Impact of wall shear stress affected by anatomical difference between acute and chronic coronary syndrome in patients with LAD proximal disease

Abstract

Abstract Recent hemodynamic studies have demonstrated that progression of coronary atherosclerosis occurs at low wall share-stress site, whereas plaque rupture frequently occurs at high share stress site. It is well recognized that wall shear stress is relatively low along the outer walls of the bifurcation. We investigated consecutive 140 patients (77 with acute coronary syndrome (ACS) and 63 with chronic coronary syndrome (CCS) performed PCI for LAD proximal lesions (AHA seg.6) from January 2016 to December 2019. In CCS group, entry criteria included stenosis of at least 90% in the LAD proximal lesion or at least 70% in the LAD proximal lesion and objective evidence of myocardial ischemia (inducible ischemia with either exercise or pharmacologic vasodilator stress or with pressure wire). Exclusion criteria were patients with maintenance dialysis, chronic total occlusion lesions, in-stent restenosis, and clinically diagnosed unstable angina without troponin I elevation. We measured the distance from LMT distal carina to the culprit site (Distance) and plaque location (Location) with intravascular ultrasound and angle between LMT and LAD with cardiovascular angiography analysis system (CAAS) (Angle). The two groups were generally well balanced with regard to baseline clinical characteristics. The mean (±SD) age of the patients was 69.0±11.8 years, and 75% were men. Medication at baseline was also similar between two groups except higher prevalence of statin prescription in CCS group. The Distance was shorter and Angle was steeper in CCS group than in ACS group. The number of patients with Angle less than 150 degrees and with Location in the lateral wall side was much more in CCS group. In this study, plaques in CCS were frequently observed at low shear stress site, whereas those in ACS at high shear stress site. Plaque progression in CCS may be associated with low wall shear stress, and high shear stress may play key role in plaque rupture in ACS. This anatomical difference can partly explain the different mechanisms of onset between of ACS and CCS. Funding Acknowledgement Type of funding sources: None. Anatomical differenceCharacteristics and results