The present study results demonstrate the capability of STE and PSSI to identify viable myocardium, predict LVEF improvement, and assess LV remodeling in STEMI patients who underwent late PCI. Previous studies have shown that PSS obtained through STE provides prognostic information about the risk of major adverse cardiovascular events (MACE), heart failure, and death in the general population (
12,
13). Some studies also indicate that PSS provides independent diagnostic information about significant CAD in patients with stable ischemic heart disease and can predict subsequent cardiovascular events (
14). Lu et al. demonstrated that the prognostic value of PSS in these patients may be higher than GLS (
15). Studies on diabetic patients have shown that PSS predicts subsequent cardiac events and provides prognostic information in these patients (
16,
17).
While previous studies have indicated that GLS and PSS are strong indices for predicting the development of heart failure in acute coronary syndrome patients who underwent PCI (
18,
19), the distinguishing aspect of our study is the assessment of PSS as a factor to predict LVEF improvement, LV systolic function recovery, and identify viable myocardium. Our study showed that LV segments with higher PSS and PSSI had better recovery after PCI, and patients with improved LVEF and no LV remodeling had higher total PSSI. In fact, it is possible that maximum shortening of ischemic segments with severely reduced wall motion does not occur during systole but may happen after aortic valve closure (PSS). Therefore, the higher this PSS is, the more likely the segment is viable.
Evaluating myocardial viability is one of the most important clinical indications for STE. Improvement of GLS during dobutamine stress echocardiography (DSE) is indicative of myocardial viability, which has diagnostic and prognostic value (
20). In 2009, Fujimoto et al. showed that in patients with a history of old MI, PSS changes during DSE can help identify hibernating myocardium and distinguish it from damaged myocardium (
21). Another study in 2011 on STEMI patients who underwent primary PCI showed that GLS obtained through STE is a predictor of LV remodeling, and there is also a moderate correlation between the level of longitudinal peak strain and irreversible dysfunctional segments (
22).
Our study demonstrated that PSS is a significant factor in ischemic myocardium in STEMI patients and, when associated with reduced wall motion, indicates potentially viable myocardium. This finding is consistent with the results of previous studies (
5,
23). In the present study, we aimed to evaluate the presence of potentially viable myocardium in STEMI patients who do not undergo PPCI by quantifying the contractile function of the ischemic myocardium and PSS through the PSSI to identify patients who may benefit from late PCI.
In a similar study, Tao Cong et al. in 2014 showed that GLS measured by STE is a strong predictor of LV remodeling in STEMI patients who underwent late PCI, predicting LV remodeling at a cut point of -10.85 with high sensitivity and specificity (
3). The results of our study align with these findings in terms of the indices assessed by STE. Additionally, the determinative role of PSSI in predicting LVEF improvement and the incidence of LV remodeling has been highlighted. Our study indicates that pre-PCI PSSI can predict LV remodeling and LVEF improvement after late PCI. The ROC curves showed that pre-PCI PSSI was higher in patients with improved LVEF and no LV remodeling after late PCI, with the best cutoff value for predicting LVEF improvement being 19%, offering the highest diagnostic accuracy.
5.1. Conclusions
The present study demonstrated that in patients with STEMI who undergo late PCI (after 24 hours), STE indicators, including the PSSI, can predict LV remodeling, LVEF improvement, and recovery of LV systolic function, thereby identifying viable myocardium.
5.2. Study Limitations
The first limitation of this study was the relatively small population and the restriction of STEMI cases to anterior circulation. The second limitation was the absence of cardiac magnetic resonance imaging (CMR) to evaluate the longitudinal strain of the myocardium and compare it to STE data. The third limitation was the lack of follow-up coronary angiography to assess the patency of PCI sites during the study.