According to background information in the article, PlGF, a member of the vascular growth factor family, acts as a primary inflammatory instigator of atherosclerotic (hardening and narrowing of the arteries) plaque instability and thus may be useful as a risk-predicting biomarker in patients with acute coronary syndromes (ACS).
Christopher Heeschen, M.D., of Johann Wolfgang Goethe University, Frankfurt, Germany and colleagues conducted a study to determine whether blood levels of PlGF predict risk for death or nonfatal heart attack in patients with acute chest pain. Various measurements were taken of 547 patients with angiographically validated ACS participating in the CAPTURE (c7E3 Fab Anti-Platelet Therapy in Unstable Refractory Angina) trial and in a cohort of 626 patients presenting with acute chest pain to an emergency department in Germany between December 1996 and March 1999.
In patients with ACS, elevated PlGF levels indicated a markedly increased risk of heart attack or death at 30 days (14.8 percent vs. 4.9 percent; more than three times increased risk). In patients with acute chest pain, elevated levels of PlGF predicted three fold increased risk of heart attack or death (21.2 percent vs. 5.3 percent).
The authors write that "... elevated PlGF levels did not only identify those patients with acute chest pain who developed ACS, 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 ACS. Measuring PlGF levels may extend the predictive and prognostic information gained from traditional inflammatory markers in patients with ACS. 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 conclude. (JAMA. 2004;291:435-441. Available post-embargo at JAMA.com)
Editor's Note: This study was entirely financed from sources at the Johann Wolfgang Goethe University.