Focal Geometry and Characteristics of Erosion-Prone Coronary Plaques in vivo Angiography and Optical Coherence Tomography Study

Abstract

Objective: This study compared focal geometry and characteristics of culprit plaque erosion (PE) vs. non-culprit plaques in ST-segment elevated myocardial infarction (STEMI) patients in whom optical coherence tomography (OCT) identified PE as the cause of the acute event. Background: Culprit PE is a distinct clinical entity with specific coronary risk factors and its own tailored management strategy. However, not all plaques develop erosion resulting in occlusive thrombus formation. Methods: Between January 2017 and July 2019, there were 484 STEMI patients in whom OCT at the time of primary percutaneous intervention identified culprit lesion PE to be the cause of the event; 484 culprit PE were compared to 1,132 non-culprit plaques within 1,196 imaged vessels. Results: Culprit PE were highly populated at "hot spots" within the proximal 40 mm in the left anterior descending artery (LAD) and tended to cluster proximal to a nearby bifurcation mainly in the LAD. Minimal lumen area (MLA) <2.51 mm² and AS (area stenosis) >64.02% discriminated culprit PE from non-culprit plaques. In the multivariable analysis, focal geometry (LAD location, distance from coronary ostium <40 mm, and location proximal to a nearby bifurcation), luminal narrowing (MLA <2.51 mm², AS > 64.02%), and TCFA phenotype were independent predictors of culprit PE overall. Cholesterol crystals were predictive of culprit PE with underlying LRP morphology while the absence of calcification and microchannels were risk factors for culprit PE with an underlying non-LRP. Similarities and differences in predictors of culprit PE were found between males and females; distance from coronary ostium <40 mm, MLA <2.51 mm², TCFA, and less spotty calcium were risk factors of culprit PE in males, but not in females while smaller RVD was associated with culprit PE only in females. Conclusions: Irrespective of underlying lesion substrates and patient risk factors, there are lesion-specific and OCT-identifiable predictors of developing culprit PE in erosion-prone vulnerable patients.

Keywords: acute coronary syndrome; erosion-prone plaque; optical coherence tomography; plaque erosion; predictors.

Figure 1

Location and longitudinal distribution of culprit PE and non-culprit plaques in STEMI patients with culprit plaque erosion. (A) Culprit PE in STEMI patients were mainly in the LAD, followed by RCA and LCX. Non-culprit plaques were evenly distributed in the RCA and LAD, followed by the LCX. The number of lesions and cumulative frequency of culprit PE and non-culprit plaques every 10 mm axial distance from the ostium of the LAD (B), LCX (C), and RCA (D) were shown. 93.8% of culprit eroded plaques in the LAD were within the proximal 40 mm of the artery. Among all plaques (culprit and non-culprit) within the proximal 40 mm of the LAD, over half represented culprit plaque erosions that were responsible for the acute event. LAD, left anterior descending artery; LCX, left circumflex artery; PE, plaque erosion; RCA, right coronary artery.

Figure 2

The distribution of culprit PE and non-culprit plaques near a bifurcation. (A) 60.5% culprit PE and 59.5% non-culprit plaques were located near a bifurcation. (B) Among them, culprit PE were mainly located in the LAD (70.3%) and most of them (61.1%) clustered proximal to a nearby bifurcation. On the contrary, most non-culprit plaques (68.8%) clustered distal to a nearby bifurcation. (C) Distance from culprit PE or the non-culprit plaque to the nearby bifurcation was shown. LAD, left anterior descending artery; LCX, left circumflex artery; PE, plaque erosion; RCA, right coronary artery.

Figure 3

ROC curves of MLA and AS for differentiating culprit PE from non-culprit plaques. The optimal cut-off value of MLA was 2.51 mm² (AUC = 0.766) (A) and the prediction probability was 76.4% for culprit PE (B). The optimal cut-off value of AS was 64.02% (AUC = 0.833) (C) and the prediction probability was 77.7% for culprit PE (D). AS, area stenosis; AUC, area under the curve; CI, confidence interval; MLA, minimal lumen area; PE, plaque erosion; ROC, receiver operating characteristic.

Figure 4

Predictors for culprit PE in overall cohort of 484 patients. Odds ratios for the presence of culprit PE overall (A), in LRPs (B), and in non-LRPs (C) according to LAD location, distance from the coronary ostium <40 mm, proximal to a nearby bifurcation, MLA <2.51 mm², AS > 64.02%, TCFA, presence of cholesterol crystals, calcification and microchannels. AS, area stenosis; CI, confidence interval; LAD, left anterior descending artery; LRP, lipid-rich plaque; MLA, minimal lumen area; OR, odds ratio; PE, plaque erosion; TCFA, thin-cap fibroatheroma.

Figure 5

Subgroup analyses of predictors for culprit PE in patients according to sex. Odd ratios for the presence of culprit PE in female (A) and male (B) according to LAD location, distance from the coronary ostium <40 mm, proximal to a nearby bifurcation, MLA <2.51 mm², AS >64.02%, RVD, TCFA and spotty calcium. AS, area stenosis; CI, confidence interval; LAD, left anterior descending artery; MLA, minimal lumen area; OR, odds ratio; PE, plaque erosion; RVD, reference vessel diameter; TCFA, thin-cap fibroatheroma.

Figure 6

Focal geometry and characteristics of erosion-prone plaques. Culprit plaque erosions selectively developed at predisposed areas within the coronary artery tree and exhibited specific features with certain focal geometry that can be used for risk-stratifying high-risk erosion-prone plaques in erosion-prone vulnerable STEMI patients. Culprit plaque erosion tended to cluster within the “hot spots,” defined as distance from the ostium to the MLA <40 mm in the LAD. LAD location, distance from coronary ostium <40 mm, proximal to a nearby bifurcation, MLA <2.51 mm², AS > 64.02% and underlying TCFA of the culprit lesion were predictors of culprit plaque erosion. AS, area stenosis; LAD, left anterior descending artery; MLA, minimal lumen area; STEMI, ST-segment elevation myocardial infarction; TCFA, thin-cap fibroatheroma.