What question did this study set out to answer?

To assess how left ventricular ejection fraction mediates the relationship between replacement fibrosis and sudden cardiac death after myocardial infarction.

January 10, 2026Open Heart1 citationsOpen Access

Replacement fibrosis, left ventricular ejection fraction and sudden cardiac death in patients after myocardial infarction: a mediation analysis

PZPengyu ZhouChinese Academy of Medical Sciences & Peking Union Medical College KAKaisaierjiang AisikaierChinese Academy of Medical Sciences & Peking Union Medical College ZDZhixiang DongChinese Academy of Medical Sciences & Peking Union Medical College

Key Result

Left ventricular ejection fraction (LVEF) mediated 19.7% of the effect of replacement fibrosis on sudden cardiac death in post-myocardial infarction patients (p <0.001).

Key Points

To assess how left ventricular ejection fraction mediates the relationship between replacement fibrosis and sudden cardiac death after myocardial infarction.
Conducted a retrospective analysis on 917 post-MI patients with cardiac MR data.
Quantified the association of late gadolinium enhancement with left ventricular ejection fraction using linear regression models.
Evaluated LGE and LVEF associations with sudden cardiac deaths using competing risk models.
Performed mediation analysis to determine LVEF's mediating effect on the relationship between LGE and SCD.
65 patients (7.1%) experienced sudden cardiac death during a median follow-up of 63.3 months.
LGE was significantly associated with lower LVEF (β=-0.35, p <0.001).
Both LGE and LVEF independently predicted sudden cardiac death.
LVEF mediated 19.7% of LGE's total effect on SCD (p <0.001), and 40.4% in patients with LVEF > 35% (p = 0.02).
No mediation was noted for patients with LVEF ≤ 35% (p = 0.08).

Structured PICO

Does left ventricular ejection fraction mediate the relationship between replacement fibrosis (assessed by LGE) and sudden cardiac death in post-myocardial infarction patients?

Population

917 post-myocardial infarction patients (mean age 56.3, 88.8% male) who underwent cardiac MR. Key inclusion: chronic MI confirmed by CMR, presence of ischemic-pattern late gadolinium enhancement (LGE). Key exclusion: concomitant non-ischemic cardiomyopathies or structural heart disease, prior cardiac surgery, previous cardiac arrest/VT/VF outside the context of MI, and recurrent MI.

Intervention

Assessment of myocardial replacement fibrosis extent via late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR)

Outcome

Composite of sudden cardiac death (SCD), aborted SCD, and appropriate implantable cardioverter-defibrillator (ICD) discharges over a median follow-up of 63.3 monthscomposite

LVEF mediates less than 20% of the association between myocardial replacement fibrosis and sudden cardiac death post-MI, suggesting fibrosis drives SCD risk largely through direct pathways independent of functional impairment.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Objective To evaluate the potential mediating role of left ventricular ejection fraction (LVEF) in the relationship between replacement fibrosis (assessed by late gadolinium enhancement (LGE)) and sudden cardiac death (SCD) post-myocardial infarction (MI) and also to assess this mediation effect in subgroups based on LVEF ≤ 35% and > 35% according to implantable cardioverter-defibrillator (ICD) selection criterion. Methods A retrospective analysis was conducted on 917 post-MI patients (mean age: 56.3±11.0 years, 88.8% male) who underwent cardiac MR from January 2017 to August 2021. The endpoint for SCDs included SCD, aborted SCD and appropriate ICD discharges. The association of LGE with LVEF was quantified using linear regression models. The associations of LGE and LVEF with SCDs were evaluated using competing risk models. Mediation analysis was then used to decompose the total effect of LGE on SCDs into direct and indirect (mediated through LVEF) effects using accelerated failure time models. Results Over a median follow-up of 63.3 (IQR, 43.6 to 76.6) months, 65 patients (7.1%) experienced SCDs. In all patients, LGE was significantly associated with lower LVEF (β=-0.35, p 35% ( p = 0.02), while no mediation was observed in patients with LVEF ≤ 35% ( p = 0.08). Conclusion LVEF partially mediated the effect of LGE on the SCD, accounting for less than one-fifth of the total effect. LVEF alone inadequately captured the whole SCD risk, irrespective of whether LVEF is greater than 35% or 35% or less.

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