Large contemporary natural history studies such as Lipid Rich Plaque 5 and PROSPECT 6 have demonstrated that plaque burden is a stronger predictor than plaque composition. As such, it is unable to depict one of the best-known and proven predictors of major adverse cardiovascular events. As mentioned, an inherent limitation with OCT is the fact that the technology is unable to penetrate deep enough to visualize the vessel wall. Plaque burden has been identified as the pinnacle of the triple ‘LLL’ ( Large plaque burden, Lipid rich, and small Lumen area) trifecta used to illustrate three major characteristics associated with poor clinical cardiovascular outcomes in follow-up. Conversely, one can think of using coronary computed tomography angiography, which allows a complete assessment of the coronary tree and is not invasive. This very low percentage of ‘vulnerable plaques’ and the inability to image the entire coronary tree with intravascular imaging puts into question this approach in the quest of high-risk plaques. This means that of the 1909 lipidic plaques, 27 (1.4%) were lipid-rich with a thin-cap and resulted in ACS as defined by the authors. Furthermore, among the 1909 lipidic plaques that were imaged, only 567 (30%) were characterized as lipid-rich, 163 (9%) as TCFA, and 83 (4%) as both LRP and TCFA. When only 129 (9%) ACS events occurred in total, 15 non-imaged lesions encompass a substantial percentage of the total (over 11% of subsequent ACS events were not characterized by OCT at all). As mentioned in the article, 15 ACS events did in fact arise from coronary segments not imaged by baseline OCT. Non-culprit plaques are not limited to one vessel in particular, and thus, it could be easily suggested that many relevant lesions were not imaged at all. In most patients (61%), single-vessel OCT was the full extent of analysis. study, triple-vessel OCT was conducted in only 11% of patients. The success of OCT in predicting ACS events from non-culprit plaques relies not only on its ability to detect lipid plaque but also the need for imaging of the entire coronary tree. 3, 4 The adaptation seems promising, as maximum lipid arc has produced high area under the curve statistics for high-risk plaque identification, but is it valid when compared to other possible criteria to define high-risk plaques such as plaque burden? In fact, studies have not agreed on a lipid arc value of the highest sensitivity and specificity, with definitions varying between 80° and 180°. Hence, if you restrict your identification of ‘vulnerable plaque’ to a certain arc degree, OCT’s performance as a diagnostic tool may be suboptimal. Therefore, the arc may not be a good surrogate of the actual lipid pool area. For example, a 180° arc and a shallow lipid pool may result in a smaller area than a 90° arc and thick lipid pool. The former is assumed to fairly represent the extent of lipid however, this is not true in most of the cases. focus on two entrance criteria for high-risk plaque detection with OCT: arc of lipid (>180°) and thin cap fibroatheroma (TCFA). However, OCT faces an inherent limitation because the infrared light is attenuated and unable to penetrate lipid deep enough to fully illustrate lipid-rich plaque down to the vessel wall therefore, clinicians are forced to adapt the vulnerable-plaque characteristics identified by OCT. 2 Clearly, identifying the lipid area of a plaque is central to OCT’s potential success. Uniquely, this retrospective study attempts to correlate non-culprit lesions imaged by OCT with the risk of subsequent lesion-specific acute coronary syndrome (ACS) events.Īutopsy studies have identified several well-known histological characteristics central to vulnerable plaque identification, including a large lipid pool (comprising >10% of the plaque area) and a thin fibrous cap. 1 aim to demonstrate the ability of optical coherence tomography (OCT) to identify in vivo high-risk plaques in patients undergoing percutaneous coronary intervention. This editorial refers to ‘Optical coherence tomography detection of vulnerable plaques at high risk of developing acute coronary syndrome’ by T.
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