[Late stent thrombosis after drug-eluting stent implantation: epidemiological, clinical and pathophysiological

Salvatore Notaristefano1, Paolo Sbarzaglia, Claudio Cavallini

  • 1S.C. di Cardiologia, Azienda Ospedaliera di Perugia, Perugia.

Giornale Italiano Di Cardiologia (2006)
|October 24, 2008
PubMed

Insights

Stent thrombosis (ST), a rare complication of percutaneous coronary intervention, may occur later with drug-eluting stents (DES). However, this very-late ST risk does not increase adverse outcomes like death or heart attack compared to bare-metal stents.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Biomaterials Science

Context:

  • Stent thrombosis (ST) is a serious complication following percutaneous coronary intervention (PCI).
  • Drug-eluting stents (DES) have been associated with concerns about very-late stent thrombosis (VLST), occurring after the first year post-PCI.
  • Existing literature suggests a potential, albeit modest, increase in VLST incidence with DES compared to bare-metal stents (BMS).

Purpose:

  • To analyze the incidence and implications of very-late stent thrombosis (VLST) in patients treated with drug-eluting stents (DES) versus bare-metal stents (BMS).
  • To explore the multifactorial causes contributing to early, late, and very-late stent thrombosis.
  • To discuss current strategies and future innovations for mitigating ST risk.

Summary:

  • While data suggest a slightly higher incidence of very-late stent thrombosis (VLST) with drug-eluting stents (DES) compared to bare-metal stents (BMS) (0.35%-0.6% annually), this has not translated into worse hard outcomes (death, myocardial infarction).
  • Stent thrombosis is multifactorial, with early ST linked to procedural aspects and antiplatelet therapy, while late and very-late ST involve patient risk factors and arterial healing.
  • Current risk reduction strategies include careful patient selection, precise implantation, and ensuring patient compliance with antiplatelet therapy. Future innovations focus on novel antiplatelet agents and next-generation DES.

Impact:

  • Understanding the nuances of ST, particularly VLST with DES, is crucial for optimizing patient selection and procedural techniques.
  • The findings underscore that despite a modest increase in VLST, DES remain a safe and effective treatment option, as hard clinical outcomes are not worsened.
  • Future advancements in DES technology and antiplatelet therapies hold promise for further reducing the risk of stent thrombosis.

Related Concept Videos

Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...