Endovascular Drug Delivery

Abstract

Drug-eluting stents (DES) and balloons revolutionize atherosclerosis treatment by targeting hyperplastic tissue responses through effective local drug delivery strategies. This review examines approved and emerging endovascular devices, discussing drug release mechanisms and their impacts on arterial drug distribution. It emphasizes the crucial role of drug delivery in modern cardiovascular care and highlights how device technologies influence vascular behavior based on lesion morphology. The future holds promise for lesion-specific treatments, particularly in the superficial femoral artery, with recent CE-marked devices showing encouraging results. Exciting strategies and new patents focus on local drug delivery to prevent restenosis, shaping the future of interventional outcomes. In summary, as we navigate the ever-evolving landscape of cardiovascular intervention, it becomes increasingly evident that the future lies in tailoring treatments to the specific characteristics of each lesion. By leveraging cutting-edge technologies and harnessing the potential of localized drug delivery, we stand poised to usher in a new era of precision medicine in vascular intervention.

Keywords: atherosclerosis; drug delivery; endovascular therapy; lesion morphology; lesion-specific treatment.

Figure 1

Bioresorbable scaffold’s mode of action. (a) Artery with atherosclerotic plaque with significant arterial stenosis (plaque represented in red spot). (b) A stent is deployed at the level of the stenosis, increasing the circulating arterial lumen and, consecutively, an increase in flow. (c) In time, due to the intimal hyperplasia, the stent is covered with hyperplasic intima and, consecutively, new plaque is formed, obstructing the lumen again, resulting in a more significant narrowing of the artery. (d) A bioresorbable scaffold is placed, this time in the obstructed arterial lumen, having the same results as the stent. (e) In time, a bioresorbable scaffold creates a film over the atherosclerotic plaque, the endothelium. The artery expands, but the intimal hyperplasia process is at a minimum. The scaffolds are resorbed, leaving a much greater lumen and, consecutively, a greater arterial flow than the stent. In the lower image (personal collection), a stent is represented by mild signs of intimal hyperplasia at the stent level.

Figure 2

Mechanism of endovascular absorbtion. The figure above considers a stent covered with a polymer drug-containing layer placed in an artery. The stent metal structure is represented in grey (d). On top of the stent structure is an inactive polymer layer that cannot release the drug molecules (e). Near the endothelium (g), a thin layer of active polymer can release the drug’s active molecules-the drug molecules are represented in ref dots (f). The drug release molecules interact with the endothelium and perform their pharmacological role. The figure below shows a section through the human artery, stained with hematoxylin–eosin (personal collection). The endothelium is shown (a), followed by the tunic media (b) and adventitia (c). The drug is released at the endothelial layer and absorbed into the tunica media.