High T1 (>1250 ms) in the noninfarcted myocardium post-STEMI was associated with a 2.5-fold increased risk of long-term MACE compared to normal T1 (HR 2.53; 95% CI 1.03-6.22; P=0.042).
Cohort (n=219)
Does acute CMR T1 mapping of infarcted and noninfarcted myocardium predict long-term MACE in patients with STEMI undergoing primary PCI?
Acute CMR T1 mapping of both infarcted and noninfarcted myocardium provides independent and incremental prognostic value for long-term MACE after STEMI.
Hazard Ratio: 2.53 (95% CI 1.03–6.22)
p-value: p=0.042
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.
Shanmuganathan et al. (Wed,) conducted a cohort in Acute ST-segment elevation myocardial infarction (STEMI) (n=219). High T1 (>1250 ms) in the noninfarcted myocardium vs. Normal T1 in the noninfarcted myocardium was evaluated on MACE (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 post-STEMI was associated with a 2.5-fold increased risk of long-term MACE compared to normal T1 (HR 2.53; 95% CI 1.03-6.22; P=0.042).