Abstract
For more than three decades, researchers in hemodynamics were led by Fry [1] and Caro [2] to focus on localized mechanical factors and their importance in arteriosclerosis development. It is believed that geometrically incited fluid shear stress plays a central role in the development of arterial lesions. Applying laser Doppler anemometry, Friedman et al [3] performed detailed flow measurements in human arterial segments selected at autopsy by passing a life-like pulsatile flow through each vessel's lumen. The time-dependent velocities at multiple sites near the walls of each case were compared with the morphometric and histologic measurements at corresponding sites in the original arteries. Their work clearly indicated that vascular geometry, particularly the detailed geometry near a vessel wall junction, posts a "geometric risk factor" for arteriosclerosis. The first successful implantation of coronary stents in human patients was reported by Sigwart et al [4]. Not until the mid-1990's have stents emerged as a safe and effective modality for treating closure of coronary arteries. To date, different types of stents have been introduced for clinically implantations in human coronary arteries. Stents are different in their composition (e.g., metallic vs. biodegradable polymer), sectional thickness, architectural design, and mode of implantation (e.g., self-expending vs. balloon-expandable). Theoretically, a coronary stent should be constructed with a nonthrombogenic material that has sufficient flexibility in its pre-expanded state to allow easy passage through the tortuous vessels following the guiding catheter. Most of the current commercial coronary stents are constructed with stainless steel, which carry a net electropositive surface change that makes it resistant to corrosion but also relatively thrombogenic. For this reason, a few current commercial stents are coated with a thin layer of less thrombogenic material (inert coating: e.g., diamond-like carbon) or slow releasing antithrombogenic drug (active coating: e.g., Drug-eluting stents). From a hemodynamic viewpoint, coronary arteries are medium size blood vessels (mostly 2.5-5.0 mm in diameter). Each vessel carries a large volumetric blood flow, and its the conduit wall flexes constantly with every movement of the myocardium walls. Implanting a man-made stent into such a conduit would inevitably alter: (1) the arterial wall shear stress, and (2) the conduit wall compliance. Either one of which may activate the blood platelets, damage the red blood cells and the vascular walls; together they should have made the coronary stent a theoretically impracticable device. However, the fact is that most of the stented coronary arteries (about 80%) works well in recipient patients. We believe that this may be attributed to two factors: (1) the timely administration of anticoagulation agents; and (2) a different mechanism is involved in the repair process of the stent induced vascular injury. The former world allow enough time for the endothelial cell to cover the bare foreign surface of the implanted stent; while the later world require focused future research to understand the reaction of blood vessel intima to hemodynamic stresses in repair of the stent induced insults. The mechanism leading to restenosis of a stented coronary may be totally different from that of the development of intimal hyperplasia in adverse hemodynamics under normal physiological conditions.
