Preventing treatment failures in coronary artery disease: what can we learn from the biology of in-stent restenosis, vein graft failure, and internal thoracic arteries?

Abstract Coronary artery disease (CAD) remains one of the most important causes of morbidity and mortality worldwide, and the availability of percutaneous or surgical revascularization procedures significantly improves survival. However, both strategies are daunted by complications which limit long-...

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Veröffentlicht in:Cardiovascular research 2020-03, Vol.116 (3), p.505-519
Hauptverfasser: Spadaccio, Cristiano, Antoniades, Charalambos, Nenna, Antonio, Chung, Calvin, Will, Ricardo, Chello, Massimo, Gaudino, Mario F L
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container_end_page 519
container_issue 3
container_start_page 505
container_title Cardiovascular research
container_volume 116
creator Spadaccio, Cristiano
Antoniades, Charalambos
Nenna, Antonio
Chung, Calvin
Will, Ricardo
Chello, Massimo
Gaudino, Mario F L
description Abstract Coronary artery disease (CAD) remains one of the most important causes of morbidity and mortality worldwide, and the availability of percutaneous or surgical revascularization procedures significantly improves survival. However, both strategies are daunted by complications which limit long-term effectiveness. In-stent restenosis (ISR) is a major drawback for intracoronary stenting, while graft failure is the limiting factor for coronary artery bypass graft surgery (CABG), especially using veins. Conversely, internal thoracic artery (ITA) is known to maintain long-term patency in CABG. Understanding the biology and pathophysiology of ISR and vein graft failure (VGF) and mechanisms behind ITA resistance to failure is crucial to combat these complications in CAD treatment. This review intends to provide an overview of the biological mechanisms underlying stent and VGF and of the potential therapeutic strategy to prevent these complications. Interestingly, despite being different modalities of revascularization, mechanisms of failure of stent and saphenous vein grafts are very similar from the biological standpoint.
doi_str_mv 10.1093/cvr/cvz214
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subjects Animals
Coronary Artery Bypass - adverse effects
Coronary Artery Disease - metabolism
Coronary Artery Disease - pathology
Coronary Artery Disease - physiopathology
Coronary Artery Disease - therapy
Coronary Restenosis - metabolism
Coronary Restenosis - pathology
Coronary Restenosis - physiopathology
Coronary Restenosis - prevention & control
Coronary Vessels - metabolism
Coronary Vessels - pathology
Coronary Vessels - physiopathology
Coronary Vessels - surgery
Graft Occlusion, Vascular - metabolism
Graft Occlusion, Vascular - pathology
Graft Occlusion, Vascular - physiopathology
Graft Occlusion, Vascular - prevention & control
Humans
Mammary Arteries - metabolism
Mammary Arteries - physiopathology
Mammary Arteries - surgery
Neointima
Percutaneous Coronary Intervention - adverse effects
Percutaneous Coronary Intervention - instrumentation
Risk Factors
Saphenous Vein - metabolism
Saphenous Vein - physiopathology
Saphenous Vein - transplantation
Stents
Time Factors
Treatment Failure
Vascular Patency
title Preventing treatment failures in coronary artery disease: what can we learn from the biology of in-stent restenosis, vein graft failure, and internal thoracic arteries?
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