What question did this study set out to answer?

To assess the association of coded steatotic liver disease with adverse outcomes after percutaneous coronary intervention in non-diabetic adults.

May 27, 2026Open Access

Effect of coded steatotic liver disease on outcomes of percutaneous coronary intervention in non-diabetic adults: insights from a multicenter real-world cohort

Key Points

To assess the association of coded steatotic liver disease with adverse outcomes after percutaneous coronary intervention in non-diabetic adults.
Retrospective cohort study using TriNetX US Collaborative Network data from 2014–2023.
Participants stratified by steatotic liver disease status, with matching performed for demographics and comorbidities.
Primary outcome was all-cause mortality, with secondary outcomes including heart failure, MI, MACE, among others.
All-cause mortality was similar between groups (2.8% vs. 3.1%, HR 0.93, 95% CI 0.77–1.13, p=0.472).
SLD was linked to higher rates of heart failure and bleeding (10.1% vs. 8.9% for heart failure, HR 1.15, p=0.027; 5.1% vs. 3.8% for bleeding, HR 1.35, p<0.001).
Risk of cardiogenic shock was highest in the first 30 days (RR 1.45, p<0.001) but decreased thereafter.

Abstract

Abstract Background Metabolic dysfunction-associated steatotic liver disease (MASLD) is a cardiovascular risk–enhancing condition. Its prognostic significance following PCI in non-diabetic adults, and the temporal distribution of that risk, remain incompletely characterized. Objectives To evaluate whether coded steatotic liver disease is associated with adverse one-year post-PCI outcomes in non-diabetic adults, and to characterize the temporal concentration of risk across early (day 0–30) and late (day 31–365) post-procedural periods. Methods Retrospective cohort study using the TriNetX US Collaborative Network (2014–2023). Non-diabetic adults undergoing PCI were stratified by steatotic liver disease (SLD) status (ICD-10-CM K76.0 and/or K75.81). Primary outcome: all-cause mortality (day 1–365). Secondary outcomes: heart failure, MI, 3-point MACE, cardiogenic shock, cardiac arrest, and bleeding. PSM (1:1) balanced demographics, cardiometabolic comorbidities, ACS type, and medications. Outcomes were further assessed across prespecified early and late windows. Results After PSM, 7,434 patients per group were well balanced (SMD < 0.10). All-cause mortality did not differ significantly (2.8% vs. 3.1%; HR, 0.93; 95% CI, 0.77–1.13; p = 0.472). SLD was significantly associated with higher one-year rates of incident heart failure (10.1% vs. 8.9%; HR, 1.15; 95% CI, 1.02–1.30; p = 0.027) and bleeding events (5.1% vs. 3.8%; HR, 1.35; 95% CI, 1.15–1.59; p < 0.001). Time-stratified analysis showed that cardiogenic shock risk was concentrated in the first 30 days (RR, 1.45; p < 0.001) and attenuated to null beyond 30 days and overall. Heart failure excess was similarly early-driven (RR, 1.17; p = 0.005), but the overall one-year signal remained significant (HR, 1.15; p = 0.027), reflecting the sustained contribution of early events. Conclusions Among non-diabetic adults undergoing PCI, coded steatotic liver disease is associated with significantly higher one-year rates of heart failure and bleeding, without a significant mortality difference. Hemodynamic vulnerability is concentrated in the early peri-procedural period, while hemorrhagic risk is sustained. These findings support heightened early surveillance and individualized antithrombotic planning for SLD patients undergoing PCI.

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