BACKGROUND: Increased lipoprotein(a) [Lp(a)] concentrations are predictive for coronary artery disease (CAD). The risk conferred by Lp(a) for other types of vascular disease compared with CAD has not been investigated within a single population. This study aimed to investigate Lp(a) risk association for 4 different types of vascular disease (including CAD) within a predominantly white population. METHODS: We used an Lp(a) ELISA that measures Lp(a) independently of apolipoprotein(a) size to measure plasma Lp(a) in patients [384 CAD, 262 peripheral vascular disease, 184 ischemic stroke (stroke), 425 abdominal aortic aneurysm] and 230 disease-free controls. We then conducted association studies with logistic regression, integrating the potential confounding effects of age, sex, diabetes, plasma lipids, and a history of previous hypertension, hypercholesterolemia, and smoking. RESULTS: Multivariate analyses with Lp(a) concentrations of >45 nmol/L (the 75th percentile value for controls) as the clinical cutoff showed increased Lp(a) concentrations to be a risk factor for all disease groups, with adjusted odds ratios ranging from 1.96 [95% confidence interval (CI) 1.24-3.08] for CAD to 2.33 (95% CI 1.39-3.89) for PVD. The risk conferred by Lp(a) appeared to be independent of other confounders, including exposure to statin/fibrate therapies. Similar odds ratios and CIs between disease groups indicated that increased Lp(a) conferred a similar risk for all groups studied. CONCLUSIONS: Lp(a) constitutes a stable risk factor of similar magnitude for 4 major forms of vascular disease. This association was not altered by exposure to standard lipid-lowering therapy.
BACKGROUND: Increased lipoprotein(a) [Lp(a)] concentrations are predictive for coronary artery disease (CAD). The risk conferred by Lp(a) for other types of vascular disease compared with CAD has not been investigated within a single population. This study aimed to investigate Lp(a) risk association for 4 different types of vascular disease (including CAD) within a predominantly white population. METHODS: We used an Lp(a) ELISA that measures Lp(a) independently of apolipoprotein(a) size to measure plasma Lp(a) in patients [384 CAD, 262 peripheral vascular disease, 184 ischemic stroke (stroke), 425 abdominal aortic aneurysm] and 230 disease-free controls. We then conducted association studies with logistic regression, integrating the potential confounding effects of age, sex, diabetes, plasma lipids, and a history of previous hypertension, hypercholesterolemia, and smoking. RESULTS: Multivariate analyses with Lp(a) concentrations of >45 nmol/L (the 75th percentile value for controls) as the clinical cutoff showed increased Lp(a) concentrations to be a risk factor for all disease groups, with adjusted odds ratios ranging from 1.96 [95% confidence interval (CI) 1.24-3.08] for CAD to 2.33 (95% CI 1.39-3.89) for PVD. The risk conferred by Lp(a) appeared to be independent of other confounders, including exposure to statin/fibrate therapies. Similar odds ratios and CIs between disease groups indicated that increased Lp(a) conferred a similar risk for all groups studied. CONCLUSIONS:Lp(a) constitutes a stable risk factor of similar magnitude for 4 major forms of vascular disease. This association was not altered by exposure to standard lipid-lowering therapy.
Authors: Monica L Bertoia; Jennifer K Pai; Jun-Hee Lee; Adam Taleb; Michel M Joosten; Murray A Mittleman; Xiaohong Yang; Joseph L Witztum; Eric B Rimm; Sotirios Tsimikas; Kenneth J Mukamal Journal: J Am Coll Cardiol Date: 2013-03-26 Impact factor: 24.094
Authors: Gregory T Jones; Andrew R Thompson; Frank M van Bockxmeer; Hany Hafez; Jackie A Cooper; Jonathan Golledge; Stephen E Humphries; Paul E Norman; Andre M van Rij Journal: Arterioscler Thromb Vasc Biol Date: 2008-01-31 Impact factor: 8.311
Authors: Gregory T Jones; Judith Marsman; Basharat Bhat; Victoria L Phillips; Aniruddha Chatterjee; Euan J Rodger; Michael J A Williams; André M van Rij; Sally P A McCormick Journal: Epigenetics Date: 2020-04-01 Impact factor: 4.528