Liver-Kidney-Metabolic Health, Sex, and Menopause Impact Total Scores and Monovessel vs. Multivessel Coronary Artery Calcification

Abstract

Introduction

Liver-kidney-metabolic health (LKMH) depends on complex interactions between metabolic dysfunction-associated steatotic liver disease (MASLD), chronic kidney disease (CKD), sex, and reproductive status. This study evaluates in a holistic manner how LKMH, sex, and menopause influence coronary artery calcification (CAC) burden.

Methods

Patients without previous cardiovascular disease were prospectively recruited. Liver fat was assessed via ultrasonography and categorized as mild or moderate-to-severe. CKD was classified using estimated glomerular filtration rate (eGFR). CAC burden was quantified as 0, 1–299, ≥ 300, single-vessel, or multivessel with coronary computed tomography. Stepwise backward multinomial logistic regression was applied for analysis.

Results

A total of 446 patients (59.2% female, average age 52.9 years) were included. Moderate-to-severe MASLD was independently associated with an increased risk of CAC 1–299 [OR 2.30 (1.21–4.36)], CAC ≥ 300 [OR 4.93 (1.46–16.59)], and single-vessel CAC [OR 2.03 (1.03–4.00)]. Mild MASLD [OR 2.47 (1.20–4.21)], moderate-to-severe MASLD [OR 3.74 (1.76–7.93)], and CKD stage 2 [OR 2.27 (1.26–4.08)] were independently associated with increased multivessel CAC risk. Liver fat content showed a dose–response association with CAC burden. Subgroup analysis revealed that MASLD and CKD increased CAC risk in male but not female patients, with menopause significantly modifying LKMH’s effect.

Conclusion

LKMH’s impact on CAC burden is significantly influenced by liver fat content, eGFR, sex, and menopause, suggesting that MASLD, CKD, sex, and reproductive status should be integrated into CAC risk prediction models.