Optical coherence tomography for imaging the vulnerable plaque

Acute myocardial infarction (AMI) is a leading cause of death in the United States and industrialized countries.^{1, 2} Research conducted over the past 15 years has demonstrated that several types of minimally or modestly stenotic atherosclerotic plaques, termed vulnerable plaques, are precursors to coronary thrombosis, myocardial ischemia, and sudden cardiac death. Postmortem studies have identified one type of vulnerable plaque, the thin-cap fibroatheroma (TCFA), as the culprit lesion in approximately 80% of sudden cardiac deaths. ^{3, 4, 5, 6, 7} Over 90% of TCFAs are found within the most proximal $5.0\mathrm{cm}$ segment of each of the main coronary arteries [left anterior descending (LAD); left circumflex (LCx); and right coronary artery (RCA)].^{3, 5} The TCFA is typically a minimally occlusive plaque characterized histologically by the following features: (1) thin fibrous cap $(<65\mathrm{\mu }\mathrm{m})$ , (2) large lipid pool, and (3) activated macrophages near or within the fibrous cap. ^{3, 5, 7, 8, 9} It is hypothesized that these features predispose TCFAs to rupture in response to biomechanical stresses.^{10, 11} Following rupture and the release of procoagulant proteins, such as tissue factor, a substrate for thrombus formation is created, leading to an acute coronary event.^{12, 13} While TCFAs are associated with the majority of AMIs, recent autopsy studies have shown that coronary plaques with erosions or superficial calcified nodules may also precipitate thrombosis and sudden occlusion of a coronary artery. ^{3, 5, 14, 15}