Jing Cao1, Brian T Steffen1, Matthew Budoff1, Wendy S Post1, George Thanassoulis1, Bryan Kestenbaum1, Joseph P McConnell1, Russell Warnick1, Weihua Guan1, Michael Y Tsai2. 1. From the Department of Laboratory Medicine and Pathology (J.C., B.T.S., M.Y.T.), Division of Biostatistics, School of Public Health (W.G.), University of Minnesota, Minneapolis; Department of Medicine, University of California, Los Angeles (M.B.); Department of Medicine, John Hopkins University, Baltimore, MD (W.S.P.); Department of Medicine, McGill University, Montreal, Québec, Canada (G.T.); Division of Nephrology, Kidney Research Institute, University of Washington, Seattle (B.K.); and Health Diagnostics Laboratory, Richmond, VA (J.P.M., R.W.). 2. From the Department of Laboratory Medicine and Pathology (J.C., B.T.S., M.Y.T.), Division of Biostatistics, School of Public Health (W.G.), University of Minnesota, Minneapolis; Department of Medicine, University of California, Los Angeles (M.B.); Department of Medicine, John Hopkins University, Baltimore, MD (W.S.P.); Department of Medicine, McGill University, Montreal, Québec, Canada (G.T.); Division of Nephrology, Kidney Research Institute, University of Washington, Seattle (B.K.); and Health Diagnostics Laboratory, Richmond, VA (J.P.M., R.W.). tsaix001@umn.edu.
Abstract
OBJECTIVE: Lipoprotein(a) [Lp(a)] is a risk factor for calcific aortic valve disease (CAVD) but has not been evaluated across multiple races/ethnicities. This study aimed to determine whether Lp(a) cutoff values used in clinical laboratories to assess risk of cardiovascular disease identify subclinical CAVD and its severity and whether significant relations are observed across race/ethnicity. APPROACH AND RESULTS: Lp(a) concentrations were measured using a turbidimetric immunoassay, and subclinical CAVD was measured by quantifying aortic valve calcification (AVC) through computed tomographic scanning in 4678 participants of the Multi-Ethnic Study of Atherosclerosis. Relative risk and ordered logistic regression analysis determined cross-sectional associations of Lp(a) with AVC and its severity, respectively. The conventional 30 mg/dL Lp(a) clinical cutoff was associated with AVC in white (relative risk: 1.56; confidence interval: 1.24-1.96) and was borderline significant (P=0.059) in black study participants (relative risk: 1.55; confidence interval: 0.98-2.44). Whites with levels ≥50 mg/dL also showed higher prevalence of AVC (relative risk: 1.72; confidence interval: 1.36-2.17) than those below this level. Significant associations were observed between Lp(a) and degree of AVC in both white and black individuals. The presence of existing coronary artery calcification did not affect these associations of Lp(a) and CAVD. There were no significant findings in Hispanics or Chinese. CONCLUSIONS: Lp(a) cutoff values that are currently used to assess cardiovascular risk seem to be applicable to CAVD, but our results suggest race/ethnicity may be important in cutoff selection. Further studies are warranted to determine whether race/ethnicity influences Lp(a) and risk of CAVD incidence and its progression.
OBJECTIVE:Lipoprotein(a) [Lp(a)] is a risk factor for calcific aortic valve disease (CAVD) but has not been evaluated across multiple races/ethnicities. This study aimed to determine whether Lp(a) cutoff values used in clinical laboratories to assess risk of cardiovascular disease identify subclinical CAVD and its severity and whether significant relations are observed across race/ethnicity. APPROACH AND RESULTS:Lp(a) concentrations were measured using a turbidimetric immunoassay, and subclinical CAVD was measured by quantifying aortic valve calcification (AVC) through computed tomographic scanning in 4678 participants of the Multi-Ethnic Study of Atherosclerosis. Relative risk and ordered logistic regression analysis determined cross-sectional associations of Lp(a) with AVC and its severity, respectively. The conventional 30 mg/dL Lp(a) clinical cutoff was associated with AVC in white (relative risk: 1.56; confidence interval: 1.24-1.96) and was borderline significant (P=0.059) in black study participants (relative risk: 1.55; confidence interval: 0.98-2.44). Whites with levels ≥50 mg/dL also showed higher prevalence of AVC (relative risk: 1.72; confidence interval: 1.36-2.17) than those below this level. Significant associations were observed between Lp(a) and degree of AVC in both white and black individuals. The presence of existing coronary artery calcification did not affect these associations of Lp(a) and CAVD. There were no significant findings in Hispanics or Chinese. CONCLUSIONS:Lp(a) cutoff values that are currently used to assess cardiovascular risk seem to be applicable to CAVD, but our results suggest race/ethnicity may be important in cutoff selection. Further studies are warranted to determine whether race/ethnicity influences Lp(a) and risk of CAVD incidence and its progression.
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