Acute Response in the Noninfarcted Myocardium Predicts Long-Term Major Adverse Cardiac Events After STEMI
Mayooran Shanmuganathan1, Ambra Masi2, Matthew K Burrage3
1Acute Vascular Imaging Centre (AVIC), University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom; Oxford Centre for Clinical Magnetic Resonance Research (OCMR), John Radcliffe Hospital, National Institute for Health Research (NIHR) Oxford Biomedical Research Centre, Oxford BHF Centre of Research Excellence, University of Oxford, Oxford, United Kingdom; Oxford University Hospitals NHS Trust, John Radcliffe Hospital, Oxford, United Kingdom.
Insights
Acute ST-segment elevation myocardial infarction (STEMI) affects both the infarcted and noninfarcted myocardium. Changes in these areas predict long-term major adverse cardiac events (MACE), offering new risk stratification strategies for STEMI patients.
Area of Science:
- Cardiology
- Biomedical Imaging
- Myocardial Infarction Research
Background:
- Acute ST-segment elevation myocardial infarction (STEMI) impacts myocardium beyond the infarct zone.
- Pathophysiology and prognostic implications of noninfarcted myocardium changes post-STEMI are not fully understood.
Purpose of the Study:
- To assess the long-term prognostic value of acute changes in both infarcted and noninfarcted myocardium after STEMI.
Main Methods:
- Cardiac magnetic resonance (CMR) and blood biomarkers were used in STEMI patients post-primary percutaneous coronary intervention.
- Evaluations were performed at 2 days and 6 months, with long-term follow-up for major adverse cardiac events (MACE).
- CMR included cine, T2-weighted, T2 2 , T1-mapping, and late gadolinium enhancement (LGE) imaging.
Main Results:
- High T1 in noninfarcted myocardium correlated with lower LVEF, higher NT-pro-BNP, and increased MACE risk.
- Lower T1 in infarcted myocardium was associated with increased MACE.
- Both noninfarct and infarct T1 were independent predictors of MACE, improving risk prediction beyond traditional markers.
Conclusions:
- Acute myocardial responses in both infarcted and noninfarcted areas are independent predictors of long-term MACE.
- These findings offer novel avenues for treatment and risk stratification in STEMI patients.
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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