We have known about the presence of inflammation in atheromas, or atherosclerotic plaques, for many years. The triggers of plaque instability may include mechanical rupture of vulnerable plaques or inflammatory activity of the vascular wall. The effects of inflammation in the vascular wall include prothrombotic and vasoconstrictive effects, expression of adhesion molecules for binding of platelets and inflammatory leukocytes, and activation of metalloproteinases, which contribute to endothelial cell detachment, matrix degradation, and plaque disruption. Systemic inflammatory markers in patients with unstable angina include activated lymphocytes, monocytes, and neutrophils, and soluble markers such as C-reactive protein, interleukin-1, and interleukin-6.

However, contrary to the beliefs of many physicians, we have found that the presence of active inflammation appears to be correlated only with unstable angina or acute coronary syndromes, but not with atherosclerosis itself or with myocardial ischemia or necrosis.

One of the best markers of inflammation is C-reactive protein, because of its long half-life. Nevertheless, while levels of C-reactive protein do not correlate with atherosclerosis and ischemia, they do provide an independent prognostic indicator of infarction, even in patients who are troponin-negative. In addition, elevated C-reactive protein levels at the time of discharge from the hospital for unstable angina correlate strongly with lower event free survival at 1 year post-discharge.

The causes of vascular inflammation in these patients is not clear, and there are many possible causes being investigated. These include infectious and non-infectious agents including bacteria, viruses, oxidants, and toxins. There may also be an enhanced inflammatory response to vascular trauma and myocardial necrosis, as well as immunologic stimuli involving modified T lymphocytes. With continuing research, the understanding of the causes of inflammation and its coronary localization may open the way to novel therapeutic strategies.