Coronary artery disease (CAD) and lower ejection fraction (EF) are two factors associated with sudden cardiac death (SCD) in patients with left ventricular (LV) systolic dysfunction [1]. About 50% of deaths in patients with CAD and LV systolic dysfunction occur suddenly [2, 3]. Attenuating the ischemic state and improving EF with coronary revascularization [4, 5, 6] have been recommended to reduce the risk of SCD [7, 8]. However, the incidence and risk of SCD in patients with CAD and LV dysfunction who underwent coronary revascularization by either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) have not been well-characterized in the literature.

Current guidelines recommend that patients with LV dysfunction undergo a reassessment of EF 3 months after revascularization to evaluate the neccesity for implantable cardioverter defibrillator (ICD) placement [9]. The rationale for waiting 3 months after revascularization is based on the LV function can improve sufficiently to raise the EF to above 35%, and in clinical trials [10, 11], ICD did not achieve the benefit of SCD prevention early after revascularization (i.e., CABG-patch [12], DINAMIT (Defibrillator in Acute Myocardial Infarction Trial) [13], and IRIS (Immediate Risk stratification Improves Survival trial) [14]). However, how the risk of SCD might develop over time after coronary revascularization is uncertain. Therefore, recognizing the distribution of the incidence of SCD over time, especially within 3 months after revascularization, is clinically significant.

Although EF is currently the most widely used and robust clinical risk factor for SCD after myocardial infarction (MI) and has become the basis for determining a patient’s eligibility for ICD therapy [15, 16], EF might be poor at distinguishing between CAD patients who will die suddenly and those who will die of other cardiovascular causes [2, 17]. Studies in patients with CAD and LV dysfunction who underwent coronary revascularization demonstrated that baseline EF was not associated with the subsequent risk of long-term SCD [18, 19]. This might be due to diverse change of EF after revascularization [7, 20] or requirement of combination with other electrical parameters [2]. Identification of patients at risk remains an issue that is not being adequately addressed.

The present study was designed to determine the incidence of SCD during long-term follow-up in patients with both CAD and LV dysfunction after coronary revascularization by either CABG or PCI, to assess how the event rate changes over time after revascularization, and to analyze clinical predictors of SCD within 3 months after revascularization, especially to understand the predictive value of EF.

In the present study, we report three main findings. First, in patients with CAD and EF $\le$40% undergoing either PCI or CABG, SCD accounted for one-third of all deaths after revascularization with a 5-year cumulative incidence of 6.40%, and 10-year cumulative incidence of 14.67%. Second, the risk of SCD was highest during the first 3 months after revascularization. Finally, a history of VT/VF or triple vessel CAD was associated with an increased risk of SCD in the 3 months after revascularization, but preoperative EF was not.

In the Multicenter Unsustained Tachycardia Trial (MUSTT) [24], patients with documented CAD, EF $\le$40%, and asymptomatic nonsustained VT were included to determine the effect of antiarrhythmic therapy guided by electrophysiological testing. With a follow-up of 5 years, the estimated incidence of SCD among patients with or without antiarrhythmic therapy was 25% and 32%, respectively. Both incidences were much higher than the incidence (6.5% at 5 years) reported in present study, which may indicate the effect of coronary revascularization on reduction of risk of SCD in patients with ischemic LV dysfunction. In addition, in contrast to the MUSTT trial with about 50% arrhythmic deaths, our study had only about one-third SCD. The incidence of SCD reported in the present study was close to the result from the Surgical Treatment for Ischemic Heart Failure (STICH) trial [19], which analyzed a patient sample with preoperative EF $\le$35% who underwent CABG and had a 5-year cumulative incidence of 8.5%.

The incident rate per month over different time intervals after revascularization indicated the extreme risk of SCD within 3 months after revascularization, especially for patients with ACS. Similar results had been reported in the STICH tial [19] and VALIANT (Valsartan in Acute Myocardial Infarction Trial) [25]. In the STICH trial, patients enrolled had chronic ischemic heart disease. The SCD/month rate at 1 month, 1–3 months, 3–6 months, 6–12 months, 1–3 years and 3–5years was 0.35%, 0.43%, 0.26%, 0.14%, 0.14%, and 0.11%, respectively. In the VALIANT trial, patients with acute MI complicated by heart failure, LV systolic dysfunction (EF $\le$40%), or both, were enrolled. Fewer than 50% of patients had primary PCI or thrombolytic therapy. The incidence of SCD at 1 month, 1–6 months, 6–12 months, 1–2 years and 2–3 years was 1.4%, 0.50%, 0.27%, 0.18% and 0.14%, respectively. Therefore, the period of extreme risk of SCD was early after revascularization.

It is recommended that patients with left ventricular dysfunction undergo a reevaluation of EF 3 months after revascularization for deciding whether to do ICD implantation or not [16]. This interval may allow LV to recover the EF from revascularization. However, the risk of SCD in this period was greatest. Early acute MI also constitutes a period of particularly high risk of death from arrhythmia [25, 26]. The effectiveness of early ICD implantation was explored by the Defibrillator in Acute Myocardial Infarction Trial (DINAMIT) [13] and Immediate Risk-stratification Improves Survival (IRIS) trial [14]. ICD was implanted 6 to 40 days or 5 to 31 days after acute MI, respectively. All the patients had EF $\le$35% or EF 40%, assessed within aforementioned intervals, and had been enrolled with additional criteria of impaired cardiac autonomic function or electrical substrate. About 62% to 75% of patients had revascularization by PCI or thrombolysis. ICD failed to reduce overall mortality in both trials, although ICD therapy was associated with a reduction in the rate of SCD. Thus, our data suggests the use of a wearable defibrillator [27] before reassessment of EF 3 months after revascularization, especially for patients with a history of VT/VF or triple vessel disease.

In the present study, a history of VT/VF or bundle branch block was a protential predictor for SCD in the first 3 months after revascularization. Bundle branch block, including both left and right bundle branch blocks, was a powerful and independent predictor of SCD in patients with reduced EF [28] and acute MI [29]. Electrical dispersion of ventricular depolarization and conduction delay, as manifested by QRS prolongation, reflect severity of electrical dysfunction. Bundle branch block with QRS duration $\ge$130 ms and a history of VT/VF might indicate an arrhythmogenic substrate that is susceptible for arrhythmic death. Electrophysiological abnormality might be more predictable for SCD than is EF [2]. In addition, triple vessel CAD was found to be another factor associated with increased risk of SCD in the 3 months after revascularization, especially for patients who underwent PCI. However, complete revascularization and antiplatelet therapy did not predict the short-term risk of SCD. The potential pathophysiological mechanism needs to be further investigated.

The present study had several limitations. (1) This was an observational study from a single center and thus might have selection bias. (2) An accurate estimate of SCD incidence requires prospective ascertainment of cases. Studies that have used a retrospective death certificate-based method to identify cases of SCD are likely to overestimate [30, 31]. (3) There were 13 patients with ICD implantation during the follow-up, but we did not have data on ICD shocks or aborted sudden cardiac arrest. However, these data were unlikely to have affected the present findings because of their uses were minimal in this cohort. (4) The medical treatments for SCD prevention were underutilized. Both prescripton rate and target-dose achievement did not align with the treatment consensus for SCD prevention, especially for patients who underwent CABG treatment. There were 97.1% who did not achieve the target dose of $\beta$-blocker and 97% were below the target dose of angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB). One potential reason was that the prescription data were from the time of patient discharge, whereas we analyzed the risk factor of SCD at 3 months after revascularization. The prescription rates of ACEI/ARB/angiotensin receptor-neprilysin inhibitor (ARNI), $\beta$-blocker, and mineralocorticoid receptor antagonist (MRA) might have increased during the period of follow-up. (5) Some other factors such as contrast-induced nephropathy [32] were reported as potential risk factors of SCD. However, those data were unavailable in the current study. Multi-center prospective studies are needed to confirm these findings.

For patients with CAD and LV systoclic dysfunction who underwent coronary revascularization, SCD accounted for one-third of all deaths. The event rate of SCD was the highest during the first 3 months after revascularization, especially in patients with a history of VT/VF or coronary triple vessel disease. Preoperative EF did not predict the short-term risk of SCD, this underscores the importance of cardiac function surveillance of patients after revascularization.

The data are available from the corresponding author upon request.

JHL and BJB conceived the concept of the study and supervision. SPW and YL contributed to the design of the research. SPW, YL, YCL, SJC, SYL, ZZ, XYG and MG were involved in data collection and analysis. SPW and YL wrote the original draft. All authors edited and approved the final version of the manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

This study was approved by the ethics committee of the Beijing Anzhen Hospital (No. 2021004X). Because this was a retrospective cohort study, written informed consent from the patients was waived. The study conforms with World Medical Association Declaration of Helsinki.

We express our gratitude to all participated staffs for completing the CRISIS Project (Coronary Revascularization In Patients with Ischemic Heart Failure and Prevention of Sudden Cardiac Death).

This research received no external funding.

The authors declare no conflict of interest.