The triglyceride/high-density lipoprotein cholesterol ratio predicts all-cause mortality in women with suspected myocardial ischemia: A Report From the Women's Ischemia Syndrome Evaluation (WISE)
Received 4 August 2008; accepted 18 November 2008.
High triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C) are important cardiovascular risk factors in women. The prognostic utility of the TG/HDL-C ratio, a marker for insulin resistance and small dense low-density lipoprotein particles, is unknown among high-risk women.
Methods
We studied 544 women without prior myocardial infarction or coronary revascularization, referred for clinically indicated coronary angiography and enrolled in the Women's Ischemia Syndrome Evaluation (WISE). Fasting lipid profiles and detailed demographic and clinical data were obtained at baseline. Multivariate Cox-proportional hazards models for all-cause mortality and cardiovascular events (death, myocardial infarction, heart failure, stroke) over a median follow-up of 6 years were constructed using log TG/HDL-C ratio as a predictor variable and accounting for traditional cardiovascular risk factors.
Results
Mean age was 57 ± 11 years; 84% were white, 55% hypertensive, 20% diabetic, 50% current or prior smokers. Triglyceride/HDL-C ranged from 0.3 to 18.4 (median 2.2, first quartile 0.35 to <1.4, fourth quartile 3.66-18.4). Deaths (n = 33) and cardiovascular events (n = 83) increased across TG/HDL-C quartiles (both P < .05 for trend). Triglyceride/HDL-C was a strong independent predictor of mortality in models adjusted for age, race, smoking, hypertension, diabetes, and angiographic coronary disease severity (hazard ratio 1.95, 95% CI 1.05-3.64, P = .04). For cardiovascular events, the multivariate hazard ratio was 1.54 (95% CI 1.05-2.22, P = .03) when adjusted for demographic and clinical variables, but became nonsignificant when angiographic results were included.
Conclusion
Among women with suspected ischemia, the TG/HDL-C ratio is a powerful independent predictor of all-cause mortality and cardiovascular events.
aDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL
bDepartment of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA
cDepartment of Pharmacy Practice and Center for Pharmacogenomics, University of Florida College of Pharmacy, Gainesville, FL
dDivision of Cardiology, Department of Medicine, Allegheny General Hospital, Pittsburgh, PA
eCardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, PA
fDivision of Cardiology, Department of Medicine, Cedars-Sinai Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA
gNational Heart, Lung and Blood Institute, NIH, Bethesda, MD
Reprint requests: Vera Bittner, MD, MSPH, Professor of Medicine, University of Alabama at Birmingham, 701 19th Street South-LHRB 310, Birmingham, Alabama 35294.
Funding sources: This work was supported by contracts from the National Heart, Lung and Blood Institutes, nos. N01-HV-68161, N01-HV-68162, N01-HV-68163, N01-HV-68164; grants U0164829, U01 HL649141, U01 HL649241, GCRC grant MO1-RR00425 from the National Center for Research Resources; and grants from the Gustavus and Louis Pfeiffer Research Foundation (Denville, NJ), The Women's Guild of Cedars-Sinai Medical Center (Los Angeles, CA), The Ladies Hospital Aid Society of Western Pennsylvania (Pittsburgh, PA), and The Edythe Broad Endowment for Women's Heart Research (Los Angeles, CA).
ABSTRACT