Dapagliflozin reduces risk of heart failure rehospitalization in diabetic acute myocardial infarction patients: a propensity score-matched analysis

In the current study, we found that in-hospital and continued use of DAPA after discharge was associated with a significant lower risk of HF rehospitalization in patients with diabetic AMI, compared with non-DAPA users. Other independent predictors of the HF rehospitalization included age, hypertension, uric acid, and Killip class. Patients with AMI and T2DM were more likely to benefit from in-hospital and continued use of DAPA. However, prospective clinical trials with a larger sample size and a longer follow-up are still required.

During the follow-up period, a total of 150 patients were hospitalized for heart failure, with a rate of 15%. It is reported in a retrospective study with a large sample of 77,363 AMI patients [30] that the heart failure rehospitalization rate was about 22% during a 5-year follow-up. The difference in this rate may be attributed to the smaller sample size in our study, as well as the geographical, dietary, climatic factors, and patients’ compliance.

We found no significant difference in the risk of HF rehospitalization between female subgroups. There are two main possible reasons. Firstly, the prevalence of AMI is higher in male than in female patients [31]. In our study, there were 66 female patients in DAPA group. The sample size is relatively small, and therefore may contribute to the lack of significant differences in the subgroup of females. Secondly, female patients have a worse prognosis post AMI [30]. During the follow-up, some female patients may have died of various reasons and could not achieve the primary endpoint. This may have also influenced the results of subgroup analysis.

In this study, we also found that most deaths occurred within 30 days post AMI and the difference in all-cause mortality was more evident in the early phase of follow-up. In another study, AMI patients undergoing percutaneous coronary intervention (PCI) and complicated with cardiogenic shock were enrolled and analyzed. Most deaths also occurred within 30 days after AMI, which is consistent with our results [32]. In the early phase post AMI, due to severe myocardial injury, cardiac dysfunction may lead to heart rupture, or papillary muscle dysfunction or rupture. These damages may end up with HF and even sudden death. In addition, various ventricular arrhythmias may appear in the early stage after heart injury, which can also result in sudden death [33]. Therefore, patients with AMI are more likely to have serious complications in the early phase after AMI. However, this study also indicated that early use of DAPA can reduce the risk of death in AMI patients more significantly.

Recurrent myocardial infarction (MI) is often followed by chronic HF, malignant arrhythmias, and cardiovascular death [34]. SGLT2 inhibitors, a novel oral hypoglycemic agent, have shown in recent clinical studies to significantly reduce the incidence of composite cardiovascular death or worsening HF events in HF patients with mildly reduced or preserved ejection fraction over a median follow-up of 2.0–2.5 years [35, 36]. However, whether SGLT2 inhibitors are effective in the early post-infarction period lacks evidence. Furthermore, considering that patients with a long history of AMI are more likely to have shared indications for SGLT2 inhibitors (e.g., T2DM or HF), it may be hasty to determine that the benefit of SGLT2 inhibitors for patients is in the context of AMI. Despite their proximate therapeutic spectra, trials in AMI populations are needed to confirm whether their treatment effects are consistent.

Existing studies suggest that in patients with T2DM and atherosclerotic cardiovascular disease, SGLT2 inhibitors reduce cardiovascular all-cause mortality and death from renal disorders, renal replacement therapy, or doubling of the serum creatinine level [37]. In contrast, this study focused on the ability of SGLT2 inhibitor in predicting rehospitalization for HF after AMI in patients combined with T2DM. One strength of this study was the introduction of propensity score matching, which allows direct comparison between the treatment and control groups, as a randomized controlled trial does [38], as well as robust error specification of the PS model [39]. In conclusion, more clinical evidence is needed in the future to confirm whether SGLT2 inhibitors should be used earlier in AMI patients.

The incidence of adverse events in this study was not high. On the one hand, this is related to the small sample size; on the other hand, our patients were all diabetic and they regularly visited a clinic for glycemic assessment and health education, which may lower the incidence of adverse events. However, the safety of SGLT2 inhibitors still requires the verification with more clinical data.

The formation of fibrous scar tissue and ventricular remodeling after AMI, along with a progressive decrease in myocardial contractility and ultimately heart failure, have been associated with death. Renal injury in the early stages of AMI has been associated with a poor prognosis in the short term and can increase long-term mortality [40]. The development of malignant arrhythmias is an important cause of early death in AMI patients [33]. Early identification of patients at a high risk of various complications is important, and an artificial intelligence model for predicting acute kidney injury risk and a new scoring system for predicting ventricular arrhythmia risk have been developed [33, 41]. In our previous studies, we have also found that a low level of free triiodothyronine is independently associated with the short-term outcomes in patients with AMI [42]. Prevention is important, but treatment is equally vital and SGLT2 inhibitors provide a new therapeutic direction for the prognosis of AMI patients. SGLT2 inhibitors may reduce the risk of acute myocardial infarction via mechanisms responsible for attenuating neurohormonal activation, cardiomyocyte necrosis, and reperfusion injury. It may also facilitate coronary blood flow and reduce ventricular load by enhancing endothelial function and vasodilation, improving myocardial energy metabolism and contractility, and other mechanisms [43,44,45,46]. With the reversal of cardiac enlargement, rhythm abnormalities, and myocardial fibrosis, HF is finally cured [47, 48]. In addition, outside the heart, SGLT2 inhibitors may also indirectly protect the cardiorenal axis by reducing intra-glomerular pressure and increasing erythropoietin production, among many other mechanisms [49, 50].

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