Myocardial bridging (MB) is a congenital defect that affects a significant fraction of the population, where a coronary artery has a short intramyocardial course, and is often found in the Left Anterior Descending (LAD) artery. All intramyocardial segments are subjected to various mechanical loads; the arterial walls are subjected to hemodynamic shear loads, and radially compressive loads during systole. Importantly, these intramyocardial courses impact blood flow in regions proximal to the bridged sections, including arterial bifurcations. Therefore, MB is known to influence the progression of atherosclerosis and myocardial ischemia. While MB can be tracked clinically from systolic compressions seen in angiography, its exact cause and impact is hard to ascertain. The bridged sections are generally known to be resistant to atherosclerotic plaque (i.e., atheroprotective) whereas the regions in proximity can become more atheroprone due to the retrograde flows. However, the exact influence of vessel/branch geometry, fluid flow, and surrounding tissue mechanics in MB as it impacts endothelial morphologies and vascular inflammation is unknown. This is practically critical to understand since patients with MB who experience severe angina often require stents in the entirety of the bridged section. Therefore, to fully understand the effects of these various parameters in MB, we present in vitro models that allow studying the endothelial morphology and permeability at arterial bifurcations. These biomimetic, reductionist models will allow us to separately chart out the impact of branching geometry, in- and out-of-phase flow profiles, and the impact of mechanical cycling - the predominant factors that influence outcomes from myocardial bridging in patients.
|Program type||Postdoctoral Fellowship|
|Effective start/end date||01/01/2020 → 12/31/2021|