LVEF is one of the most general indicators of LVSD and is widely available in clinical settings. Evaluation of LVEF after STEMI treated with PPCI is well established as an important predictor of clinical outcome[9]. By using the Kaplan‒Meier method, we found significant differences in the survival rate between the rLVEF group and pLVEF group. Cox proportional hazard regression analysis demonstrated that LVSD was an independent predictor of survival. A lower baseline LVEF and larger infarct size have been associated with failure of LV recovery[10]. Timely identification of subjects at risk for HF development using a multimodality approach and early initiation of guideline-directed HF therapy in these patients can decrease the HF burden[11]. In this study, we found that age, HR at admission, number of STELs, peak CK, and STW time may be used to identify the high risk of HF in a timely manner and initiate early standard therapy for patients with anterior wall STEMI whose LAD artery was completely occluded and reperfused by PPCI.
1. Age
The number of individuals who develop HF after AMI undergoing PCI increases with age[12]. In an observational study of elderly patients with first MI, 75% of survivors developed HF in the subsequent 5 years[13]. In young patients, only nearly one-third presented with LV dysfunction post-MI, and LVEF recovery occurred in more than 40%[14]. The following reasons can explain this phenomenon. The mechanical contractility of the heart, function of the conduction system, heart reserve capacity and tolerance to ischemia or hypoxia are reduced in elderly individuals. In addition, the severity and extent of coronary artery disease increase with age. Patients with multivessel coronary artery disease have diminished coronary flow reserve and more severe myocardial damage after AMI.
2. Heart Rate at Admission
Accelerated HR is an important external manifestation of sympathetic nerve excitement, which is one of the primary internal mechanisms for the occurrence and development of HF after AMI. In the early stage of AMI, increased HR further promotes myocardial oxygen consumption and shortens myocardial perfusion time, which can directly cause the expansion of the infarction size. As the stroke volume decreases and coronary perfusion decreases, HR increases in an attempt to regain cardiac output and maintain sufficient perfusion of the heart[15]. The formation of a vicious cycle leads to a rapid deterioration of heart function. A study showed that prehospital HR ≥ 100 bpm in STEMI was independently associated with larger infarct size, reduced LVEF and an increased risk of all-cause mortality and HF[16]. In our study, AAW-STEMI patients with HR ≥ 80 bpm at admission were more likely to develop LVSD than patients with HR < 70 bpm. Therefore, HR at admission serves as an easily obtainable and powerful tool to identify STEMI patients at high risk.
3. Number of ST-segment Elevation Leads
The greater the number of ST elevation leads that appear, the wider the myocardial injury and infarct range will be. The number of leads with ST-segment elevation was associated with LV remolding occurrence[17]. The degree of LV function impairment is closely related to the location of MI. Anterior wall infarction location is an important independent predictor of LVSD, particularly when the apical region is involved[18]. The results of this study showed that peak CK was positively correlated with the number of STELs. The LVSD of AAW-STEMI after PPCI was negatively correlated with the number of STELs. The LVSD group had a higher proportion of patients with extensive anterior wall combined with high sidewall ST-segment elevation and a lower proportion of patients with anterior septal MI.
4. Peak Creatine Kinase
A large infarct size is associated with progressive LV remodeling. Patients with higher peak CK are more likely to experience left ventricular remodeling after STEMI and present more often with a lower LVEF[19, 20]. Patients with AAW-STEMI are at increased risk for higher CK[21]. In this study, peak CK had the closest negative correlation with LVEF and could be used to predict LVSD in patients with AAW-STEMI who underwent PPCI. Opening or proximal occlusion can cause more extensive MI than middle or distal occlusion of the LAD artery, leading to a significant increase in CK. Peak CK was higher in extensive anterior wall combined with high sidewall STEMI and lower in anterior septal STEM. The peak CK was higher in young patients. This may be due to decreased protein synthesis and lower levels of CK in the aged cardiomyocytes of elderly individuals[22]. In addition, because of the lack of ischemic preconditioning and less collateral circulation, the tolerance of cardiomyocytes to acute ischemia was reduced in younger patients.
5. Symptoms to Wire-crossing Time
Shortening the STW time is very important to reduce the risk of HF in patients, especially those with anterior wall STEMI[23]. STW time includes the time from onset of symptoms to first medical contact (STF) and FTW time. In this study, the STW time was approximately 30 minutes longer in the ≥ 60 years group than in the < 60 years group. It is considered that it may be the cognitive and socioeconomic factors of older patients contributing further to the delay. The average FTW time was 77.11 minutes, the fastest time was 19 minutes, the longest time was 237 minutes, the proportion of patients with less than 90 minutes was 75.24%, and only 37.79% achieved the currently advocated FTW of < 60 minutes. Several reasons could explain the prolonged FTW time, including the complicated treatment process in the emergency department for STEMI patients during the COVID-19 pandemic, the extremely low ratio of patients admitted directly to the catheterization laboratory, the occupancy of the catheter room and the hesitation of the patient’s family on the PCI operation. STW time is an independent negative influencing factor of LVEF in patients with anterior wall STEMI in the acute phase. It is still necessary to strengthen the publicity of AMI knowledge among the public to emphasize the importance of timely consultation for patients with chest pain. All efforts should be extended to shorten the STW time by educating the public to activate emergency medical services early to bypass the emergency department and allow timely PPCI for the best outcome[23].
6. Recommendations for Early Treatment and Follow-up
LV remodeling is an important pathophysiological process from anterior wall STEMI to HF. In this study, early application of ACEIs/ARBs or ARNIs and β-blockers failed to improve the LVEF level in the acute phase. However, it has been confirmed that the early application of ACEIs/ARBs or ARNIs and β-blockers can inhibit myocardial remodeling and improve long-term prognosis[24]. Improvement in LVEF commonly begins within 3 days in patients who are revascularized with myocardial stunning and improved function of viable myocardium as the mechanisms, and the main improvement in LVEF occurs within 1 month[25, 26]. The first month following primary reperfusion is a critical period during which the greatest degree of cardiac remodeling occurs[27]. Early prediction of LVSD and timely application of recombinant human brain natriuretic peptide, levosimendan, aldosterone antagonist or sodium-glucose cotransporter type 2 inhibitors may reduce the occurrence of HF after AMI [28–31]. In this study, LVSD occurred in more than one-third of patients with AAW-STEMI. Closer follow-up is recommended for patients with LVSD to benefit from early optimization of HF treatment, thereby reducing or delaying cardiogenic death.