40 Years of Percutaneous Coronary Intervention: History and Future Directions

John Canfield, Hana Totary-Jain, John Canfield, Hana Totary-Jain

Abstract

The field of interventional cardiology has evolved significantly since the first percutaneous transluminal coronary angioplasty was performed 40 years ago. This evolution began with a balloon catheter mounted on a fixed wire and has progressed into bare-metal stents (BMS), first-generation drug-eluting stents (DES), second- and third-generation biodegradable polymer-based DES, and culminates with the advent of bioabsorbable stents, which are currently under development. Each step in technological advancement has improved outcomes, while new persisting challenges arise, caused by the stent scaffolds, the polymers employed, and the non-selective cytostatic and cytotoxic drugs eluted from the stents. Despite the promising technological advances made in stent technology, managing the balance between reductions in target lesion revascularization, stent thrombosis, and bleeding remain highly complex issues. This review summarizes the evolution of percutaneous coronary intervention with a focus on vascular dysfunction triggered by the non-selective drugs eluted from various stents. It also provides an overview of the mechanism of action of the drugs currently used in DES. We also discuss the efforts made in developing novel cell-selective drugs capable of inhibiting vascular smooth muscle cell (VSMC) proliferation, migration, and infiltration of inflammatory cells while allowing for complete reendothelialization. Lastly, in the era of precision medicine, considerations of patients' genetic variance associated with myocardial infarction and in-stent restenosis are discussed. The combination of personalized medicine and improved stent platform with cell-selective drugs has the potential to solve the remaining challenges and improve the care of coronary artery disease patients.

Keywords: angioplasty; coronary artery disease; percutaneous intervention; reendothelialization; restenosis; stent.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Evolutionary history of percutaneous coronary intervention (PCI). 1 BMS: Bare-metal stent. 2 DES: Drug-eluting stent.
Figure 2
Figure 2
Graphic schematic depicting the cell-selective therapy capable of preventing restenosis and allowing for reendothelialization. Balloon injury and control green fluorescent protein (GFP) treated rat coronary artery results in neotintimal hyperplasia, infiltration of inflammatory cells, and an increased risk of thrombosis, accompanied by a severe reduction in reendothelialization and loss of endothelial cell-dependent vasodilation. Balloon injury and non-cell selective p27 treated rat coronary artery decreased neointimal hyperplasia and inflammation, but increased thrombosis due to decreased reendothelialization endothelial cell-dependent vasodilation. However, balloon injury and treatment with the cell-selective p27-126TS decreased neotintimal hyperplasia and inflammation, but also allowed for complete reendothelialization and effective endothelial cell-dependent vasodilation and greatly diminished the risk of thrombosis. EC: endothelial cell; CMV: Cytomegalovirus.
Figure 3
Figure 3
Treatment with p27-126TS prevents restenosis and allows for complete reendothelialization of the vascular wall. (A–D). Representative images of uninjured (A), or balloon injured rat carotid arteries treated with GFP (B), p27 (C), or p27-126TS (D) followed by hematoxylin and eosin (H&E) stain. Original magnification 10×, scale bars represent 500 μM. (E–H) Representative images of uninjured (E), or balloon injured rat carotid arteries treated with GFP (F), p27 (G), or p27-126TS (H) immunostained for vascular endothelial cell marker vascular endothelial-cadherin (VE-Cadherin). White arrows indicate VE-Cadherin positive endothelial cells. (I–L) Representative images of uninjured (I), or balloon injured rat carotid arteries treated with GFP (J), p27 (K), or p27-126TS (L) immunostained for the pan-inflammatory marker CD45. (E–L) Nuclei were counterstained with DAPI. Original magnification 60×, scale bars represent 100 μM.

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