CMR-derived myocardial perfusion reserve was significantly associated with multi-beat Ees/Ea (β=0.11; 95% CI 0.00-0.21; p=0.047) and discriminated RV-PA uncoupling with an AUC of 0.80.
Observational (n=16)
No
Does CMR-derived myocardial perfusion reserve correlate with invasive right ventricular-pulmonary arterial coupling in patients with suspected pulmonary hypertension?
CMR-derived myocardial perfusion reserve is significantly associated with invasive RV-PA coupling measures and can effectively discriminate RV-PA uncoupling in patients with suspected pulmonary hypertension.
Effect estimate: β 0.11 (95% CI 0.00-0.21)
p-value: p=0.047
Abstract Rationale Impaired myocardial perfusion may contribute to right ventricular (RV) maladaptation in pulmonary hypertension (PH). Myocardial perfusion reserve (MPR) is an emerging cardiac magnetic resonance (CMR)-based index that compares myocardial blood flow between stress and rest. In this study, we investigated whether MPR in the RV reflects RV-pulmonary arterial (PA) coupling and may serve as a noninvasive marker of RV adaptation in PH. Methods Sixteen patients evaluated for suspected PH between 2008-2023 at Johns Hopkins Hospital underwent same-day right heart catheterization with baseline hemodynamics and multi-beat RV pressure-volume (PV) loop analysis followed by CMR imaging. MPR was calculated as the ratio of RV myocardial perfusion during adenosine stress to perfusion at rest using gadolinium-enhanced first-pass imaging. Gold standard RV-PA coupling measurements were taken by calculating the ratio of end-systolic to arterial elastances (Ees/Ea) using multi-beat PV loops. The association between log-transformed MPR and multi-beat Ees/Ea was assessed with age- and sex-adjusted linear regression. Receiver operating characteristic (ROC) analysis evaluated MPR’s ability to discriminate RV-PA uncoupling, defined as Ees/Ea 0.78 as previously determined (Rosen et al, ERJ in press). Results Participants had a median age of 59 42-64; 75% were female, 69% had PAH, and 60% had systemic sclerosis. Median MPR was 1.5 1.2-1.9 and median Ees/Ea was 1.0 0.7-1.9. Thirty-one percent of patients met criteria for RV-PA uncoupling (Ees/Ea 0.78). A 10% increase in MPR was associated with a 0.11-unit increase in Ees/Ea (β = 0.11; 95% CI 0.00-0.21; p = 0.047). MPR effectively discriminated RV-PA uncoupling with an AUC = 0.80 (Figure 1). The Youden index of 1.17 corresponded to a sensitivity of 0.91, specificity 0.6, positive likelihood ratio of 2.3, and negative likelihood ratio of 0.15. Conclusions To our knowledge, this is the first demonstration that CMR-derived MPR is significantly associated with multi-beat Ees/Ea. MPR exhibits strong discriminatory performance for identifying RV-PA uncoupling (Ees/Ea 0.78), which is a strong predictor of mortality in PH. These findings suggest MPR may serve as a promising surrogate marker for RV-PA coupling, facilitating noninvasive assessment of RV adaptation. Further studies are warranted to validate these results and explore MPR’s potential in predicting outcomes. This abstract is funded by: None
Rosen et al. (Fri,) conducted a observational in Pulmonary hypertension (n=16). Myocardial perfusion reserve (MPR) via CMR vs. Multi-beat Ees/Ea via right heart catheterization was evaluated on Association between log-transformed MPR and multi-beat Ees/Ea (β 0.11, 95% CI 0.00-0.21, p=0.047). CMR-derived myocardial perfusion reserve was significantly associated with multi-beat Ees/Ea (β=0.11; 95% CI 0.00-0.21; p=0.047) and discriminated RV-PA uncoupling with an AUC of 0.80.
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