Key result
Hepatic T1 times 4 months post-STEMI are linked to ~186% greater MACE risk.
Why the study?
The presence and clinical significance of hepatic tissue alterations assessed by CMR in patients with STEMI were unclear.
Hepatic tissue alterations assessed by CMR T1 mapping persist into the chronic phase after STEMI and are independently associated with a higher risk of major adverse cardiovascular events.
Hepatic T1 mapping may aid post-STEMI risk stratification; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: The presence and clinical significance of hepatic tissue alterations as assessed by cardiac magnetic resonance imaging in patients with ST-segment–elevation myocardial infarction (STEMI), are unclear. This study aimed to investigate associations of hepatic T1 patterns with myocardial tissue damage and clinical outcomes in patients suffering from STEMI. METHODS: We analyzed 485 patients with STEMI treated with percutaneous coronary intervention who were enrolled in the prospective MARINA STEMI study (Magnetic Resonance Imaging In Acute ST-Elevation Myocardial Infarction). Myocardial function and left and right ventricular (RV) infarct characteristics were assessed by cardiac magnetic resonance within the first week after STEMI. Native hepatic T1 times and extracellular volume were evaluated from standard cardiac T1 maps at baseline and 4 months thereafter. RESULTS: Median hepatic T1 times were 559 ms (interquartile range, 514–605) at baseline and decreased to 542 ms (interquartile range, 507–577) at 4 months ( P <0.001). Hepatic T1 times at baseline were independently associated with female sex (β 0.116; P =0.008), hyperlipidemia (β −0.116; P =0.008), and myocardial tissue damage (infarct size: β 0.178; P <0.001; microvascular obstruction: β 0.193; P <0.001; RV infarction: β 0.161; P <0.001). Determinants of hepatic T1 times at 4 months were female sex (β 0.123; P =0.002), multivessel disease (β 0.121; P =0.002), N-terminal pro–B-type natriuretic peptide (β 0.101; P =0.010), RV infarction (β 0.501; P <0.001), and RV end-systolic volume index (β 0.087; P =0.031). Patients without a decrease exhibited a higher frequency of major adverse cardiovascular events (13% versus 5%; P =0.003). Hepatic T1 times at baseline (hazard ratio, 1.87 [95% CI, 1.40–2.50]; P <0.001), 4 months (hazard ratio, 2.69 [95% CI, 2.15–3.36]; P <0.001), and hepatic extracellular volume at 4 months (hazard ratio, 1.59 [95% CI, 1.33–1.90]; P <0.001) were associated with major adverse cardiovascular events. After adjustment for univariable associates, only hepatic T1 times at 4 months were independently associated with adverse outcomes (hazard ratio, 2.86 [95% CI, 1.99–4.12]; P <0.001). CONCLUSIONS: Hepatic tissue alterations determined by T1 mapping were associated with female sex, hyperlipidemia, multivessel disease, N-terminal pro–B-type natriuretic peptide, and left and RV myocardial tissue damage. These alterations can persist into the chronic phase after STEMI and indicate a worse clinical outcome. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04113356.
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Lechner et al. (2024) studied this question. Hepatic T1 times at 4 months post-STEMI were independently associated with major adverse cardiovascular events (HR 2.86, 95% CI 1.99-4.12, P<0.001).
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