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Published on: December 11, 2016
Hepatic Tissue Alterations in ST-Elevation Myocardial Infarction: Determinants and Prognostic Implications
Ivan Lechner1, Martin Reindl1, Sebastian von der Emde1
1University Clinic of Internal Medicine III, Cardiology and Angiology (I.L., M.R., S.v.d.E., A.D., F.O., C.T., M.H., T.K., J.F., A.B., B.M., S.J.R.), Medical University of Innsbruck Innsbruck, Austria.
Insights
Hepatic T1 patterns in ST-segment-elevation myocardial infarction (STEMI) patients are linked to myocardial damage and worse outcomes. Persistent hepatic alterations at 4 months post-STEMI indicate a higher risk of major adverse cardiovascular events.
Area of Science:
- Cardiology
- Radiology
- Biomedical Imaging
Background:
- The clinical significance of hepatic tissue changes in ST-segment-elevation myocardial infarction (STEMI) patients, assessed via cardiac magnetic resonance imaging (CMR), remains unclear.
- This study investigates the relationship between hepatic T1 patterns and myocardial damage, as well as clinical outcomes in STEMI patients.
Purpose of the Study:
- To explore the association of hepatic T1 patterns with myocardial damage and clinical outcomes in STEMI patients.
- To determine if hepatic tissue alterations detected by CMR T1 mapping predict adverse cardiovascular events post-STEMI.
Main Methods:
- Analysis of 485 STEMI patients from the MARINA STEMI study, treated with percutaneous coronary intervention.
- Assessment of myocardial function, infarct characteristics, and ventricular function using CMR within the first week post-STEMI.
- Evaluation of native hepatic T1 times and extracellular volume from cardiac T1 maps at baseline and 4-month follow-up.
Main Results:
- Median hepatic T1 times decreased from baseline (559 ms) to 4 months (542 ms) post-STEMI (P<0.001).
- Baseline hepatic T1 times were associated with female sex, hyperlipidemia, infarct size, microvascular obstruction, and right ventricular (RV) infarction.
- Hepatic T1 times at 4 months were linked to female sex, multivessel disease, N-terminal pro-B-type natriuretic peptide, RV infarction, and RV end-systolic volume index.
- Patients without a decrease in hepatic T1 times had a higher incidence of major adverse cardiovascular events (13% vs. 5%; P=0.003).
- Hepatic T1 times at baseline and 4 months, and hepatic extracellular volume at 4 months, were associated with major adverse cardiovascular events.
- After adjustment, only 4-month hepatic T1 times independently predicted adverse outcomes (HR, 2.86; P<0.001).
Conclusions:
- Hepatic tissue alterations, identified by T1 mapping, correlate with patient characteristics and myocardial damage in STEMI.
- These hepatic changes can persist into the chronic phase after STEMI.
- Persistent hepatic T1 alterations are indicative of a worse clinical prognosis and increased risk of major adverse cardiovascular events.
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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