary interventions, 12 allograft dysfunction. Unadjusted Cox analysis showed a significant reduction in event-free survival in patients with PET1 stress MBF < 2.1 (HR: 2.43, 95% CI 1.11-5.29 P = 0.047) and persistent abnormal PET1 to PET2 CVR > 76 (HR: 2.19, 95% CI 0.87-5.51 Christiane Wiefels and Aws Almufleh contributed equally to this work (First co-authors). The authors have also provided an audio summary of the article, which is available to download as ESM, or to listen to via the JNC/ASNC Podcast. Funding Dr. Wiefels is supported by the University of Ottawa Heart Institute Division of Cardiology Kaufman-Chan Endowed Fellowship and by CAPES (Coordenac¸a˜o de Aperfeic¸oamento de Nı´vel Superior) from Brazil. Dr. Beanlands is supported by the University of Ottawa Heart Institute Heart Institute Vered Chair in Cardiology and University of Ottawa Tier 1 chair in Cardiac Research. He was supported as a Career Investigator from the Heart and Stroke Foundation Ontario. Dr. Chih is supported by a Heart and Stroke Foundation (HSF) of Ontario Clinician Scientist award. This work was supported in part by the HSF of Canada (Grant #G-170018310).
Electronic supplementary material The online version of this article (doi:https://doi.org/10.1007/s12350-020-02342-7) contains supplementary material, which is available to authorized users. The authors of this article have provided a PowerPoint file, available for download at SpringerLink, which summarises the contents of the paper and is free for re
Data Loading...
