In this prospective study of older Vietnamese patients with MI, we found a 12.8% incidence of post-MI HFrEF 3 months after hospital discharge. Previous studies have reported an incidence of post-MI HF ranging from 11–50%, although with different post-MI HF definitions and without ejection fraction classification [1, 14–16, 18–21]. Notably, in older populations, Ezekowitz et al. reported a 46% incidence of post-MI HF after 1 year, whereas Kochar et al. reported a 10% incidence [14, 15]. The relatively lower incidence in the present study may be partly explained by differences in the study design and population compared with those in previous reports. Notably, many previous studies utilised retrospective analyses of registry data with post-MI HF diagnosis based on ICD codes during rehospitalisation or follow-up visits without standardised ejection fraction measurement. In contrast, the prospective design of the present study involved systematic echocardiographic follow-up at approximately 3 months post-discharge to evaluate the ejection fraction and HF-related symptoms for HFrEF diagnosis based on the latest guidelines. In addition, most patients in the present study underwent invasive treatment for MI, with 94% undergoing invasive coronary angiography and 92% undergoing coronary revascularisation, reflecting a contemporary optimal MI treatment. Previous studies were conducted decades ago when revascularisation was less prevalent, especially among high-risk older adults. Advances in acute MI management may translate into less adverse remodelling and HFrEF development in more recent cohorts. For example, Ezekowitz et al. reported only a 15% and 3% rate of PCI and coronary artery bypass grafting, respectively, possibly contributing to the higher incidence observed [15]. Kochar et al. found an incidence similar to that in the present study despite reporting lower revascularisation rates (38% rate of PCI), which suggested that factors other than revascularisation, including the timing of revascularisation, severity, or other characteristics of MI, affect post-MI HF development. However, these details were unavailable for comparison in the study by Kochat et al. [14]. The present study’s finding that one in 10 older MI survivors developed new HFrEF despite high revascularisation rates underscores the need for ongoing improvements in both acute MI treatment and post-MI care for this high-risk population.
In the three multivariate models, we identified female sex, highest troponin T levels, and reduced pre-discharge LVEF as independent factors associated with post-MI HfrEF The association between female sex and an increased risk of post-MI HF has been inconsistent across previous studies, with some identifying female sex as an independent predictor of post-MI HF development. This discrepancy may be due to older age, higher comorbidity, geriatric syndrome burden, and treatment disparities in women with post-MI HF, who tend to receive less invasive management and secondary prevention [6]. In addition, systemic inflammation due to excess adipose tissue in postmenopausal women may contribute to this discrepancy [33]. The sex sub-analysis in the present study confirmed the association between the female sex and post-MI HF development despite no differences in revascularisation rates between sexes.
Infarct size is an established risk factor for post-MI HF and is the most important predictor of adverse remodelling and, consequently, left ventricular dysfunction after MI [34, 35]. Infarct size can be assessed clinically using cardiac imaging, the location and extent of ST elevations, or indirectly through the culprit coronary arteries combined with the severity of the CAD burden through invasive coronary angiography. In addition, late reperfusion and no or minimal collateral flow after revascularisation can lead to a larger infarct size, thus impacting the development of post-MI HF. Cardiac troponin is an established marker of MI severity that reflects infarct size, with peak levels proportional to the extent of irreversible cardiac damage measured using magnetic resonance imaging [36]. In the multivariate analysis in the present study, the highest troponin T level was significantly associated with post-MI HFrEF, whereas the timing of reperfusion and the severity of CAD were not. Given the different invasive approach timings between NSTEMI and STEMI, the impact of the total ischaemic time may be diluted in the highly revascularised cohort with almost equal STEMI and NSTEMI ratios in the present study. Furthermore, inaccurate symptom reporting in older patients can present a bias in the determination of the ischaemic time [37]. The findings of the present study contradict those of Gerber et al., who identified the severity of angiographic coronary disease as a predictor of post-MI HF [17]. We hypothesised that in high-risk older patients, underlying coronary disease would likely be already present, and the infarct size of acute MI, as indicated by the culprit arteries, might more precisely reflect MI severity. Notably, we also found no significant association with MI, as determined by the BCIS-JS, which, to the best of our knowledge, has only been previously utilised in the setting of ischaemic chronic HFrEF. However, the results of the present study align with the post-MI HFrEF pathophysiology, in which peak cardiac troponin most objectively indicates infarct magnitude.
Reduced ejection fraction (LVEF ≤ 40%) before discharge was the strongest independent factor associated with post-MI HFrEF in the present study. Lower pre-discharge LVEF indicates a higher risk of post-MI HFrEF development, with every 5% decrease associated with 1.59 times higher odds (95% confidence interval: 1.32–1.89) in the univariate analysis (Supplementary Table 4, Supplementary Appendix). This finding is consistent with that of previous studies, indicating that impaired LVEF early post-MI predicts patients prone to adverse remodelling [38, 39]. Notably, most (70%) patients in the post-MI HFrEF group developed reduced LVEF before discharge, as shown in Fig. 3. Furthermore, among patients with reduced pre-discharge LVEF, 35% (21 patients) did not recover LVEF > 40% at 3 months post-discharge. Wohlfahrt et al. reported an even higher rate (55%) of patients with unrecovered LVEF 3 months post-discharge, although their cohort was younger (mean age, 66 years) with more STEMI cases (85%) [40]. Despite the high revascularisation rates in both studies, a significant proportion of patients with acute MI who had low pre-discharge LVEF experienced no LVEF improvement at 3 months, facing an increased risk of adverse remodelling and potentially subsequent adverse cardiac events. Further research is warranted to elucidate the specific factors affecting LVEF recovery post-discharge and to develop interventions to eliminate maladaptive processes in this high-risk group, especially in the current modern era of invasive MI therapy.
The present study has some limitations. First, echocardiography was performed at two individual study sites without core laboratory confirmation of LVEF measurements. Second, we lacked long-term follow-up data on major adverse cardiac events. However, this study provides important contemporary prospective data on post-MI HFrEF epidemiology, specifically among older patients treated with modern standards of care, as evidenced by our study at two high-volume PCI-capable tertiary centres in Vietnam. Given the shifts in patient demographics, cardiovascular risk profiles, and advances in acute MI management in recent decades, updated information is critical. Our findings highlight the persistent knowledge gaps in the pathophysiology and prevention of post-MI HF despite optimal revascularisation. This underscores the need for further research to enhance risk prediction and identify tailored monitoring and treatment approaches, particularly for high-risk subgroups, as identified in our analysis.