Non-infarcted myocardium inflammation predicts outcomes after myocardial infarction
Authors: Pavon A , Bergamaschi L , Maurizi N , Landi A , Pizzi C , Valgimigli M , Leo L A , Iglesias J F , Eeckhout E , Schwitter J , Masci P G 
Published: June 2023

Funding Acknowledgements

Type of funding sources: None.

Background

ST segment elevated myocardial infarction (STEMI) is associated with a systemic inflammatory response. In animal model of STEMI, a sustained inflammatory response has also been described in the non-infarcted myocardium (NIM) with potential detrimental consequences for the left ventricular (LV) remodelling.

Purpose

to characterize inflammation of the NIM in relation with infarct size (IS) and other inflammatory markers and its prognostic role after STEMI.

Methods

171 consecutive patients with STEMI who underwent CMR after primary angioplasty were analysed in terms of standard infarct characteristics. Inflammation of the NIM was assessed based on T2 mapping. The primary endpoint was major adverse cardiac events (MACE), defined as deaths, myocardial infarction (MI), unplanned non-infarct-related artery revascularization or re-hospitalization for heart failure at follow-up.

Results

NIM T2 values were directly correlated with IS (r=0.610; p&lt;0.001), area at risk (r = 0.503, p &lt;0.001) and inversely correlated with LVEF (−0.397, p &lt;0.001). T2 values of NIM followed a bimodal distribution with a mean and median values of 45 ms. A total of 78 patients (46%) presented high, defined as above the median, T2 values. Patients with high, compared with non-high NIM T2 values, had lower LVEF (46.04±12.29% vs 54.63±10.99%, p &lt; 0.001), larger IS (median value: 19.9 vs 9.0 gr p value &lt; 0.001), greater AAR (median value: 25.00 vs 18.61 gr, p-value &lt; 0.001), higher T2 values in the infarcted area (64.31±7.18 vs 61.53±5.44 ms, p 0.028), and more frequent MVO (60.3% vs 32.3%, p &lt; 0.001). At logistic multivariable analyses, IS (OR 1.116, 95%CI 1.080 – 1.258, p &lt; 0.001) and T2 values in the infarcted area (OR 1.102, 95%CI 1.007 – 1.206, p = 0.035), were the only independent predictors of high NIM T2 values. At median follow-up of 30 [27–34] months, patients with high (&gt;45 ms) T2 values in the non-infarcted area incurred greater MACE risk (21.5% vs 7.7% for T2 values &lt;45 ms, p &lt;0.001). Multivariable Cox regression analysis showed that elevated NIM T2 values (HR 2.768, 95%CI 1.262 – 6.073, p = 0.011), LVEF&lt;50% % (HR 2.182, 95%CI 1.058–4.497, p = 0.035) and larger IS (HR 2.830, 95%CI 1.303–6.149, p = 0.009) were independently associated with MACE occurrence (HR 2.126, 95%CI 1.023 – 4.417, p = 0.043) and myocardial re-infarction (HR 10.928, 95%CI 1.441 – 83.686, p = 0.021) after correction for the main CMR parameters.

Conclusions

High NIM T2 values after STEMI are independently associated with worse outcomes, mainly owing to higher MI risk. Importantly, the prognostic information of NIM T2 values was incremental in addition to established CMR outcome markers, including IS. Additional studies are needed to validate weather therapeutic interventions that influence remote zone native T2 improve event-free survival after revascularized STEMI or not.