Key result
High noninfarcted myocardial T1 linked to ~2.5-fold higher long-term MACE risk post-STEMI.
Why the study?
Pathophysiologic changes in the noninfarcted myocardium after acute STEMI and their long-term prognostic implications remain unclear.
Does high T1 in the noninfarcted myocardium predict major adverse cardiac events in patients post-STEMI?
Cohort (n=219)
No
Does high T1 in the noninfarcted myocardium predict major adverse cardiac events in patients post-STEMI?
Acute myocardial injury in the noninfarcted territory measured by CMR T1-mapping provides independent and incremental prognostic value beyond traditional markers for long-term MACE after STEMI.
High noninfarct T1 may refine post-STEMI risk assessment; leaves open whether T1-mapping improves stratification or outcomes.
BACKGROUND: Acute ST-segment elevation myocardial infarction (STEMI) has effects on the myocardium beyond the immediate infarcted territory. However, pathophysiologic changes in the noninfarcted myocardium and their prognostic implications remain unclear. OBJECTIVES: The purpose of this study was to evaluate the long-term prognostic value of acute changes in both infarcted and noninfarcted myocardium post-STEMI. METHODS: Patients with acute STEMI undergoing primary percutaneous coronary intervention underwent evaluation with blood biomarkers and cardiac magnetic resonance (CMR) at 2 days and 6 months, with long-term follow-up for major adverse cardiac events (MACE). A comprehensive CMR protocol included cine, T2-weighted, T2∗, T1-mapping, and late gadolinium enhancement (LGE) imaging. Areas without LGE were defined as noninfarcted myocardium. MACE was a composite of cardiac death, sustained ventricular arrhythmia, and new-onset heart failure. RESULTS: Twenty-two of 219 patients (10%) experienced an MACE at a median of 4 years (IQR: 2.5-6.0 years); 152 patients returned for the 6-month visit. High T1 (>1250 ms) in the noninfarcted myocardium was associated with lower left ventricular ejection fraction (LVEF) (51% ± 8% vs 55% ± 9%; P = 0.002) and higher NT-pro-BNP levels (290 pg/L [IQR: 103-523 pg/L] vs 170 pg/L [IQR: 61-312 pg/L]; P = 0.008) at 6 months and a 2.5-fold (IQR: 1.03-6.20) increased risk of MACE (2.53 [IQR: 1.03-6.22]), compared with patients with normal T1 in the noninfarcted myocardium (P = 0.042). A lower T1 (<1,300 ms) in the infarcted myocardium was associated with increased MACE (3.11 [IQR: 1.19-8.13]; P = 0.020). Both noninfarct and infarct T1 were independent predictors of MACE (both P = 0.001) and significantly improved risk prediction beyond LVEF, infarct size, and microvascular obstruction (C-statistic: 0.67 ± 0.07 vs 0.76 ± 0.06, net-reclassification index: 40% [IQR: 12%-64%]; P = 0.007). CONCLUSIONS: The acute responses post-STEMI in both infarcted and noninfarcted myocardium are independent incremental predictors of long-term MACE. These insights may provide new opportunities for treatment and risk stratification in STEMI.
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Shanmuganathan et al. (2022) conducted a cohort in Acute STEMI (n=219). High T1 (>1250 ms) in noninfarcted myocardium vs. Normal T1 (≤1250 ms) in noninfarcted myocardium was evaluated on Major adverse cardiac events (composite of cardiac death, sustained ventricular arrhythmia, and new-onset heart failure) (HR 2.53, 95% CI 1.03-6.22, p=0.042). High T1 (>1250 ms) in the noninfarcted myocardium was associated with a 2.53-fold increased risk of long-term major adverse cardiac events post-STEMI.
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