USED TO GAUGE a patient's risk of coronory heart disease (CHD) and stroke, the PLAC test measures lipoprotein-associated phospholipase A2 (Lp-PLA2) levels in the blood. A cardiovascular-specific inflammatory enzyme, Lp-PLA2resides mainly on low-density lipoprotein (LDL) cholesterol and contributes to the formation of atherosclerotic plaque that's vulnerable to rupture.
According to the Atherosclerosis Risk in Communities study, elevated blood Lp-PLA2 levels can provide early evidence of risk even when blood LDL levels are normal (less than 130 mg/dL). This study found an elevation of Lp-PLA2 to be independently associated with CHD, even after adjustment for traditional risk factors and C-reactive protein (CRP).
Arterial plaque is thought to result largely from an inflammatory process. At areas of disruption to the intima, LDL and Lp-PLA2 enter the intima, where LDL is oxidized and Lp-PLA2 triggers proinflammatory and proatherogenic activities. Monocytes then enter the intima, mature into macrophages, engulf the LDL, and develop into foam cells that form plaque with a fibrous cap. Over time, the macrophages secrete substances that cause the cap to thin, threatening rupture and clot formation.
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