Intracoronary Stents

Excerpt

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality worldwide, with acute coronary syndrome (ACS) being one of its most critical clinical manifestations. Plaque rupture or erosion within coronary vessels triggers a cascade of platelet activation, thrombosis, and potential vessel occlusion, often requiring urgent revascularization. Percutaneous coronary intervention (PCI) has emerged as the primary modality for restoring coronary blood flow in these patients, evolving significantly since its inception.

The modern era of coronary revascularization began on September 16, 1977, in Zurich, Switzerland, when Andreas Grüntzig performed the first successful percutaneous transluminal coronary angioplasty using a DG 20-30 balloon catheter. While this landmark procedure demonstrated long-term vessel patency in select cases, balloon angioplasty alone was limited by several complications, most notably acute vessel closure due to arterial recoil, dissection, and thrombus formation at sites of plaque disruption. These issues led to abrupt occlusion in 5% to 10% of cases and a high restenosis rate due to neointimal hyperplasia.

In response to these limitations, bare-metal stents (BMS) were developed in the 1980s as mechanical scaffolds to maintain vessel patency. The introduction of coronary stents eliminated coronary dissection and vascular recoil, as the expandable metallic meshwork prevented negative remodeling. Initially constructed from thick stainless-steel struts, early BMS devices effectively reduced the acute complications of balloon angioplasty. However, they introduced new challenges, particularly stent thrombosis, which was mitigated by the adoption of dual antiplatelet therapy (DAPT). Despite these advancements, long-term follow-up revealed significant in-stent restenosis rates, occurring in 20% to 50% of cases, driven by vascular injury-induced smooth muscle cell (SMC) proliferation and neointimal hyperplasia.

Drug-eluting stents (DES) were developed in the early 2000s to overcome these limitations, marking a major milestone in interventional cardiology. DES consists of 3 critical components—a metal stent platform, a polymer coating to control drug release, and an antiproliferative agent designed to inhibit neointimal growth. Early-generation DES featured stainless steel frameworks with relatively thick struts and closed-cell designs, limiting deliverability in complex and calcified lesions. Paclitaxel and sirolimus were the first antiproliferative drugs used—paclitaxel disrupted microtubule function during mitosis, whereas sirolimus inhibited the mammalian target of rapamycin (mTOR) pathway to suppress SMC proliferation.

The introduction of DES significantly reduced restenosis rates and the need for repeat revascularization. However, early designs were associated with delayed endothelial healing and an increased risk of late stent thrombosis. Ongoing advancements have led to newer-generation DES with thinner struts, more biocompatible or biodegradable polymers, and improved antiproliferative agents. These innovations enhance safety and efficacy, minimize adverse vascular responses, and improve outcomes in complex patient populations, including those with diabetes, calcified lesions, or bifurcation disease. Today, coronary stents remain a cornerstone of CAD management, with continuous technological advancements refining their design, performance, and clinical utility.