AIMS: Prospective studies indicate that apolipoprotein measurements predict coronary heart disease (CHD) risk; however, evidence is conflicting, especially in the US. Our aim was to assess whether measurements of apolipoprotein B (apoB) and apolipoprotein A-I (apoA-I) can improve the ability to predict CHD death beyond what is possible based on traditional cardiovascular (CV) risk factors and clinical routine lipid measurements. METHODS AND RESULTS: We analysed prospectively associations of apolipoprotein measurements, traditional CV risk factors, and clinical routine lipid measurements with CHD mortality in a multi-ethnic representative subset of 7594 US adults (mean age 45 years; 3881 men and 3713 women, median follow-up 124 person-months) from the Third National Health and Nutrition Examination Survey mortality study. Multiple Cox-proportional hazards regression was applied. There were 673 CV deaths of which 432 were from CHD. Concentrations of apoB [hazard ratio (HR) 1.98, 95% confidence interval (CI) 1.09-3.61], apoA-I (HR 0.48, 95% CI 0.27-0.85) and total cholesterol (TC) (HR 1.17, 95% CI 1.02-1.34) were significantly related to CHD death, whereas high density lipoprotein cholesterol (HDL-C) (HR 0.68, 95% CI 0.45-1.05) was borderline significant. Both the apoB/apoA-I ratio (HR 2.14, 95% CI 1.11-4.10) and the TC/HDL-C ratio (HR 1.10, 95% CI 1.04-1.16) were related to CHD death. Only apoB (HR 2.01, 95% CI 1.05-3.86) and the apoB/apoA-I ratio (HR 2.09, 95% CI 1.04-4.19) remained significantly associated with CHD death after adjusting for CV risk factors. CONCLUSION: In the US population, apolipoprotein measurements significantly predict CHD death, independently of conventional lipids and other CV risk factors (smoking, dyslipidaemia, hypertension, obesity, diabetes and C-reactive protein). Furthermore, the predictive ability of apoB alone to detect CHD death was better than any of the routine clinical lipid measurements. Inclusion of apolipoprotein measurements in future clinical guidelines should not be discarded.
AIMS: Prospective studies indicate that apolipoprotein measurements predict coronary heart disease (CHD) risk; however, evidence is conflicting, especially in the US. Our aim was to assess whether measurements of apolipoprotein B (apoB) and apolipoprotein A-I (apoA-I) can improve the ability to predict CHD death beyond what is possible based on traditional cardiovascular (CV) risk factors and clinical routine lipid measurements. METHODS AND RESULTS: We analysed prospectively associations of apolipoprotein measurements, traditional CV risk factors, and clinical routine lipid measurements with CHD mortality in a multi-ethnic representative subset of 7594 US adults (mean age 45 years; 3881 men and 3713 women, median follow-up 124 person-months) from the Third National Health and Nutrition Examination Survey mortality study. Multiple Cox-proportional hazards regression was applied. There were 673 CV deaths of which 432 were from CHD. Concentrations of apoB [hazard ratio (HR) 1.98, 95% confidence interval (CI) 1.09-3.61], apoA-I (HR 0.48, 95% CI 0.27-0.85) and total cholesterol (TC) (HR 1.17, 95% CI 1.02-1.34) were significantly related to CHD death, whereas high density lipoprotein cholesterol (HDL-C) (HR 0.68, 95% CI 0.45-1.05) was borderline significant. Both the apoB/apoA-I ratio (HR 2.14, 95% CI 1.11-4.10) and the TC/HDL-C ratio (HR 1.10, 95% CI 1.04-1.16) were related to CHD death. Only apoB (HR 2.01, 95% CI 1.05-3.86) and the apoB/apoA-I ratio (HR 2.09, 95% CI 1.04-4.19) remained significantly associated with CHD death after adjusting for CV risk factors. CONCLUSION: In the US population, apolipoprotein measurements significantly predict CHD death, independently of conventional lipids and other CV risk factors (smoking, dyslipidaemia, hypertension, obesity, diabetes and C-reactive protein). Furthermore, the predictive ability of apoB alone to detect CHD death was better than any of the routine clinical lipid measurements. Inclusion of apolipoprotein measurements in future clinical guidelines should not be discarded.
Authors: John D Brunzell; Michael Davidson; Curt D Furberg; Ronald B Goldberg; Barbara V Howard; James H Stein; Joseph L Witztum Journal: J Am Coll Cardiol Date: 2008-04-15 Impact factor: 24.094
Authors: John D Brunzell; Michael Davidson; Curt D Furberg; Ronald B Goldberg; Barbara V Howard; James H Stein; Joseph L Witztum Journal: Diabetes Care Date: 2008-04 Impact factor: 19.112
Authors: Abel Romero-Corral; Victor M Montori; Virend K Somers; Josef Korinek; Randal J Thomas; Thomas G Allison; Farouk Mookadam; Francisco Lopez-Jimenez Journal: Lancet Date: 2006-08-19 Impact factor: 79.321
Authors: Oemer-Necmi Goek; Anna Köttgen; Ron C Hoogeveen; Christie M Ballantyne; Josef Coresh; Brad C Astor Journal: Nephrol Dial Transplant Date: 2012-01-28 Impact factor: 5.992
Authors: Heidi T May; John R Nelson; Seth T Lirette; Krishnaji R Kulkarni; Jeffrey L Anderson; Michael E Griswold; Benjamin D Horne; Adolfo Correa; Joseph B Muhlestein Journal: Eur J Prev Cardiol Date: 2015-10-19 Impact factor: 7.804
Authors: Brian T Steffen; Weihua Guan; Alan T Remaley; James H Stein; Mathew C Tattersall; Joel Kaufman; Michael Y Tsai Journal: J Clin Lipidol Date: 2017-07-12 Impact factor: 4.766
Authors: Chandra A Reynolds; Margaret Gatz; Jonathan A Prince; Stig Berg; Nancy L Pedersen Journal: J Am Geriatr Soc Date: 2010-03 Impact factor: 5.562
Authors: Paramjit K Sandhu; Salma M A Musaad; Alan T Remaley; Stephanie S Buehler; Sonya Strider; James H Derzon; Hubert W Vesper; Anne Ranne; Colleen S Shaw; Robert H Christenson Journal: J Appl Lab Med Date: 2016-08-01
Authors: M V Papavasileiou; A G Karamanou; P Kalogeropoulos; G Moustakas; S Patsianis; A Pittaras Journal: J Hum Hypertens Date: 2015-07-02 Impact factor: 3.012