Key result
Myocardial work index was the strongest determinant of rejection-related myocardial damage in heart transplant recipients (AUC 0.812, 95% CI 0.69-0.94, P<0.0001) with 77% specificity.
Why the study?
RV dysfunction is an important cause of graft failure after HTx, prompting investigation into the relative merits of echocardiographic tools and CMR with T1 mapping for assessing RV functional adaptation and remodelling.
Do echocardiographic myocardial work index and CMR T1 mapping accurately detect right ventricular remodelling and rejection-related myocardial damage in heart transplant recipients compared to endomyocardial biopsy?
Cross-Sectional (n=61)
Do echocardiographic myocardial work index and CMR T1 mapping accurately detect right ventricular remodelling and rejection-related myocardial damage in heart transplant recipients compared to endomyocardial biopsy?
Effect estimate: AUC 0.812 (95% CI 0.69-0.94)
p-value: p=< 0.0001
Myocardial work index is a specific and strong non-invasive marker for detecting rejection-related right ventricular myocardial damage in heart transplant recipients, capable of distinguishing functional adaptation from subclinical structural damage.
MWI may help identify subclinical RV damage post-HTx; leaves open whether it refines surveillance or biopsy timing.
AIMS: Right ventricular (RV) dysfunction is an important cause of graft failure after heart transplantation (HTx). We sought to investigate relative merits of echocardiographic tools and cardiac magnetic resonance (CMR) with T1 mapping for the assessment of functional adaptation and remodelling of the RV in HTx recipients. METHODS AND RESULTS: Sixty-one complete data set of echocardiography, CMR, right heart catheterization, and biopsy were obtained. Myocardial work index (MWI) was quantified by integrating longitudinal strain (LS) with invasively measured pulmonary artery pressure. CMR derived RV volumes, T1 time, and extracellular volume (ECV) were quantified. Endomyocardial biopsy findings were used as the reference standard for myocardial microstructural changes. In HTx recipients who never had a previous allograft rejection, longitudinal function parameters were lower than healthy organ donors, while ejection fraction (EF) (52.0 ± 8.7%) and MWI (403.2 ± 77.2 mmHg%) were preserved. Rejection was characterized by significantly reduced LS, MWI, longer T1 time, and increased ECV that improved after recovery, whereas RV volumes and EF did not change MWI was the strongest determinant of rejection related myocardial damage (area under curve: 0.812, P < 0.0001, 95% CI: 0.69-0.94) with good specificity (77%), albeit modest sensitivity. In contrast, T1 time and ECV were sensitive (84%, both) but not specific to detect subclinical RV damage. CONCLUSION: Subclinical adaptive RV remodelling is characterized by preserved RV EF despite longitudinal function abnormalities, except for MWI. While ultrastructural damage is reflected by MWI, ECV, and T1 time, only MWI has the capability to discriminate functional adaptation from transition to subclinical structural damage.
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Sade et al. (2022) conducted a cross-sectional in Heart transplant recipients (n=61). Myocardial work index (MWI) vs. Endomyocardial biopsy (reference standard) was evaluated on Rejection related myocardial damage (AUC 0.812, 95% CI 0.69-0.94, p=< 0.0001). Myocardial work index was the strongest determinant of rejection-related myocardial damage in heart transplant recipients (AUC 0.812, 95% CI 0.69-0.94, P<0.0001) with 77% specificity.
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