Blood levels of the biomarker placental growth factor (PlGF) may predict the risk of myocardial infarction or death for patients with coronary heart disease, according to a study in the January 28th issue of The Journal of the American Medical Association.

According to background information in the article, the vascular growth factor acts as a primary inflammatory trigger of instability in atherosclerotic plaques; thus, it may be useful as a risk-predicting biomarker in patients with acute coronary syndromes.

Christopher Heeschen, M.D., and his German colleagues conducted a study to determine whether biomarker levels predict risk for death or nonfatal myocardial infarction in patients with acute chest pain. Various measurements were taken of 547 patients with angiographically validated acute coronary syndrome participating in the CAPTURE (c7E3 Fab Anti-Platelet Therapy in Unstable Refractory Angina) trial and in 626 patients presenting with acute chest pain to a single emergency department between December 1996 and March 1999.

In patients with acute coronary syndrome, elevated growth factor levels indicated a markedly increased risk of myocardial infarction or death at 30 days (14.8 percent versus 4.9 percent; more than 3 times an increase in risk). In patients with acute chest pain, elevated levels of growth factor predicted a 3-fold increased risk of myocardial infarction or death (21.2 percent versus 5.3 percent).

The authors wrote that "... elevated PlGF levels did not only identify those patients with acute chest pain who developed acute coronary syndrome, but also those patients with an increased risk of recurrent instability after hospital discharge."

"In summary, PlGF plasma levels represent a potentially powerful clinical biomarker of vascular inflammation and adverse outcome in patients with acute coronary syndrome. Measuring PlGF levels may extend the predictive and prognostic information gained from traditional inflammatory markers in patients with acute coronary syndrome. Since the proinflammatory effects of PlGF can be specifically inhibited by blocking its receptor, ... these findings may also provide a rationale for a novel anti-inflammatory therapeutic target in patients with coronary artery disease," the authors concluded.