Since its inception in the 1960s, coronary artery bypass graft (CABG) evolved as one of the most common, best documented, and most effective of all major surgical treatments for ischemic heart disease. Despite its widespread use, however, the outcome is not always completely satisfactory. The objective of this review is to highlight the physical determinants of biomechanical design of CABG so that future procedures would have prolonged patency and better outcome. Our central axiom postulates the existence of a mechanical homeostatic state of the blood vessel, i.e., the variation in vessel wall stresses and strains are relatively small under physiological conditions. Any perturbation of mechanical homeostasis leads to growth and remodeling. In this sense, stenosis and failure of a graft may be viewed as an adaptation process gone awry. We outline the principles of engineering design and discuss the biofluid and biosolid mechanics principles that may have the greatest bearing on mechanical homeostasis and the long-term outcome of CABG.

The intra-aortic filter can be safely deployed and captures particulate emboli, the predominant origin of which is atheromatous. The beneficial effects of this device on neurologic outcomes have yet to be determined.

It is well known that flow patterns at the anastomosis of coronary artery bypass graft (CABG) are complex and may affect the long-term patency. Various attempts at optimal designs of anastomosis have not improved long-term patency. Here, we hypothesize that mild anastomotic stenosis (area stenosis of about 40–60%) may be adaptive to enhance the hemodynamic conditions, which may contribute to slower progression of atherosclerosis. We further hypothesize that proximal/distal sites to the stenosis have converse changes that may be a risk factor for the diffuse expansion of atherosclerosis from the site of stenosis. Twelve (12) patient-specific models with various stenotic degrees were extracted from computed tomography images using a validated segmentation software package. A 3-D finite element model was used to compute flow patterns including wall shear stress (WSS) and its spatial and temporal gradients (WSS gradient, WSSG, and oscillatory shear index, OSI). The flow simulations showed that mild anastomotic stenosis significantly increased WSS (>15 dynes⋅cm−2) and decreased OSI (<0.02) to result in a more uniform distribution of hemodynamic parameters inside anastomosis albeit proximal/distal sites to the stenosis have a decrease of WSS (<4 dynes⋅cm−2). These findings have significant implications for graft adaptation and long-term patency.

Atrial fibrillation (AF) is the most common sustained dysfunction in heart rhythm clinically and has been identified as an independent risk factor for stroke through formation and embolization of thrombi. AF is associated with reduced cardiac output and short and irregular cardiac cycle length. Although the effect of AF on cardiac hemodynamic parameters has been reported, it remains unclear how the hemodynamic perturbations affect the potential embolization of blood clots to the brain that can cause stroke. To understand stroke propensity in AF, we performed computer simulations to describe trajectories of blood clots subject to the aortic flow conditions that represent normal heart rhythm and AF. Quantitative assessment of stroke propensity by blood clot embolism was carried out for a range of clot properties (e.g., 2–6 mm in diameter and 0–0.8 m/s ejection speed) under normal and AF flow conditions. The simulations demonstrate that the trajectory of clot is significantly affected by clot properties as well as hemodynamic waveforms which lead to significant variations in stroke propensity. The predicted maximum difference in stroke propensity in the left common carotid artery was shown to be about 60% between the normal and AF flow conditions examined. The results suggest that the reduced cardiac output and cycle length induced by AF can significantly increase the incidence of carotid embolism. The present simulations motivate further studies on patient-specific risk assessment of stroke in AF.

The potential of the coronary veins for revascularization has been evaluated by many investigators for more than a century. The major hurdle has been the damage of veins during sudden exposure to arterial pressure. The solution to this problem has typically involved the use of intricate and complicated apparatus and devices, which has prevented routine clinical utility in the catheterization laboratory. This review examines this old concept from a new perspective and proposes a novel hypothesis to address previous shortcomings. We speculate on an approach that may serve to eliminate the edema and hemorrhage that result during venous retroperfusion as the pressure is suddenly increased to arterial values. We propose the rationale to increase the venous pressure to arterial values more gradually to allow prearterializations of the veins before full exposure of arterial pressure. Finally, we discuss various possible indications for this selective autoretroperfusion strategy to combat myocardial ischemia in cardiogenic shock patients, ST-elevation myocardial infarct patients, no-option patients, and beyond.