Fasting Compared With Nonfasting Lipids and Apolipoproteins for Predicting Incident Cardiovascular Events . Circulation on line first
Samia Mora MD, MHS*, Nader Rifai PhD, Julie E. Buring ScD, and Paul M Ridker MD, MPH
From the Donald W. Reynolds Center for Cardiovascular Research (S.M., J.E.B., P.M.R.), Leducq Center for Molecular and Genetic Epidemiology (S.M., P.M.R.), and Center for Cardiovascular Disease Prevention (S.M., P.M.R.), Division of Preventive Medicine (S.M., J.E.B., P.M.R.), and Division of Cardiovascular Medicine (S.M., P.M.R.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; Department of Epidemiology, Harvard School of Public Health, Boston, Mass (J.E.B., P.M.R.); and Department of Laboratory Medicine, Children's Hospital and Harvard Medical School, Boston, Mass (N.R.).
* To whom correspondence should be addressed. E-mail: smora@partners.org
Background—Although guidelines recommend measuring fasting lipids for initial screening of adults without cardiovascular disease (CVD), recent studies suggest that nonfasting triglycerides may be superior to fasting. Whether fasting status alters associations of nontriglyceride lipids with CVD is unclear.
Methods and Results—In a prospective study of 26 330 healthy women (19 983 fasting; 6347 nonfasting), associations of baseline lipids with incident CVD (754 fasting; 207 nonfasting) were examined over an 11-year follow-up. Except for triglycerides, lipid concentrations differed minimally (<5%) for fasting versus nonfasting. However, stronger associations with CVD were noted for fasting total cholesterol (adjusted fasting hazard ratio [HR], 1.22 per 1-SD increment; 95% CI, 1.14 to 1.30; nonfasting HR, 1.07; 95% CI, 0.93 to 1.21), low-density lipoprotein (LDL) cholesterol (fasting HR, 1.21; 95% CI, 1.13 to 1.29; nonfasting HR, 1.00; 95% CI, 0.87 to 1.15), apolipoprotein B-100 (fasting HR, 1.36; 95% CI, 1.27 to 1.45; nonfasting HR, 1.20; 95% CI, 1.05 to 1.36), non–high-density lipoprotein (HDL) cholesterol (fasting HR, 1.29; 95% CI, 1.21 to 1.38; nonfasting HR, 1.15; 95% CI, 1.01 to 1.31), and apolipoprotein B-100/A-1 ratio (fasting HR, 1.39; 95% CI, 1.30 to 1.48; nonfasting HR, 1.18; 95% CI, 1.09 to 1.27). Compared with fasting levels, nonfasting HDL cholesterol, apolipoprotein A-1, and total/HDL cholesterol ratio had similar associations, and triglycerides had a stronger association, with CVD. Significant interactions were seen for LDL cholesterol and apolipoprotein B-100/A-1 ratio with fasting status (P for interaction=0.03 and <0.001, respectively).
Conclusions—This study demonstrates that HDL cholesterol, triglycerides, total/HDL cholesterol ratio, and apolipoprotein A-1 predict CVD when measured nonfasting. By contrast, total, LDL, and non-HDL cholesterol, in addition to apolipoprotein B-100 and B-100/A-1 ratio, provide less useful CVD risk information when nonfasting, despite small changes in their concentrations. Guidelines for lipid screening may need to consider these differences.
From the Donald W. Reynolds Center for Cardiovascular Research (S.M., J.E.B., P.M.R.), Leducq Center for Molecular and Genetic Epidemiology (S.M., P.M.R.), and Center for Cardiovascular Disease Prevention (S.M., P.M.R.), Division of Preventive Medicine (S.M., J.E.B., P.M.R.), and Division of Cardiovascular Medicine (S.M., P.M.R.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; Department of Epidemiology, Harvard School of Public Health, Boston, Mass (J.E.B., P.M.R.); and Department of Laboratory Medicine, Children's Hospital and Harvard Medical School, Boston, Mass (N.R.).
* To whom correspondence should be addressed. E-mail: smora@partners.org
Background—Although guidelines recommend measuring fasting lipids for initial screening of adults without cardiovascular disease (CVD), recent studies suggest that nonfasting triglycerides may be superior to fasting. Whether fasting status alters associations of nontriglyceride lipids with CVD is unclear.
Methods and Results—In a prospective study of 26 330 healthy women (19 983 fasting; 6347 nonfasting), associations of baseline lipids with incident CVD (754 fasting; 207 nonfasting) were examined over an 11-year follow-up. Except for triglycerides, lipid concentrations differed minimally (<5%) for fasting versus nonfasting. However, stronger associations with CVD were noted for fasting total cholesterol (adjusted fasting hazard ratio [HR], 1.22 per 1-SD increment; 95% CI, 1.14 to 1.30; nonfasting HR, 1.07; 95% CI, 0.93 to 1.21), low-density lipoprotein (LDL) cholesterol (fasting HR, 1.21; 95% CI, 1.13 to 1.29; nonfasting HR, 1.00; 95% CI, 0.87 to 1.15), apolipoprotein B-100 (fasting HR, 1.36; 95% CI, 1.27 to 1.45; nonfasting HR, 1.20; 95% CI, 1.05 to 1.36), non–high-density lipoprotein (HDL) cholesterol (fasting HR, 1.29; 95% CI, 1.21 to 1.38; nonfasting HR, 1.15; 95% CI, 1.01 to 1.31), and apolipoprotein B-100/A-1 ratio (fasting HR, 1.39; 95% CI, 1.30 to 1.48; nonfasting HR, 1.18; 95% CI, 1.09 to 1.27). Compared with fasting levels, nonfasting HDL cholesterol, apolipoprotein A-1, and total/HDL cholesterol ratio had similar associations, and triglycerides had a stronger association, with CVD. Significant interactions were seen for LDL cholesterol and apolipoprotein B-100/A-1 ratio with fasting status (P for interaction=0.03 and <0.001, respectively).
Conclusions—This study demonstrates that HDL cholesterol, triglycerides, total/HDL cholesterol ratio, and apolipoprotein A-1 predict CVD when measured nonfasting. By contrast, total, LDL, and non-HDL cholesterol, in addition to apolipoprotein B-100 and B-100/A-1 ratio, provide less useful CVD risk information when nonfasting, despite small changes in their concentrations. Guidelines for lipid screening may need to consider these differences.
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