All implantable coronary artery stents have been made of either stainless steel or nitinol. In the premarket evaluations of these coronary stents over the past seven years there have been no differences observed in terms of primary restenosis and/or major cardiac endpoints. Balloon-expanded stents are deployed in the coronary artery with a high-pressure strategy while nitinol self-extending stents expand over time and are often deployed at lower pressures. Several angiographic and intravascular ultrasound follow-up studies have not shown any significant difference in terms of the degree of intimal hyperplasia or abnormal vessel behavior in the stent body or at the stent edges. However, differences in stent morphology have been noted over time between self-expanded stents and balloon-expanded stents. For example, in the ASSURE trial self-expanding stents were seen to increase in size within six months to an average of 28% in overall volume. Although the length of the stent did not change, this chronic growth was associated with a concomitant increase in intimal hyperplasia. Compared to a randomized arm of balloon-expanded stents, this increase in stent volume was compensated by an increase in intimal hyperplasia so that there was no difference in the late lumen loss in either strategy. However, at the stent edge in the self-expanding group the late volume loss was significantly less compared to balloon-expandable stents.
As we enter a new era of exposing several pharmacologic approaches and energy forms to the imbedded metal struts within the vessel wall, the exact vessel response is unknown. For example, ionizing radiation drastically inhibits intimal hyperplasia; however, the exposed metal struts following this therapy may be at increased risk for late thrombosis. The inappropriate dosing of either a pharmacologic agent or ionized energy dose may result in unfavorable effects within stents and, in particular, at the edges. This phenomenon has most recently been seen with certain ionizing radiation sources where vessel constriction and intimal hyperplasia outside the stents are predominant mechanisms for late lumen loss. Several of the stent configurations may provide an opportunity to compensate for these vascular responses to ionizing radiation and are the subject of several ongoing trials.