Correlation between regional post systolic index and culprit artery in NSTEMI with preserved left ventricular function

Background Patients with non-ST-segment elevation myocardial infarction (NSTEMI) typically present critical arterial stenosis, defined as the stenosis≥70% of the culprit artery. In addition, myocardial shortening that occurs after end-systole, called post-systolic shortening index (PSI), has been acknowledged as a sign of myocardial ischemia, which is easily measurable by the two-dimensional speckle-tracking echocardiography (2D-STE). Aim This study was to investigate the correlation between regional average PSI and coronary angiography (CAG)-identified culprit artery among patients with NSTEMI and preserved left ventricular ejection fraction (LVEF). Methods Applying a descriptive-correlational research design, the present study was conducted on 54 patients with NSTEMI and LVEF≥50%, admitted to the emergency department of our hospital between 2022 and 2023. All patients underwent a transthoracic 2D-STE within the first day of admission. An 16-left ventricular (LV) segment model of myocardial perfusion territories was then utilized, and regional strain was further explained according to the perfusion territory of each major epicardial artery. Besides, CAG was performed for all patients during 24–48 h of admission. The patients with an identifiable culprit artery on CAG were subsequently divided into two groups based on the location of the culprit artery: Group I ( n = 28) with the culprit artery within the left anterior descending (LAD) territory, and Group II ( n = 26) with the culprit artery in the right coronary (RCA) or left circumflex (LCX) artery. Results The PSI LAD was found to be higher in Group I than Group II (3.00 [0.33–9.92] vs. 0.63 [0.06–5.50], respectively, p = 0.019). The logistic regression analysis (LRA) of different variables additionally revealed that only the average PSI LAD (odds ratio [OR] 1.115, 95% confidence interval [CI]: 1.005–1.239, p = 0.04) was independently correlated with the CAG-identified culprit artery in the LAD. Moreover, the receiver operating characteristic (ROC) curve analysis demonstrated that the area under the curve (AUC) for the average PSI LAD to predict the CAG-identified LAD culprit artery was 0.679 ( p = 0.016; 95% CI [0.540–0.818]). Conclusion Regional average PSILAD was independently associated with LAD culprit lesions identified by coronary angiography in a selected population of NSTEMI patients with preserved LVEF. Given the modest diagnostic performance and limited sample size, these findings should be considered exploratory and require validation in larger and more representative NSTEMI cohorts.