Triglyceride to High-Density Lipoprotein Cholesterol Ratio as a Marker of Subclinical Coronary Atherosclerosis and Hepatic Steatosis in Familial Hypercholesterolemia.

Abstract

Objective: Features of the cardiometabolic syndrome are prevalent in patients with familial hypercholesterolemia (FH). Triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio, a surrogate marker of insulin resistance, may be a robust predictor of cardiac events in the general population. We explored the association between TG/HDL-C ratio and high-risk coronary artery plaque (HRP) and hepatic steatosis (HS) in asymptomatic patients with FH.

Methods: We conducted a cross-sectional study of 290 patients (mean age = 49 years, 44% male) who underwent computed tomography coronary angiography for cardiovascular risk assessment. HRP and HS were assessed from computed tomography coronary angiography, and TG/HDL-C ratio was derived from the fasting lipid panel collected around time of scanning. Associations were assessed using binary logistic and Kaplan-Meier analysis.

Results: TG/HDL-C ratio was significantly associated with HRP (odds ratio, 1.27; 95% CI, 1.04-1.56; P = .020) and HS (odds ratio, 1.71; 95% CI, 1.17-2.51; P = .005) after adjusting for age, body mass index, smoking, and coronary calcium score. TG/HDL-C ratio was associated with HRP in patients treated with lipid-lowering medications (P = .042) and inclusion in a predictive model outperformed the FH-Risk-Score (area under receiver operating characteristic 0.74 vs 0.63; P = .004). An elevated TG/HDL-C ratio predicted myocardial infarction or coronary revascularization over a median follow-up of 91 months with 10 cardiac events recorded (P = .043). TG/HDL-C ratio was strongly positively correlated (P < .001 for all) with markers of cardiometabolic dysfunction: lipid accumulation product (r = 0.81), visceral adiposity index (r = 0.96), and triglyceride-glucose index (r = 0.91).

Conclusion: TG/HDL-C ratio was strongly associated with HRP, HS, and cardiac events in patients with FH treated with long-term cholesterol-lowering therapy.