Prognostic significance of infarct core pathology revealed by quantitative non-contrast in comparison with contrast cardiac magnetic resonance imaging in reperfused ST-elevation myocardial infarction survivors

Abstract

Aims: To assess the prognostic significance of infarct core tissue characteristics using cardiac magnetic resonance (CMR) imaging in survivors of acute ST-elevation myocardial infarction (STEMI).

Methods and results: We performed an observational prospective single centre cohort study in 300 reperfused STEMI patients (mean ± SD age 59 ± 12 years, 74% male) who underwent CMR 2 days and 6 months post-myocardial infarction (n = 267). Native T1 was measured in myocardial regions of interest (n = 288). Adverse remodelling was defined as an increase in left ventricular (LV) end-diastolic volume ≥20% at 6 months. All-cause death or first heart failure hospitalization was a pre-specified outcome that was assessed during follow-up (median duration 845 days). One hundred and sixty (56%) patients had a hypo-intense infarct core disclosed by native T1. In multivariable regression, infarct core native T1 was inversely associated with adverse remodelling [odds ratio (95% confidence interval (CI)] per 10 ms reduction in native T1: 0.91 (0.82, 0.00); P = 0.061). Thirty (10.4%) of 288 patients died or experienced a heart failure event and 13 of these events occurred post-discharge. Native T1 values (ms) within the hypo-intense infarct core (n = 160 STEMI patients) were inversely associated with the risk of all-cause death or first hospitalization for heart failure post-discharge (for a 10 ms increase in native T1: hazard ratio 0.730, 95% CI 0.617, 0.863; P < 0.001) including after adjustment for left ventricular ejection fraction, infarct core T2 and myocardial haemorrhage. The prognostic results for microvascular obstruction were similar.

Conclusion: Infarct core native T1 represents a novel non-contrast CMR biomarker with potential for infarct characterization and prognostication in STEMI survivors. Confirmatory studies are warranted. CLINICALTRIALS.

Gov identifier: NCT02072850.

Keywords: Adverse remodelling; Cardiac magnetic resonance; Percutaneous coronary intervention; ST-elevation myocardial infarction.

Figure 1

Three patients with acute ST-elevation myocardial infarction treated by primary PCI and with the same anti-thrombotic therapies, including aspirin, clopidogrel, heparin, and intravenous tirofiban. Each patient had normal thrombolysis in myocardial infarction Grade 3 flow at the end of PCI. Cardiac magnetic resonance imaging was performed for each patient 2 days later. (A) Patient with no T1 hypo-intense infarct core and no microvascular obstruction. Native T1 within the injury zone (middle) measured 1211 ms. Acute infarct size revealed by late gadolinium enhancement (right) was 22.2%. The left ventricular ejection fraction and left ventricular end-diastolic volume were 55.2% and 143.1 mL, respectively. Analysis of the repeat magnetic resonance imaging scan after 6 months follow-up indicated that the final infarct size was 15.6% of left ventricular mass and the left ventricular end-diastolic volume had reduced to 103.0 mL. This patient had an uncomplicated clinical course. (B) Patient with both T1 hypo-intense infarct core and microvascular obstruction. T1 mapping (middle) revealed a hypo-intense region within the infarct core, corresponding to the area of microvascular obstruction on contrast-enhanced magnetic resonance imaging (right). Native T1 within the infarct core measured 1036 ms, which was substantially lower than the T1 value measured at the periphery of the infarct zone (1193 ms). Acute infarct size revealed by late gadolinium enhancement (right) was 33.0%. Microvascular obstruction depicted as the central dark zone within the infarct territory was 3.6% of left ventricular mass. The left ventricular ejection fraction and end-diastolic volume were 45.8% and 199.3 mL, respectively. The final infarct size at 6 months was 22.6% of left ventricular mass and the left ventricular end-diastolic volume had increased to 221.8 mL. This patient was re-hospitalized for new onset heart failure during follow-up.

Figure 2

Flow diagram of the cohort study.

Figure 3

Kaplan–Meier survival curves for 160 ST-elevation myocardial infarction patients grouped according to the native T1 value in the infarct core with patients grouped by thirds (lowest T1 tertile vs. tertiles 2 and 3) and all-cause death or first heart failure hospitalization (n = 13) after discharge from hospital to the end of follow-up [censor time 839 (598–1099) days]. Infarct core native T1 values in the lowest tertile were associated with all-cause death or heart failure hospitalization.