Segmental circumferential strain values in reperfused infarcted myocardial segments are mainly influenced by the transmurality of infarction, not by MVO

Abstract

Purpose: Microvascular obstruction (MVO) after primary percutaneous coronary intervention (PPCI) for acute myocardial infarction is a known parameter for impaired functional recovery. This study explored the relationship between MVO, regional infarct transmurality and detailed segmental systolic and diastolic function using CMR strain analysis. Methods: CMR was performed 3-7 days after PPCI and at 4 months follow-up in 33 patients, using cine imaging, single breath-hold tagging (retrospective CSPAMM sequence, TR 42ms) and late gadolinium enhancement (LGE). Peak circumferential strain (PCS), peak systolic and diastolic circumferential strain rate (PSCSR/PDCSR), and absolute systolic wall thickening (SWT) were calculated in a 16-segment model. Results: Mean LVEF was 47±10% at baseline and 54±10% at follow up. Infarct size (% LV mass) was 18±10% at baseline and 13±9% at follow up. 273 segments were non-infarcted and 255 were infarcted; infarcted segments were stratified into four groups according to the amount of enhancement: 75% (n=48) enhancement. Infarcted segments had impaired systolic function (2±2mm vs. 4±2mm, p<0.001), decreased PCS (-9±5 vs. -15±4%, p<0.001), decreased PSCSR (-75±29 vs. -97±26%/ms, p<0.001) and decreased PDCSR (78±49 vs. 118±41%/ms, p<0.001) compared to non-infarcted segments. In infarcted segments, a significant correlation existed between infarct transmurality and baseline PCS (r=0.61, p<0.001), PSCSR (r=0.40, p<0.001) and PDCSR (r=-0.49, p<0.001). In the 75-100% group, no difference in transmurality was found between segments with and without MVO (88±7 vs. 91±5%, p=0.204). However, analysis of covariance in this group demonstrated worse PSCSR in segments with MVO (effect 24.0%/ms [95% CI: 8 to 40%/ms], p=0.003). MVO did not further influence PCS (effect 0.7% [95% CI: -1 to 2%], p=0.37) or PDCSR (effect -8.3%/ms [95% CI: -31 to 15%/ms], p=0.47). At follow-up, correlation between transmurality and PCS (r=0.61, p<0.001), PSCSR (r=0.40, p<0.001) and PDCSR (r=-0.50, p<0.001) persisted. Between the different transmurality groups, no significant difference was found for strain recovery. In the 75-100% group, segments with MVO did not have a different strain recovery compared to segments without MVO (p-values 0.27-0.95). Conclusion: Circumferential strain values in infarcted myocardial segments are mainly influenced by the transmurality of infarction. The presence of MVO at baseline does not have an additional effect on the recovery of peak strain or peak strain rates.