Biochemist Alexei A. Bogdanov, Jr., Ph.D., and colleagues at Massachusetts General Hospital and Harvard Medical School are using a cell-culture model and magnetic resonance imaging (MRI) to develop their non-invasive method. They aim to detect and trace elevated levels of an enzyme that other research groups have linked to plaque instability and cardiac risk.
Bogdanov emphasizes much work remains before the technique could reach the clinic. However, results to date are so encouraging that he presented them today at the 228th national meeting of the American Chemical Society, the worlds largest scientific society.
If doctors have early warning that a particular plaque is unstable, they may be able to prioritize or target their patients treatment to that artery, perhaps averting an attack or at least minimizing its damage.
When a plaque ruptures, it exposes a surface that is thrombogenic, or clot-inducing, Bogdanov explains. So instead of a partial blockage of the artery, a complete blockage can develop. That leads to oxygen deprivation in surrounding tissue and then, depending on location, either heart attack or stroke.
The chemical sequence of events is still unclear, but at the root appears to be myeloperoxidase (MPO), an enzyme secreted by white blood cells infectious bacteria.
But studies have found MPO seems to exert another, unwanted effect in arterial plaques.
A breakdown product of MPO triggers the release of an enzyme that degrades the fibrous cap surrounding a plaque, says Bogdanov. Rupture occurs when the cap gets too thin.
Research published in the New England Journal of Medicine last year found that patients