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[Standards in interventional therapy of coronary artery disease]
Wolfgang Rutsch1, Volker Gliech, Hans-Peter Dübel
1Medizinische Klinik und Poliklinik, Schwerpunkt Kardiologie, Angiologie und Pneumologie, Universitätsklinikum Charité, Humboldt-Universität Berlin, Germany. wolfgang.rutsch@charite.de
Insights
Percutaneous coronary intervention (PCI) techniques have advanced for coronary artery disease, but abrupt closure and restenosis remain challenges. Coronary artery stents reduce complications but can lead to in-stent restenosis, necessitating new strategies like drug-eluting stents.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Biomedical Engineering
Context:
- Percutaneous coronary intervention (PCI) has expanded for acute and chronic coronary artery disease.
- Balloon angioplasty is limited by short-term abrupt vessel closure and long-term restenosis.
- PCI-induced arterial injury activates coagulation and platelet aggregation, risking intracoronary thrombus formation.
Purpose:
- To review current percutaneous coronary interventional techniques for coronary artery disease.
- To discuss limitations of PCI, including abrupt closure, restenosis, and in-stent restenosis.
- To explore emerging strategies for preventing and treating restenosis after PCI.
Summary:
- Coronary artery stents improve acute outcomes and reduce restenosis compared to balloon angioplasty.
- In-stent restenosis, particularly in diffuse lesions, remains a significant challenge.
- New techniques like drug-eluting stents and gene therapy show promise for inhibiting restenosis.
Impact:
- PCI advancements have broadened treatment indications for coronary artery disease.
- Coronary artery stents are crucial adjuncts but introduce the challenge of in-stent restenosis.
- Future research focuses on novel therapies to overcome restenosis and improve long-term PCI outcomes.
Abstract:
This review provides an overview of current percutaneous coronary interventional techniques (PCI) in patients with acute and chronic coronary artery disease. The indications for PCI have expanded during the past two decades, and no absolute contraindications remain. The chief limitations to event free survival following balloon angioplasty have been abrupt vessel closure in the short term and restenosis in the long term. The therapeutic effect of arterial vessel enlargement through PCI is accompanied by various degrees of arterial injury with exposure of thrombogenic components. Depending on the degree of activation of the coagulation cascade, as well as platelet adhesion and aggregation, this may result in intracoronary thrombus formation and subsequent ischemic sequelae. Therefore, inhibition of platelets and the coagulation system has always been central to interventional investigations. Restenosis has been the most important long-term limitation of PCI. Coronary artery stents have become an important adjunct to conventional balloon angioplasty owing to their dual function of reducing acute complications and the long term risk of restenosis. Although coronary artery stents serve as antirestenosis devices and reduce target vessel revascularisation requirements compared with balloon angioplasty, they themselves become a source of restenosis. In-stent restenosis is a major challenge for the interventionalist. None of the available interventional modalities provides optimal acute results, and long-term results are even poorer. This is especially true for diffuse in-stent restenosis lesions which have high recurrence rates. Thus, mechanical treatment modalities for evolved in-stent restenosis can only be one step in a comprehensive strategy for prevention and treatment. Brachytherapy as an adjunct seems to be especially promising, but late thrombosis, delayed restenosis and the potential for very late fibrosis are matters of concern. As attention has turned towards the prevention of in-stent restenosis new techniques such as drug delivering stents and gene therapy to inhibit the biological reaction of the vessel wall are likely to obtain greater importance.