Microcracks in concrete can coalesce into larger cracks that further propagate under repetitive load cycles. Complex process of crack formation and growth are essentially involved in the failure mechanism of concrete. Understanding the crack formation and propagation is one of the core issues in fatigue damage evaluation of concrete materials and components. In this regard, a numerical model was formulated to simulate the thorough failure process, ranging from microcracks growth, crack coalescence, macrocrack formation and propagation, to the final rupture. This model is applied to simulate the fatigue rupture of three-point bending concrete beams at different stress levels. Numerical results are qualitatively consistent with the experimental observations published in literature. Furthermore, in the framework of damage mechanics, one damage variable is defined to reflect stiffness reduction caused by fatigue loading. S-N curve is subsequently computed and the macroscopic damage evolution of concrete beams are achieved. By employing the combined approaches of fracture mechanics and damage mechanics, made possible is the damage evolution of concrete beam as well as the microscopic multiple fatigue crack simulation. The proposed approach has the potential to be applied to the fatigue life assessment of materials and components at various scales in engineering practice.

Background.Calcification is commonly believed to be associated with cardiovascular disease burden. But whether or not the calcifications have a negative effect on plaque vulnerability is still under debate.Methods and Results.Fatigue rupture analysis and the fatigue life were used to evaluate the rupture risk. An idealized baseline model containing no calcification was first built. Based on the baseline model, we investigated the influence of calcification on rupture path and fatigue life by adding a circular calcification and changing its location within the fibrous cap area. Results show that 84.0% of calcified cases increase the fatigue life up to 11.4%. For rupture paths 10Dfar from the calcification, the life change is negligible. Calcifications close to lumen increase more fatigue life than those close to the lipid pool. Also, calcifications in the middle area of fibrous cap increase more fatigue life than those in the shoulder area.Conclusion.Calcifications may play a positive role in the plaque stability. The influence of the calcification only exists in a local area. Calcifications close to lumen may be influenced more than those close to lipid pool. And calcifications in the middle area of fibrous cap are seemly influenced more than those in the shoulder area.

Rupture of atheromatous plaque is the major cause of stroke or heart attack. Considering that the cardiovascular system is a classic fatigue environment, plaque rupture was treated as a chronic fatigue crack growth process in this study. Fracture mechanics theory was introduced to describe the stress status at the crack tip and Paris' law was used to calculate the crack growth rate. The effect of anatomical variation of an idealized plaque cross-section model was investigated. The crack initiation was considered to be either at the maximum circumferential stress location or at any other possible locations around the lumen. Although the crack automatically initialized at the maximum circumferential stress location usually propagated faster than others, it was not necessarily the most critical location where the fatigue life reached its minimum. We found that the fatigue life was minimum for cracks initialized in the following three regions: the midcap zone, the shoulder zone, and the backside zone. The anatomical variation has a significant influence on the fatigue life. Either a decrease in cap thickness or an increase in lipid pool size resulted in a significant decrease in fatigue life. Comparing to the previously used stress analysis, this fatigue model provides some possible explanations of plaque rupture at a low stress level in a pulsatile cardiovascular environment, and the method proposed here may be useful for further investigation of the mechanism of plaque rupture based on in vivo patient data.