Background: Plaque rupture occurs if stress within coronary lesions exceeds the protection capacity of  the fibrous cap overlying the necrotic lipid core. However, very little is known about biomechanical plaque stress contributing to this disrupting force. This study aimed to examine the biomechanical stress distribution in coronary lesions in patients with or without acute coronary syndrome (ACS) and investigate its relationship with plaque rupture.

Methods: Employing optical coherence tomography, we compared 10 ruptured coronary lesions of ACS patients with 10 non-ruptured lesions of stable patients. We generated a 3D plaque model based on 2D segmentation of the lesion; we then used this reconstruction for mechanistic finite element analysis to simulate the stress distribution within the vessel wall. Ethics Committee approval was obtained.

Results: In ruptured lesions, peak cap stress (PCS: 174±67 vs. 52±42 kPa, p<0.001) and maximal stress within the vessel wall (MPS: 399±233 vs. 90±95 kPa, p=0.001) were significantly higher compared to non-ruptured plaques. Ruptures arose in the immediate proximity of maximal stress concentrations (21.8±30.3° from PCS, 20.7±23.7° from MPS). PCS (AUC 0.940) and MPS (AUC 0.950) predicted plaque rupture with excellent accuracy, significantly superior to single plaque vulnerability features such as fibrous cap thickness (AUC 0.630, respectively p=0.027 and p=0.036) and extent of plaque macrophage infiltration (AUC 0.545, respectively p=0.003 and p=0.001).

Conclusion: Our proof-of-concept study shows that OCT-based finite element analysis is a feasible tool to determine plaque biomechanics, which predicts plaque rupture in patients. Our data highlight the importance of morpho-mechanic analysis assessing the disrupting effects of plaque stress.