Acute myocardial infarction (AMI) remains a leading cause of cardiovascular morbidity and mortality worldwide (Zheng et al., 2025). It is characterized by myocardial necrosis resulting from acute or sustained coronary ischemia and hypoxia, with persistent chest pain as its hallmark symptom (Liu et al., 2024). Globally, an estimated 3 million individuals experience AMI annually, underscoring its significant clinical burden (Tin et al., 2023). Despite advances in therapeutic strategies, patients with AMI continue to face a significant risk for adverse cardiovascular outcomes (Ma et al., 2024). Among these, heart failure (HF) is one of the most common and severe complications following an initial infarction and is strongly associated with worse in-hospital and long-term prognosis (Ma et al., 2024). Clinically, HF is defined by the heart’s inability to maintain adequate cardiac output, resulting in symptoms such as dyspnea, fatigue, and fluid retention (Roghani et al., 2024). It is typically classified into three phenotypes based on left ventricular ejection fraction (LVEF), with reduced ejection fraction (HFrEF) accounting for up to 60% of cases in developed countries (Brennan et al., 2024). The development of HF post-AMI is primarily driven by extensive cardiomyocyte loss and subsequent scar formation, triggering chronic neurohormonal activation. This includes upregulation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, which ultimately contribute to progressive ventricular remodeling (Takeuchi et al., 2024). The risk of HF and mortality is further elevated in post-AMI patients, especially those with persistent congestion or reduced LVEF (Butler et al., 2024).

Current pharmacological management for AMI involves a comprehensive regimen including antithrombotic agents, β-blockers, lipid-lowering drugs, nitrates, calcium channel blockers, and angiotensin-converting enzyme inhibitors (Dong et al., 2025). Among these, β-blockers play a pivotal role, particularly in patients with HFrEF (Roghani et al., 2024). Substantial clinical evidence supports their efficacy in improving symptoms, reducing rehospitalization rates, and decreasing mortality in HF patients (Roghani et al., 2024). Long-term β-blocker therapy following MI has been associated with an approximate 20% reduction in all-cause mortality (Yndigegn et al., 2024). Large-scale randomized controlled trials and meta-analyses have confirmed the benefits of evidence-based β-blockers—specifically bisoprolol, carvedilol, and metoprolol succinate—in terms of improving symptoms, reversing left ventricular remodeling, reducing hospitalizations and mortality, and enhancing overall survival and quality of life in patients with HFrEF (Hassen et al., 2025).

Diuretics have long been a cornerstone of HF management (Wu et al., 2024). Loop diuretics, prescribed in over 90% of HF cases, are indispensable for alleviating volume overload by reducing both central and peripheral edema (Palazzuoli et al., 2024). They play a dual role in achieving decongestion during acute decompensated HF and maintaining euvolemia in chronic HF (Chopra et al., 2023). Although furosemide remains the most widely used loop diuretic, emerging evidence suggests that torasemide may offer superior clinical benefits, including lower rates of rehospitalization and morbidity (Li et al., 2025). Torasemide has favorable pharmacokinetic and pharmacodynamic properties, such as high oral bioavailability, hepatic metabolism, food-independent absorption, a prolonged half-life, and a rapid onset of action (Chopra et al., 2023). Furthermore, it may exert antifibrotic effects on the myocardium, mitigate ventricular hypertrophy and dilation, and exhibit mineralocorticoid receptor antagonistic activity. These attributes have been associated with improved New York Heart Association (NYHA) functional class and a lower incidence of hypokalemia (Palazzuoli et al., 2024).

Although bisoprolol and torasemide are both widely utilized in clinical settings, evidence regarding their combined effects on cardiac electrophysiology in AMI patients complicated by HF remains scarce. Therefore, this study aims to assess the efficacy of bisoprolol in conjunction with short-term torasemide therapy in enhancing electrophysiological parameters, improving cardiac function and clinical symptoms, and ultimately optimizing outcomes in this high-risk population. The findings may offer new insights into the clinical benefits of this combination therapy and support its potential application in routine practice.

We investigated the effects of bisoprolol combined with torasemide on cardiac electrophysiology in patients with AMI complicated by HF. Our findings suggest that this combination therapy can improve cardiac electrophysiological parameters, cardiac function, clinical symptoms, and hemodynamic status after 2 weeks of treatment.

Both groups showed reductions in QTc interval and QT dispersion, with more pronounced improvements observed in the experimental group. Regarding the influence of medications on QTc interval, QT dispersion, and arrhythmia incidence, the review by Koev et al. (2023) on preventing sudden cardiac death provides valuable context. β-blockers are well-established in attenuating arrhythmogenic risk in HF and ischemic heart disease, especially in those with impaired left ventricular function (Cotton et al., 2022). In our study, bisoprolol likely contributed to improved QT parameters through its known antiarrhythmic mechanisms (Nakamura et al., 2016; Li et al., 2011). Torasemide’s antifibrotic properties—including inhibition of type I collagen synthesis via downregulation of procollagen type I carboxy-terminal proteinase—may further homogenize myocardial conduction (Chopra et al., 2023). Myocardial fibrosis disrupts electrical conduction pathways and increases the risk of arrhythmias (Czubryt and Hale, 2021). By attenuating fibrosis, torasemide may improve myocardial structure and conduction, potentially lowering the risk of arrhythmias, which may be reflected in improved QT parameters. However, the precise relationship between these agents and arrhythmia incidence warrants further study. Overall, the observed reductions in QTc interval and QT dispersion may signal enhanced myocardial electrical stability and a reduced arrhythmic risk to some extent.

Furthermore, BNP levels decreased and LVEF improved in both groups, with the experimental group showing more significant improvements at 2 weeks post-treatment. The reduction in BNP indicates decreased cardiac load and improved hemodynamic status, while the increase in LVEF suggests enhanced myocardial contractility. These findings align with the improvements seen in QT parameters, collectively highlighting the benefit of combining bisoprolol and torasemide. Bisoprolol mitigates neurohormonal activation and preserves myocardial integrity (Nakamura et al., 2016), whereas torasemide enhances these effects through potent diuresis and possible direct antifibrotic activity (Chopra et al., 2023). Prior trials have noted torasemide’s superiority over furosemide in augmenting ejection fraction and shortening hospital stays (Mentz et al., 2023). Meta-analyses further support long-term β-blocker use for reducing all-cause and cardiovascular mortality, as well as major adverse cardiac events in post-MI cohorts (Liang et al., 2022). Additionally, large registries have linked β-blocker therapy with improved survival in HFpEF patients following decompensation (Ibrahim et al., 2024). Notably, after 2 weeks of treatment, the experimental group had lower serum potassium levels than the control group, likely due to torasemide’s diuretic effect (K et al., 2025). The absence of a significant difference in creatinine levels suggests that torasemide’s impact on renal function may be relatively modest.

Improvements in NYHA class and Borg dyspnea scores were also more pronounced in the experimental group, alongside a higher rate of edema resolution after 2 weeks. These findings indicate that the combination therapy can effectively alleviate clinical symptoms. Torasemide blocks Na⁺/K⁺/2Cl^- cotransporters in the thick ascending limb of Henle—responsible for 20%–30% of filtered sodium reabsorption—thereby promoting natriuresis and diuresis (Palazzuoli et al., 2024). It also exerts reversible inhibition of NKCC2 and acts on distal nephron sites, enhancing fluid removal (Wu et al., 2024).

Both groups experienced significant reductions in SBP, DBP, and HR, with the experimental group exhibiting lower SBP and DBP than the control group. β-blockers reduce HR, myocardial oxygen demand, and adverse sympathetic activity by blocking β-adrenergic receptors (Roghani et al., 2024). Bisoprolol’s efficacy in improving long-term cardiovascular outcomes and blood pressure control has been documented in hypertensive populations (Kim Tran et al., 2023). Although one trial found no superiority of torasemide over furosemide regarding mortality or quality of life post-HF hospitalization (Verbrugge and Menon, 2022), bisoprolol combined with torasemide may producesynergistic antihypertensive effects.

While intergroup differences in VA and AFL/AF incidence were not statistically significant, the experimental group experienced a lower incidence of VA and AFL/AF after 3 months of treatment than at baseline. Torasemide has a relatively long half-life (Mentz et al., 2023), with a faster onset, longer duration of action, and lower risk of abrupt diuresis compared to furosemide (Balsam et al., 2019). These findings may be attributed to torasemide’s ability to maintain effective plasma concentrations over an extended period, thereby sustaining its diuretic effects and reducing cardiac preload and afterload. Even after discontinuation, residual drug levels may continue to exert therapeutic effects. Additionally, the limited sample size in this study may have influenced the observed incidence rate. Long-term β-blocker use after ST elevation myocardial infarction and percutaneous coronary intervention is associated with reduced all-cause mortality (Maqsood et al., 2021). Systematic reviews support β-blockers’ role in decreasing recurrent infarction and long-term mortality, although their impact on short-term mortality remains inconclusive (Safi et al., 2019), especially in patients with preserved LVEF (Sabina et al., 2024). The trend toward reduced arrhythmia incidence in the experimental group may suggest potential long-term survival benefits, but this warrants validation through longer follow-up. Notably, no significant differences in cardiovascular or all-cause mortality were observed between groups during the treatment period. Early initiation of oral carvedilol post-percutaneous coronary intervention has been shown to reduce long-term mortality (Dai et al., 2024), and β-blockers, including bisoprolol, consistently demonstrate survival benefits in HF by attenuating catecholamine effects and preventing arrhythmias (Roghani et al., 2024). Although the TRANSFORM-HF trial found no mortality difference between furosemide and torasemide (Verbrugge and Menon, 2022), meta-analyses have favored torasemide for reducing HF hospitalization rates without a clear effect on mortality (Singh et al., 2023). Given the complex interplay of drug mechanisms and clinical effects, mortality outcomes require further validation in long-term studies.

From a mechanistic perspective, torasemide, as a novel loop diuretic, may offer cardiovascular protection beyond its diuretic action due to its multifaceted properties. Evidence suggests that torasemide can reverse myocardial fibrosis, inhibit type I collagen synthesis, and improve cardiac remodeling in chronic HF patients (Acuna, 2010). These effects are particularly important during post-MI remodeling, as they may reduce the arrhythmogenic substrate by enhancing myocardial structural uniformity. Additionally, torasemide exhibits unique aldosterone antagonistic activity, inhibiting aldosterone binding and downstream signaling (Acuna, 2010; Potter et al., 2019). Aldosterone promotes myocardial fibrosis, inflammation, and oxidative stress by activating mineralocorticoid receptors in cardiomyocytes, thereby increasing arrhythmia risk (Tsai et al., 2024; Khan et al., 2024). When combined with β-blockers, torasemide may synergistically counteract excessive neurohormonal activation, further stabilizing myocardial electrophysiology.

It is important to note that while both furosemide and torasemide are loop diuretics used in HF management (Li et al., 2025), they differ in pharmacokinetic and pharmacodynamic profiles. Torasemide has higher bioavailability and a longer half-life than furosemid (Mentz et al., 2023), resulting in faster onset, sustained action, and a lower risk of rapid diuresis (Balsam et al., 2019). Moreover, torasemide’s anti-aldosterone, vasodilatory, and antifibrotic properties may confer additional cardiovascular benefits beyond fluid removal. In contrast, furosemide primarily acts as a diuretic and natriuretic agent without direct protective effects on myocardial remodeling (Mentz et al., 2023; Balsam et al., 2019). Recent TRANSFORM-HF trials have reported no significant differences in all-cause mortality or HF rehospitalization rates between torasemide and furosemide among patients discharged after HF hospitalization (Kittipibul et al., 2024). Regardless of LVEF or baseline status, patient-reported outcomes appear similar between the two agents (Kapelios et al., 2024; Greene et al., 2023). Future multi-center, large-scale studies are needed to further clarify the comparative benefits of torasemide and furosemide.

In conclusion, bisoprolol combined with torasemide improved cardiac electrophysiological parameters, cardiac function, symptoms, and hemodynamics in patients with AMI complicated by HF after 2 weeks of treatment. This combination regimen may provide clinicians with an additional therapeutic option to optimize management and improve patient outcomes. However, this study has several limitations. First, the short follow-up period precludes assessment of the long-term effects of bisoprolol-torasemide therapy on cardiac electrophysiology, function, and prognosis in AMI-HF patients; extended observation is needed to evaluate its sustained efficacy and safety. Second, the small sample size may introduce bias and limit the generalizability of the findings, particularly for mortality and arrhythmia endpoints. Additionally, metabolic parameters such as blood glucose and lipid profiles were not monitored, potentially overlooking the drugs’ metabolic impact. Future research should extend follow-up duration, expand the sample size, and adopt multi-center, randomized controlled trial designs to enhance external validity. Furthermore, comprehensive monitoring of metabolic markers will help elucidate the full spectrum of effects. Finally, in-depth mechanistic studies exploring how bisoprolol combined with torasemide improves cardiac electrophysiology and function could identify novel therapeutic targets and provide theoretical support for developing more effective treatment strategies.