Acute coronary syndromes (ACS) remain a challenging and global health problem responsible for an enormous number of major adverse cardiac events (MACE) [1]. The three underlying pathobiologic mechanisms responsible for ACS include plaque rupture, plaque erosion, and calcified nodules [2]. Plaque erosion is defined as a thrombus overlying a plaque with an intact fibrous cap (IFC), caused mainly by endothelial denudation [3,4]. Autopsy and optical coherence tomography (OCT) studies showed that plaque erosion could be the causative mechanism in about 20–40% of patients presenting with ACS [[5], [6], [7], [8], [9]].

The role of endothelial shear stress (ESS), the biomechanical force due to the tangential friction of blood flowing over the arterial endothelium, in the natural history of plaque formation, progression, and destabilization has been studied, but its role in plaque erosion remains unknown [10,11]. Focal areas of high ESS and, in particular, high ESS gradient (ESSG, the ESS value of immediately adjacent plaque endothelial areas) have been hypothesized to promote erosion [12,13]. In addition, no studies examined the detailed mechanistic relationships between longitudinal location of plaque erosion/thrombus, i.e., proximal vs. distal to the minimal luminal area (MLA) of the culprit erosion plaque, and its relationship to the maximum magnitude of upslope vs. downslope of the lumen obstruction topography. Therefore, this study is a hypothesis generating study aimed [1]: to compare ESS and ESSG metrics between plaques with erosion and similar non-culprit control plaques that remained stable and [2], among erosion plaques, to study the mechanistic implications of maximum slope steepness up- and down-stream from the culprit plaque MLA on thrombus location.