Longitudinal Change and Predictors of Myocardial Flow Reserve by Positron Emission Tomography for the Evaluation of Cardiac Allograft Vasculopathy Following Heart Transplantation
•Myocardial flow reserve (MFR) on positron emission tomography longitudinally declines over time after heart transplantation and is prognostic for adverse post-transplant events.•Cardiometabolic risk factors, allograft rejection and cytomegalovirus infection are associated with reduced MFR and, ther...
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Published in: | Journal of cardiac failure Vol. 30; no. 7; pp. 915 - 925 |
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Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Elsevier Inc
01-07-2024
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Subjects: | |
Online Access: | Get full text |
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Summary: | •Myocardial flow reserve (MFR) on positron emission tomography longitudinally declines over time after heart transplantation and is prognostic for adverse post-transplant events.•Cardiometabolic risk factors, allograft rejection and cytomegalovirus infection are associated with reduced MFR and, therefore, the development and progression of cardiac allograft vasculopathy.•The use of moderate- to high-intensity statin therapy is associated with a higher MFR, and escalation of statin intensity may reduce the incidence of cardiac allograft vasculopathy.
Positron emission tomography (PET) myocardial flow reserve (MFR) is a noninvasive method of detecting cardiac allograft vasculopathy in recipients of heart transplants (HTs). There are limited data on longitudinal change and predictors of MFR following HT.
We conducted a retrospective analysis of HT recipients undergoing PET myocardial perfusion imaging at an academic center. Multivariable linear and Cox regression models were constructed to identify longitudinal trends, predictors and the prognostic value of MFR after HT.
Of HT recipients, 183 underwent 658 PET studies. The average MFR was 2.34 ± 0.70. MFR initially increased during the first 3 years following HT (+ 0.12 per year; P = 0.01) before beginning to decline at an annual rate of -0.06 per year (P < 0.001). MFR declines preceding acute rejection and improves after treatment. Treatment with mammalian target of rapamycin (mTOR) inhibitors (37.2%) slowed the rate of annual MFR decline (P = 0.03). Higher-intensity statin therapy was associated with improved MFR. Longer time post-transplant (P < 0.001), hypertension (P < 0.001), chronic kidney disease (P < 0.001), diabetes mellitus (P = 0.038), antibody-mediated rejection (P = 0.040), and cytomegalovirus infection (P = 0.034) were associated with reduced MFR. Reduced MFR (HR: 7.6, 95% CI: 4.4–13.4; P < 0.001) and PET-defined ischemia (HR: 2.3, 95% CI: 1.4–3.9; P < 0.001) were associated with a higher risk of the composite outcome of mortality, retransplantation, heart failure hospitalization, acute coronary syndrome, or revascularization.
MFR declines after the third post-transplant year and is prognostic for cardiovascular events. Cardiometabolic risk-factor modification and treatment with higher-intensity statin therapy and mechanistic target of rapamycin inhibitors are associated with a higher MFR.
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1071-9164 1532-8414 1532-8414 |
DOI: | 10.1016/j.cardfail.2023.09.013 |