Ventricular tachyarrhythmias (VTA), encompassing ventricular tachycardia (VT), ventricular flutter, and ventricular fibrillation (VF), represents life-threatening complications that frequently manifest in the aftermath of acute myocardial infarction (AMI). The occurrence of VTA brings about a significant medical challenge, given the association with a substantial proportion of sudden cardiac deaths (SCD). In-hospital mortality approaches 20 percent or more in patients who accompany with VTA following by AMI [1, 2]. Rapid identification and treatment of high-risk patients susceptible to VTA is paramount in clinical cardiology. The interplay between renal function and cardiac disease is a subject of intricate reciprocity which could be summarized as cardiorenal syndrome (CRS). It describes a spectrum of disorders involving both the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ [3]. Impaired renal function is increasingly recognized as a risk factor for adverse cardiovascular events including SCD [4, 5]. In this context, the estimated glomerular filtration rate (eGFR) emerges as a pivotal biological marker. Beyond its conventional role as an indicator of renal health, eGFR assumes significance as a predictive factor for cardiovascular events.

This premise leads us to a critical research question: Dose decrease in eGFR is an independent risk factor of the occurrence of VTA in patients with AMI? A brief retrospective review of existing literature reveals Anna C van der Burgh demonstrated that every 10 mL/min/1.73 m${}^2$ eGFR-cys decrease was associated with 23% increase in the prevalence of SCD (HR = 1.23, with 95% confidence interval (CI) as 1.12–1.34, p 0.001 [6]). However, due to interference from multiple risk factors, the specific investigation into the relationship between eGFR and the risk of VTA in patients with AMI remains inadequacy.

In this research, we employ the propensity score matching (PSM) method, which attempts to adjust post hoc for recognized unbalanced factors at baseline such that the data once analyzed will hopefully approximate or indicate what a prospective randomized dataset. It is well-regarded for its capacity to enhance the robustness of observational studies, allowing for an ideal assessment of correlation of interested variables in situations where randomized controlled trials may not be feasible [7]. Thus, the study aims to systematically explore the association between eGFR and VTA in the context of AMI rigorously, and provide more supporting evidence to the prevention of SCD.

The definition and classification of chronic kidney disease (CKD) based on glomerular filtration rate (GFR), raised in 2002 and acknowledged since 2004, has been followed until today [12, 13]. eGFR is a common indicator based on serum creatinine levels, age, sex and cystatin C (according to the 2012 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) cystatin C equation), which is ideal for reflecting kidney function and is considered an alternative to GFR in clinical practice [14]. The relationship between kidney damage and major adverse cardiovascular events remains a concern for researchers. In this study, we aimed to explore the relationship between the decrease in eGFR and the incidence rate of VTA in AMI patients. The PSM method was applied to simulate the cohort as a randomized controlled trial, to reduce the effects of different confounding factors. The result of PSM analysis showed that 86 of 91 patients with renal dysfunction were matched. The univariate (eGFR) logistic regression analysis demonstrated that the OR of the original cohort was 6.442 (95% CI = 3.770–11.05), and the OR of the cohort after PSM analysis was 3.654 (95% CI = 1.764–7.993). The study concluded that the decrease in eGFR (60 mL/min/1.73 m${}^2$) is a risk factor associated with the concurrence of VTA in patients with AMI.

According to previous studies, CKD is considered to be one of the strongest risk factors for the development of cardiovascular disease [15]. The prevalence of cardiovascular disease among patients older than 65 years of age with CKD in the United States is 64.5%, compared with only 32.4% among those without CKD [16]. Several meta-analyses with large samples have shown that a decrease in eGFR (60 mL/min/1.73 m${}^2$) was significantly associated with an increased risk of all-cause and cardiovascular mortality, regardless of the high-risk population or the general population cohort, or independent of traditional risk factors (such as hypertension, diabetes, and hyperlipidemia) [17, 18]. According to the 2018 U.S. Renal Data System data, non-atherosclerotic adverse cardiovascular events, such as SCD or fatal arrhythmias, are more common in patients with end-stage renal disease (ESRD) than in those with atherosclerosis-related complications, such as AMI or stroke. The report noted that up to 40% of ESRD patients died of SCD, while 18% died of acute myocardial infarction [16]. A recent study highlighted a 6 to 20-fold increased risk of SCD in patients exposed to chronic kidney failure compared with the non-exposed population [19]. Our previous study suggested that eGFR 60 mL/min/1.73 m${}^2$, especially 30 mL/min/1.73 m${}^2$ is a significant variable in the prediction model of SCD after AMI [20]. This opinion is supported by both Faxén et al. [21] and Docherty et al. [22]. All this clinical evidence confirmed that the decrease in eGFR was an independent risk factor for ventricular tachyarrhythmias after AMI.

Cardiac structural remodeling and electrophysiological changes in patients with CKD are the main causes of fatal arrhythmias. Sympathetic hyperactivity is evident at the earliest stage of CKD, which can trigger adratic-related ventricular tachyarrhythmias in susceptible individuals and is directly related to the progression of renal failure [23, 24]. Several studies have demonstrated that renal denervation can decrease the susceptibility of the heart to ventricular fibrillation, in dog and rabbit CKD models [25, 26]. Cardiac structural remodeling includes left ventricular hypertrophy (LVH) and myocardial fibrosis. LVH is easily detected on electrocardiography or echocardiography. The Framingham study followed more than 3000 samples over 14 years and concluded that SCD in the normal population was 1.64%, while SCD in the LVH population was up to 21.5% [27]. Overactivity of the renin–angiotensin–aldosterone system (RAAS) is the most important mechanism of myocardial hypertrophy as it can promote vasoconstriction, cardiac ischemia, myocardial apoptosis, and fibrosis, which are fundamental to ventricular tachyarrhythmias [28]. Myocardial fibrosis is a common pathological state in various cardiac diseases and is an essential cause of ventricular tachyarrhythmia caused by reentrant activity and initiation trigger mechanisms. Cardiac magnetic resonance imaging can directly reflect the degree of myocardial fibrosis through late gadolinium enhancement (LGE) [29]. Multiple clinical studies and meta-analyses have shown that ventricular fibrosis detected using LGE is a powerful predictor of SCD events in patients with ischemic heart disease, dilated cardiomyopathy, and hypertrophic cardiomyopathy [30, 31, 32]. Moreover, ventricular arrhythmias and SCD in patients with ESRD may be related to sharp changes in blood pressure, hypovolemia, and electrolyte disturbance caused by dialysis treatment [33, 34].

Nevertheless, some limitations need to be mentioned. First, this was a single-center retrospective study and the selective bias was inevitable. Moreover, the risk factors related to VTA were numerous, while the study did not cover certain aspects, such as body mass index, drug treatment, the location of the culprit’s vessel, and history of heart failure.

The result of our study has demonstrated the decrease in eGFR (60 mL/min/1.73 m${}^2$) as an independent risk factor of VTA after AMI by PSM analysis.

eGFR, estimated glomerular filtration rate; VTA, ventricular tachyarrhythmia; AMI, acute myocardial infarction; PSM, propensity score matching; OR, odds ratio; CI, confidence interval; LVEF, left ventricular ejection fraction; ESRD, end-stage renal disease; CKD, chronic kidney disease.

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

ML and CZ were involved in the conception, statistics, article writing and revision. ZH was responsible for the conception, statistics and scientific supervision. XZ and CC were involved in data collection. All authors contributed to editorial changes in the manuscript. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

The study and waiver of informed consent was approved by the Ethics Committee of the Affiliated Hospital of Guangdong Medical University (KT2023-062-01). Informed consent was waived due to the retrospective nature of the analysis. All methods were carried out in accordance with relevant guidelines and regulations (Declaration of Helsinki). Researchers tried their best to protect the information from disclosure.

We would like to thank Burcu from Editage (www.editage.cn) for English language editing.

The research was funded by “Affiliated Hospital of Guangdong Medical University Clinical Research Program, No. LCYJ2022B004”.

The authors declare no conflict of interest.