title: Oxidative stress and pathological changes after coronary artery interventions.
abstract: Oxidative stress greatly influences the pathogenesis of various cardiovascular disorders. Coronary interventions, including balloon angioplasty and coronary stent implantation, are associated with increased vascular levels of reactive oxygen species in conjunction with altered endothelial cell and smooth muscle cell function. These alterations potentially lead to restenosis, thrombosis, or endothelial dysfunction in the treated artery. Therefore, the understanding of the pathophysiological role of reactive oxygen species (ROS) generated during or after coronary interventions, or both, is essential to improve the success rate of these procedures. Superoxide O2(·-) anions, whether derived from uncoupled endothelial nitric oxide synthase, nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, or mitochondria, are among the most harmful ROS. O2(·-) can scavenge nitric oxide, modify proteins and nucleotides, and induce proinflammatory signaling, which may lead to greater ROS production. Current innovations in stent technologies, including biodegradable stents, nitric oxide donor-coated stents, and a new generation of drug-eluting stents, therefore address persistent oxidative stress and reduced nitric oxide bioavailability after percutaneous coronary interventions. This review discusses the molecular mechanisms of ROS generation after coronary interventions, the related pathological events-including restenosis, endothelial dysfunction, and stent thrombosis-and possible therapeutic ways forward.
authors.affiliation: Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Maastricht, the Netherlands.
authors.forename: Rio P
authors.initials: RP
authors.lastname: Juni
authors.forename: Henricus J
authors.initials: HJ
authors.lastname: Duckers
authors.forename: Paul M
authors.initials: PM
authors.lastname: Vanhoutte
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
authors.forename: An L
authors.initials: AL
authors.lastname: Moens
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000379:methods; D023903:Coronary Restenosis / Q000473:pathology* / Q000628:therapy; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000401:mortality / Q000628:therapy; D054855:Drug-Eluting Stents; D004730:Endothelium, Vascular / Q000201:enzymology / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects* / Q000379:methods*; D011182:Postoperative Care / Q000379:methods; D011183:Postoperative Complications / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D011379:Prognosis; D011859:Radiography; D016032:Randomized Controlled Trials as Topic; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018570:Risk Assessment; D015607:Stents; D016019:Survival Analysis; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D017382:Reactive Oxygen Species; D014665:Vasodilator Agents; D052250:Nitric Oxide Synthase Type III