Left Ventricular Aneurysm (LVA) is a well-recognized consequence of myocardial infarction that can lead to life-threatening sequelae, such as cardiac arrhythmia, cardiac rupture, and heart failure [1]. A recent review by Jan et al. reported that patients with apical aneurysms had an overall mortality rate of approximately 9%-10.5% over a follow-up period of 2 to 6.5 years [2]. Following a Myocardial Infarction (MI) and the replacement of the ventricular wall with fibrous tissue, the weakened wall tends to develop a bulged area on the ventricular wall, a dyskinetic outpouching of the left ventricular wall, and contributes to diminished left ventricular ejection fraction [3, 4]. The reported incidence of LVA following Myocardial Infarction (MI) ranges from 10% to 35%. However, it has declined to approximately 5% to 15%, due to the benefits of rapid reperfusion therapy and medications that prevent ventricular remodeling [5, 6]. Surgical resection of the aneurysm and reconstruction of the myocardial wall are performed to improve hemodynamics and to improve LV geometry and function [4]. However, despite the benefits of LVA repair, postoperative cardiac arrhythmias remain a significant concern, impacting morbidity and mortality. Cardiac arrhythmias following LVA resection result from multiple pathophysiological mechanisms. The development of malignant ventricular pathways, particularly at the interface between viable and fibrotic myocardium [7].

Myocardial fibrosis and scarring, which are inherent to both the infarction and surgical intervention, can create substrates for reentrant arrhythmias [8]. Moreover, surgical manipulations and direct mechanical irritation of the myocardium and pericardium are among the postoperative arrhythmias after cardiothoracic surgery. Increased sympathetic and hormonal activity, systemic inflammatory response, and complement pathway activation may also contribute to electrical instability [9]. Among post-surgical arrhythmias, ventricular arrhythmias, including Ventricular Fibrillation (VF) and Ventricular Tachycardia (VT), have the highest risk of sudden cardiac death [10, 11]. They often develop from reentry cycles in scarred tissue of infarcted myocardium and require immediate management. The treatment encompasses antiarrhythmic therapy, catheter ablation, or Implantable Cardioverter-Defibrillator (ICD) placement [10, 12]. Supraventricular arrhythmias, such as Atrial Fibrillation (AF), are also prevalent following LVA resection, particularly in patients with preexisting atrial enlargement or structural heart disease [13]. AF can lead to hemodynamic deterioration and an increased risk of thromboembolism, necessitating the implementation of anticoagulation and rhythm- or rate-control strategies [14]. Despite numerous studies focusing on arrhythmias after LVA resection, notable gaps persist in the existing literature. While previous research has investigated treatment outcomes of LVA resection and the prognosis of arrhythmias, few studies have examined patient-specific risk factors, such as sex-related differences and metabolic influences, including lipid profiles [15, 16]. Additionally, to the best of our knowledge, long-term post-surgical follow-up of patients with LVA resection has not yet been studied. Therefore, this study aimed to investigate the incidence of cardiac arrhythmias following LVA resection and to identify their clinical and perioperative correlates.

This cross-sectional study offers insights into the incidence, characteristics, and outcomes of cardiac arrhythmias following LVA resection, a procedure performed to restore ventricular geometry and subsequently improve cardiac function. The results confirm that ventricular arrhythmias, particularly PVCs, are a significant postoperative complication, affecting 20.7% of the study's cohort. One of the most notable findings is the high incidence of PVCs in both preoperative and postoperative stages, suggesting a possible persistent electrophysiological abnormality following myocardial infarction and subsequent LVA. The study's findings can be explained by several factors. First, the pathophysiology of arrhythmias post-surgery is multifactorial. LVAs are often the result of prior myocardial infarction, which leads to myocardial scarring and fibrosis [17]. The fibrotic architecture of the aneurysm acts as a substrate for electrical instability, primarily by altering myocardial conduction properties and fostering reentrant circuits [8, 17, 18]. The resection of LVA may mitigate some of these abnormalities, as evidenced by the significant improvement in LVEF from a mean of 33.4% preoperatively to 42.9% at two years post-surgery. This suggests that while surgery improves overall cardiac function, it does not entirely resolve the arrhythmic risk, likely due to the presence of scar tissue and impaired electrical conduction in the remaining myocardium [12, 19-21]. The pathogenesis of arrhythmias following LVA resection reflects an interaction between a pre-existing scar-based substrate and acute perioperative triggers, consistent with contemporary concepts of scar-related ventricular arrhythmogenesis and postoperative rhythm vulnerability [22, 23]. Although aneurysmectomy removes dyskinetic scar, the peri-scar/border-zone where surviving myocyte strands are interspersed with fibrosis often remains a critical site for slow, heterogeneous conduction and re-entrant VT circuits [22, 24]. Experimental mapping in healed MI demonstrates that the infarct scar border supports VT circuits, with conduction impairment and spatial electrophysiologic heterogeneity playing a key mechanistic role [25]. More broadly, electrical remodeling and conduction slowing in structurally remodeled myocardium are well-recognized prerequisites for reentry and complex ventricular ectopy [25]. Additionally, the occurrence of arrhythmias post-surgery could be partly due to surgical trauma and ischemia-reperfusion injury, both of which contribute to electrical disturbances in the heart [23, 26]. The early postoperative period (ICU phase) is a high-risk window during which acute triggers act upon the underlying substrate. Post-cardiac surgery reviews identify multiple contributors, including hemodynamic stress, metabolic abnormalities, electrolyte disturbances (notably K⁺/Mg²⁺ shifts), and increased adrenergic tone (including stress response and inotropic agents) [23, 27].

Regarding mechanical factors, sudden changes in loading conditions can acutely influence electrophysiology via mechano-electric feedback; direct intraoperative human data demonstrate that abrupt increases in ventricular loading can measurably alter electrophysiologic parameters, providing physiologic support for “mechanical stress” as a plausible trigger on a vulnerable substrate [28]. Contemporary reviews also emphasize “electromechanical reciprocity” as a clinically relevant contributor to arrhythmogenesis in susceptible hearts [29]. One of the most consistent findings in our study was the significant improvement in LVEF after surgery. The preoperative LVEF was 33.4% ± 8.1%, and it increased to 42.9% ± 6.9% two years postoperatively. Sartipy et al. (2008) examined the prevalence of arrhythmias in patients with both ventricular aneurysms and ventricular tachycardia following surgery. In their study of 63 patients, they observed a decrease in arrhythmia rates post-surgery, with a two-year survival rate of approximately 85% and a five-year survival rate of 62%. The leading cause of death was severe heart failure. Our findings align closely with those of Sartipy et al., as we also observed a reduction in pathological ECG changes post-surgery. Additionally, our two-year survival rate was approximately 80%, consistent with their results [30]. Another finding of interest is the increased mortality rate among patients who developed postoperative complications. A total of six patients (20.7%) died after surgery, with the majority of deaths attributed to low cardiac output syndrome (4 patients) and cardiac tamponade (2 patients). The role of low cardiac output syndrome in post-surgical mortality is well-documented, often resulting from inadequate myocardial function following the removal of an aneurysmal segment [31]. The observation that tamponade, a condition in which fluid accumulates in the pericardial sac and restricts normal cardiac filling and reduces cardiac output, was also a significant contributor to mortality, and it highlights the need for close postoperative monitoring, particularly in patients with impaired ventricular function [32, 33].

Our data showed a significant correlation between dyslipidemia and pathological postoperative ECG changes, which is another critical aspect of the study, consistent with previous studies [34]. Liu et al.'s (2006) study, examining eight patients with acute MI, revealed that higher levels of low-density Lipoprotein Cholesterol (LDL-C) were significantly associated with an increased risk of developing VT or VF during the acute stage of MI [34]. Mechanistically, changes in membrane lipid composition (including cholesterol content) can influence membrane protein conformation and function, with downstream effects on cardiac excitability. In near-native membrane experiments, cholesterol depletion significantly reduced Na⁺/K⁺-ATPase activity and altered reaction kinetics, supporting the principle that membrane lipid environment can modulate key electrogenic transporters relevant to resting membrane potential stability and ectopy thresholds [35]. In our study, patients with a history of dyslipidemia were more likely to exhibit abnormal postoperative ECGs, as well as more severe arrhythmias such as AF and PVCs. This finding suggests that dyslipidemia may contribute to the underlying pathophysiology of arrhythmias, possibly through its effects on myocardial ischemia, endothelial dysfunction, and the promotion of fibrosis [36, 37]. The increased vulnerability to arrhythmias in these patients could be related to a combination of factors, including the accelerated progression of coronary artery disease and the resulting impact on the electrical stability of the myocardium. Interestingly, no significant statistical correlation was found between specific arrhythmia types and age groups in our cohort. This apparent lack of an age-related effect may be attributable to the relatively small sample size, which likely limited the statistical power to detect subtle differences. However, the broader literature suggests that the incidence of arrhythmias generally increases with age [38, 39]. In terms of comorbidities, our findings indicated no significant association between preoperative pulmonary disease and arrhythmias (p > 0.05). This contrasts with the study by Serrano Jr. et al. (2010) [40], which demonstrated that aneurysmectomy in patients with severe left ventricular dysfunction was associated with a higher rate of pulmonary tract infections (73% in patients who expired). The discrepancy between our findings and those of Serrano Jr. et al. (2010) [40] may be attributed to our smaller sample size, which may have limited the detection of significant associations. The relationship between surgical complications and hospital admission duration is also an essential topic of discussion. While patients with intraoperative or postoperative complications and arrhythmias tended to have more extended hospital stays, statistical analysis did not reveal a significant association. This could be due to a variety of factors, including the complexity of each individual's recovery process and the hospital's discharge criteria, which may not be based solely on arrhythmia resolution.

Recent advancements have significantly refined the management of post-LVA arrhythmias. Beyond traditional resection, the integration of preoperative/intraoperative 3D Electroanatomic Mapping (EAM) enables more precise identification of arrhythmogenic substrate/foci and can guide targeted ablation strategies during hybrid or open surgical procedures [41-43]. Furthermore, combining LVA resection/ surgical ventricular reconstruction (SVR) with adjunctive surgical VT procedures (eg, cryoablation/endocardial substrate modification) has been reported to improve long-term VT control, supporting the concept that geometric reconstruction alone may not fully eliminate re-entrant circuits [30, 42, 44, 45]. In terms of prevention, early perioperative beta-blocker optimization remains a key evidence-based strategy for reducing post-cardiac-surgery tachyarrhythmias, and perioperative amiodarone prophylaxis has RCT-level evidence for reducing postoperative tachyarrhythmias, with reported reduction in sustained ventricular tachyarrhythmias as well [46, 47]. However, for patients deemed high-risk (eg, persistent complex ventricular ectopy/NSVT, sustained VT, or markedly reduced LVEF after optimization), timely ICD implantation is a guideline-supported standard of care for prevention of sudden cardiac death in eligible patients (eg, ischemic cardiomyopathy with LVEF ≤35% despite optimal therapy, per contemporary guideline criteria) [22]. Finally, improved imaging, particularly Late Gadolinium Enhancement (LGE) cardiac MRI for scar and border-zone characterization, is increasingly central for arrhythmic risk stratification and may inform downstream ICD selection and/or VT ablation planning [48-50].

While this study provides valuable insights into postoperative outcomes following ventricular aneurysm surgery, several limitations warrant consideration. Primarily, the relatively small sample size constrained the statistical power of the study, precluding the feasibility of multivariate analysis to adjust for potential confounders. Consequently, our findings regarding gender-based differences and clinical correlations should be interpreted as exploratory and hypothesis-generating rather than definitive. Additionally, the single-center nature of the research may limit the generalizability of the results to broader clinical settings. Future research should focus on larger, multicenter prospective trials to validate these findings and refine risk stratification models. Long-term studies assessing arrhythmia recurrence, survival rates, and quality of life post-LVA resection are necessary to further establish the durability of surgical benefits and the impact of postoperative complications. Furthermore, integrating advanced imaging and electrophysiological mapping could offer deeper insights into the underlying mechanisms of post-surgical arrhythmias.

Patients with dyslipidemia are at a higher risk of preoperative and postoperative arrhythmias. Aggressive management of lipid profiles, including statin therapy, should be prioritized before surgery to reduce arrhythmic risk. Male patients exhibited a higher incidence of arrhythmias post-LVA resection. Clinicians should be vigilant in monitoring male patients for arrhythmias and consider prophylactic antiarrhythmic therapy or closer postoperative surveillance. Given the high incidence of postoperative arrhythmias (20.7%), continuous ECG monitoring in the immediate postoperative period is essential. Early detection of ventricular arrhythmias (e.g., PVCs, VT) and AF can guide timely interventions such as antiarrhythmic medications, catheter ablation, or ICD placement. Low cardiac output syndrome and cardiac tamponade were the leading causes of in-hospital mortality. Therefore, hemodynamic monitoring and early use of inotropic support or mechanical circulatory assistance should be considered in high-risk patients. Cardiac tamponade contributed to mortality in this cohort. Meticulous surgical hemostasis and postoperative pericardial drainage protocols should be emphasized to prevent this complication.

The significant improvement in LVEF (from 33.4% to 42.9% at two years) underscores the benefits of LVA resection in restoring cardiac function. However, the persistence of arrhythmias suggests that surgical intervention alone may not fully address electrical instability. Long-term follow-up with echocardiography and arrhythmia monitoring is recommended. Despite improved LVEF, patients remain at risk for heart failure. Guideline-Directed Medical Therapy (GDMT) for heart failure, including beta-blockers, ACE inhibitors, and aldosterone antagonists, should be optimized postoperatively. Dyslipidemia was strongly associated with abnormal ECG findings and severe arrhythmias. Postoperative lipid-lowering therapy should be intensified, and lifestyle modifications should be encouraged to reduce arrhythmic risk. Hypertension and diabetes were prevalent in the cohort. Tight control of blood pressure and blood glucose levels may reduce the risk of arrhythmias and improve overall outcomes. The study highlights the role of surgical manipulation in triggering arrhythmias. Surgeons should aim to minimize myocardial trauma and ischemia-reperfusion injury during LVA resection. Patients with intraoperative or postoperative complications had more extended hospital stays. Implementing Enhanced Recovery After Surgery (ERAS) protocols may reduce complications and shorten hospitalization. While no significant association was found between age and arrhythmias, older patients may still be at higher risk due to comorbidities. Individualized risk assessment and tailored postoperative care are essential. Although no significant link was found between pulmonary disease and arrhythmias, patients with COPD or other pulmonary conditions should receive optimized respiratory care to prevent postoperative pulmonary complications.

In conclusion, this study underscores that while ventricular aneurysmectomy significantly improves left ventricular systolic function, it does not eliminate the risk of postoperative arrhythmias. Additionally, dyslipidemia emerged as a critical clinical marker, strongly associated with pathological ECG changes and complex arrhythmias. Although the relatively small sample size necessitates an exploratory interpretation of these results, the data suggest that surgical success should be measured not only by hemodynamic recovery but also by long-term electrical stability. Future management strategies should prioritize aggressive lipid-lowering therapy and vigilant postoperative monitoring, particularly in high-risk patients, to mitigate the burden of arrhythmic events and improve overall survival.