PLAC Science
CHD Facts
Approximately 15.5 million Americans ≥20 years of age have CHD.1
| Condition | Total/year | Males/year | Females/year |
|---|---|---|---|
| Coronorary heart disease (CHD) | 15,500,000 | 8,900,000 | 6,600,000 |
| CHD deaths | 375,295 | 206,908 | 168,387 |
| Heart attack, new and and recurrent (>35 y) | 735,000 | 430,000 | 305,000 |
| Heart attack deaths | 119,905 | 66,765 | 53,140 |
- 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