Mechanical stress is a well-recognized driver of plaque rupture. Likewise, investigating the role of mechanical forces in plaque erosion has recently begun to provide some important insights, yet the knowledge is by far less advanced. The most significant example is that of shear stress, which has early been proposed as a possible driver for focal endothelial death and denudation. Recent findings using optical coherence tomography, computational sciences and mechanical models show that plaque erosion occurs most likely around atheromatous plaque throats with specific stress pattern. In parallel, we have recently shown that neutrophil-dependent inflammation promotes plaque erosion, possibly through a noxious action on ECs. Most importantly, spontaneous thrombosis - associated or not with EC denudation - can be impacted by hemodynamics, and it is now established that neutrophils promote thrombosis and platelet activation, highlighting a potential relationship between, mechanical stress, inflammation, and EC loss in the setting of coronary plaque erosion. Here, we review our current knowledge regarding the implication of both mechanical stress and neutrophils, and we discuss their implication in the promotion of plaque erosion via EC loss and thrombosis.