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Lipids, Lipoproteins, and Cardiovascular Risk Factors |
1 Department of Pathology and Laboratory Medicine and
2 Department of Medicine–Cardiology Unit, University of Rochester School of Medicine and Dentistry, Rochester, NY.
3 Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, TX.
aAddress correspondence to this author at: Department of Pathology and Laboratory Medicine, Box 608, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642. Fax 585-273y3003; e-mail James_Corsetti{at}urmc.rochester.edu.
Background: Recent studies demonstrate that lipoprotein-associated phospholipase A2 (Lp-PLA2) is a risk factor for cardiovascular disease presumably deriving from generation of proinflammatory and proatherogenic species through its hydrolytic activity on lipoprotein-associated phospholipids. The goal of this study was to assess the relationship of Lp-PLA2 with a set of thrombogenic, lipid, inflammatory, and metabolic blood markers and to determine whether plasma Lp-PLA2 is a risk factor for recurrent coronary events in postinfarction patients.
Methods: Factor analysis on the set of blood markers and Lp-PLA2 was performed for 766 patients of the Thrombogenic Factors and Recurrent Coronary Events (THROMBO) postinfarction study. Recurrent coronary event risk was assessed as a function of blood marker concentrations and Lp-PLA2 by Cox proportional hazards multivariable regression adjusted for significant clinical covariates.
Results: Factor analysis revealed that Lp-PLA2 was associated with one factor dominated by cholesterol and apolipoprotein B and another factor dominated by HDL-cholesterol and triglycerides, with little association with an inflammatory factor dominated by C-reactive protein. Multivariable analysis demonstrated as significant and independent predictors of risk of secondary coronary events only apolipoprotein B in a model without Lp-PLA2 (hazard ratio, 1.66; 95% confidence interval, 1.14–2.40) and only Lp-PLA2 in a model with Lp-PLA2 included [1.90 (1.31–2.75)].
Conclusions: Lp-PLA2 is a significant and independent predictor of risk for recurrent coronary events in postinfarction patients, and Lp-PLA2 is related to both hypercholesterolemia and high triglyceride–low HDL dyslipidemia in this study population.
The following articles in journals at HighWire Press have cited this article:
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  S. Tsimikas, J. Willeit, M. Knoflach, M. Mayr, G. Egger, M. Notdurfter, J. L. Witztum, C. J. Wiedermann, Q. Xu, and S. Kiechl Lipoprotein-associated phospholipase A2 activity, ferritin levels, metabolic syndrome, and 10-year cardiovascular and non-cardiovascular mortality: results from the Bruneck study Eur. Heart J., January 1, 2009; 30(1): 107 - 115. [Abstract] [Full Text] [PDF]
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 J. P. Corsetti, D. Ryan, A. J. Moss, D. L. Rainwater, W. Zareba, and C. E. Sparks Plasminogen Activator Inhibitor-1 Polymorphism (4G/5G) Predicts Recurrence in Nonhyperlipidemic Postinfarction Patients Arterioscler Thromb Vasc Biol, March 1, 2008; 28(3): 548 - 554. [Abstract] [Full Text] [PDF]
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M. S. Sabatine, D. A. Morrow, M. O'Donoghue, K. A. Jablonksi, M. M. Rice, S. Solomon, Y. Rosenberg, M. J. Domanski, J. Hsia, and for the PEACE Investigators Prognostic Utility of Lipoprotein-Associated Phospholipase A2 for Cardiovascular Outcomes in Patients With Stable Coronary Artery Disease Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2463 - 2469. [Abstract] [Full Text] [PDF]
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N. S. Jenny Lipoprotein-associated phospholipase A2: novel biomarker and causal mediator of atherosclerosis? Arterioscler Thromb Vasc Biol, November 1, 2006; 26(11): 2417 - 2418. [Full Text] [PDF]
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F. D. Kolodgie, A. P. Burke, K. S. Skorija, E. Ladich, R. Kutys, A. T. Makuria, and R. Virmani Lipoprotein-Associated Phospholipase A2 Protein Expression in the Natural Progression of Human Coronary Atherosclerosis Arterioscler Thromb Vasc Biol, November 1, 2006; 26(11): 2523 - 2529. [Abstract] [Full Text] [PDF]
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 A. Zalewski, J. J. Nelson, L. Hegg, and C. Macphee Lp-PLA2: A New Kid on the Block Clin. Chem., September 1, 2006; 52(9): 1645 - 1650. [Abstract] [Full Text] [PDF]
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