Weihua Guan1, Jing Cao1, Brian T Steffen1, Wendy S Post1, James H Stein1, Mathew C Tattersall1, Joel D Kaufman1, Joseph P McConnell1, Daniel M Hoefner1, Russell Warnick1, Michael Y Tsai2. 1. From the Division of Biostatistics, School of Public Health (W.G.) and Department of Laboratory Medicine and Pathology (J.C., B.T.S., M.Y.T.), University of Minnesota, Minneapolis; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD (W.S.P.); Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison (J.H.S., M.C.T.); Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle (J.D.K.); and Health Diagnostics Laboratory, Richmond, VA (J.P.M., D.M.H., R.W.). 2. From the Division of Biostatistics, School of Public Health (W.G.) and Department of Laboratory Medicine and Pathology (J.C., B.T.S., M.Y.T.), University of Minnesota, Minneapolis; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD (W.S.P.); Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison (J.H.S., M.C.T.); Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle (J.D.K.); and Health Diagnostics Laboratory, Richmond, VA (J.P.M., D.M.H., R.W.). tsaix001@umn.edu.
Abstract
OBJECTIVE: We aimed to examine associations of lipoprotein(a) (Lp(a)) concentrations with coronary heart disease (CHD) and determine whether current Lp(a) clinical laboratory cut points identify risk of disease incidence in 4 races/ethnicities of the Multi-Ethnic Study of Atherosclerosis (MESA). APPROACH AND RESULTS: A subcohort of 1323 black, 1677 white, 548 Chinese American, and 1044 Hispanic MESA participants were followed up during a mean 8.5-year period in which 235 incident CHD events were recorded. Lp(a) mass concentrations were measured using a turbidimetric immunoassay. Cox regression analysis determined associations of Lp(a) with CHD risk with adjustments for lipid and nonlipid variables. Lp(a) concentrations were continuously associated with risk of CHD incidence in black (hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.09-2.04] and white participants (HR, 1.22; 95% CI, 1.02-1.45). Examining Lp(a) risk by the 50 mg/dL cut point revealed higher risks of incident CHD in all races except Chinese Americans: blacks (HR, 1.69; 95% CI, 1.03-2.76), whites (HR, 1.82; 95% CI, 1.15-2.88); Hispanics (HR, 2.37; 95% CI, 1.17-4.78). The lower Lp(a) cut point of 30 mg/dL identified higher risk of CHD in black participants alone (HR, 1.87; 95% CI, 1.08-3.21). CONCLUSIONS: Our findings suggest that the 30 mg/dL cutoff for Lp(a) is not appropriate in white and Hispanic individuals, and the higher 50 mg/dL cutoff should be considered. In contrast, the 30 mg/dL cutoff remains suitable in black individuals. Further research is necessary to develop the most clinically useful Lp(a) cutoff values in individual races/ethnicities.
OBJECTIVE: We aimed to examine associations of lipoprotein(a) (Lp(a)) concentrations with coronary heart disease (CHD) and determine whether current Lp(a) clinical laboratory cut points identify risk of disease incidence in 4 races/ethnicities of the Multi-Ethnic Study of Atherosclerosis (MESA). APPROACH AND RESULTS: A subcohort of 1323 black, 1677 white, 548 Chinese American, and 1044 Hispanic MESAparticipants were followed up during a mean 8.5-year period in which 235 incident CHD events were recorded. Lp(a) mass concentrations were measured using a turbidimetric immunoassay. Cox regression analysis determined associations of Lp(a) with CHD risk with adjustments for lipid and nonlipid variables. Lp(a) concentrations were continuously associated with risk of CHD incidence in black (hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.09-2.04] and white participants (HR, 1.22; 95% CI, 1.02-1.45). Examining Lp(a) risk by the 50 mg/dL cut point revealed higher risks of incident CHD in all races except Chinese Americans: blacks (HR, 1.69; 95% CI, 1.03-2.76), whites (HR, 1.82; 95% CI, 1.15-2.88); Hispanics (HR, 2.37; 95% CI, 1.17-4.78). The lower Lp(a) cut point of 30 mg/dL identified higher risk of CHD in black participants alone (HR, 1.87; 95% CI, 1.08-3.21). CONCLUSIONS: Our findings suggest that the 30 mg/dL cutoff for Lp(a) is not appropriate in white and Hispanic individuals, and the higher 50 mg/dL cutoff should be considered. In contrast, the 30 mg/dL cutoff remains suitable in black individuals. Further research is necessary to develop the most clinically useful Lp(a) cutoff values in individual races/ethnicities.
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