Increased hepatic T1 values are correlated with right ventricular involvement and congestion after ST-segment elevation myocardial infarction

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background ST-segment elevation myocardial infarction (STEMI) may have a multiorgan impact. Due to its proximity to the heart, a large portion of the liver is imaged during T1 mapping in Cardiovascular Magnetic Resonance (CMR) and recently higher T1 have been found associated with signs of right heart failure (RHF) in patients with non-ischemic cardiomyopathy, but no data are available in STEMI population. Purpose To evaluate the role of early hepatic native T1 in detecting the presence of right ventricle (RV) involvement after STEMI. Methods 133 patients with STEMI who underwent early CMR after primary angioplasty (PPCI) were enrolled. Patients with known hepatic disease were excluded from the study. Hepatic T1 was evaluated considering the mean value obtained from three regions of interest, free from fat and blood vessels. RV involvement was diagnosed in the presence of RV ejection fraction (EF) reduction according to current guidelines, RV wall motion abnormalities and the presence of necrosis in late gadolinium enhancement (LGE) sequences. Results Overall, the mean age was 59.72 ± 13.32 years and 28.2% were female. Fifty-two (39.1%) patients had an anterior myocardial infarction. The median time from PPCI to CMR was 3 [IQR 2.00–5.00] days. T1 mapping was available in all patients and mean hepatic T1 value of the population was 622.91 ± 100.14 ms. According to the Youden index the optimal hepatic T1 cut-off value to predict RV involvement was 605 ms. A total of 72 (54.1%) patients presented high hepatic T1 values (>605 ms). No significant correlations were found between high hepatic T1 values and left ventricle EF, infarct size, area at risk and the presence of microvascular obstruction. High hepatic T1 values were correlated with larger RV end-diastolic volume index (RVEDVi) (median 83.03 ml/m2 vs 53.16 ml/m2, p<0.001), lower RVEF (median 39.4% vs 57.62%, p<0.001) and presence of LGE in RV (26.5% vs 9.8%, p = 0.015). White blood cells (WBC), C-reactive protein and hs-Tn T peak values did not differ in the two study groups but NT-proBNP values were significantly higher in patients with high hepatic T1 (median 3531.22 vs 111.25 pg/mL, p<0.001). A strong positive correlation was found between hepatic T1 and NTproBNP (r = 0.754, p<0.001, Figure 1). At the univariable analysis, RV EF (OR 0.848, 95%CI 0.806–0.893, p<0.001), RVEDVi (OR 1.026, 95%CI 1.013–1.038, p<0.001) and the presence of RV infarct at the CMR evaluation (OR 3.286, 95%CI 1.218–8.865, p = 0.019) were found predictors of high hepatic T1 values. On multivariable logistic regression, RVEDVi (OR 1.022, 95%CI 1.006–1.038, p = 0.008) and RV-EF (OR 0.854, 95%CI 0.809–0.902, p<0.001) resulted as independent predictors of increased hepatic T1 values. Conclusions RV involvement after STEMI may lead to hepatic congestion and high hepatic T1 values are associated with early RV dysfunction parameters (RVEDVi, RV-EF and LGE) at CMR and higher levels of NT-proBNP.