PLAC Science

CHD Facts

Approximately 15.5 million Americans ≥20 years of age have CHD.1

Coronorary heart disease (CHD)15,500,0008,900,0006,600,000
CHD deaths375,295206,908168,387
Heart attack, new and and recurrent (>35 y)735,000430,000305,000
Heart attack deaths119,90566,76553,140
  • 1 of every 7 deaths in the US is attributed to CHD1
  • Each year, an estimated 635,000 Americans will have a new coronary event (hospitalization for heart attack or heart attack-related death)1
  • Every 43 seconds, an American will suffer a heart attack1
  • Every 1 minute and 24 seconds, an American will die from a heart attack1
  • Patients with low and moderate CHD risk still have a significant risk for events over 10 years2
  • 50% of myocardial infarctions occur in individuals with normal low-density lipoprotein (LDL)3
  • 44% of the decrease in rates of CHD events from 1980 to 2000 has been attributed to changes in risk factors1,4

Basic science of Lp-PLA2

  • The PLAC® Test for Lp-PLA2 Activity identifies the atherosclerotic disease process and is the only FDA-cleared blood test that measures the activity of Lp-PLA2, a vascular-specific inflammatory marker critical in the formation of rupture-prone plaque5
  • Lp-PLA is a calcium-independent phospholipase A2 enzyme that is associated with both low-density lipoprotein (LDL) and, to a lesser extent, high-density lipoprotein (HDL) in human plasma and serum6
  • Lp-PLA2 is distinct from other phospholipases such as cPLA2 and sPLA27,8
  • Lp-PLA2 is produced by macrophages and other inflammatory cells and is expressed in greater concentrations in advanced atherosclerotic lesions than in early-stage lesions5,9
  • Evidence suggests that oxidation of LDL plays a critical role in the development and progression of atherosclerosis10,11
  • Lp-PLA2 participates in the breakdown of oxidized LDL in the vascular wall by hydrolyzing the oxidized phospholipid, producing lysophosphatidylcholine and oxidized free fatty acids, both of which are potent pro-inflammatory products that contribute to the formation of atherosclerotic plaques12-14
  • Lp-PLA2 has demonstrated modest intra- and interindividual variation, commensurate with other cardiovascular lipid markers and substantially less variability than high-sensitivity C-reactive protein (hs-CRP)15-18
  • Lp-PLA2 is not elevated in systemic inflammatory conditions, has relatively small biological variation, and may be a more specific marker of vascular inflammation19-21

Lp-PLA2 Mechanism of Action