Re-infarction after primary percutaneous coronary intervention

PURPOSE OF REVIEW: Thrombus formation, usually on a ruptured atherosclerotic plaque, is pivotal in the pathogenesis of ST segment elevation myocardial infarction (STEMI). This thrombus formation provides the milieu for re-occlusion of the infarct-related artery, the main location of re-infarction post-STEMI. Although rates of re-infarction are lower after reperfusion by primary percutaneous coronary intervention (PCI) than after fibrinolytic therapy, re-infarction remains a major cause of morbidity and mortality. RECENT FINDINGS: The predominant cause of re-infarction after primary PCI is stent thrombosis. Two recent trials [A Prospective, Randomized Trial of Ambulance Initiation of Bivalirudin vs. Heparin ± Glycoprotein IIb/IIIa Inhibitors in Patients with STEMI Undergoing Primary PCI (EUROMAX) and Unfractionated heparin versus bivalirudin in primary percutaneous coronary intervention (HEAT-PPCI)] have each reported higher rates of stent thrombosis in the first 24 h after primary PCI in patients assigned to receive bivalirudin, which affects the balance of risks and benefit of bivalirudin post-STEMI. Also, in a subanalysis of the Platelet Inhibition And Patient Outcomes trial, ticagrelor reduces re-infarction compared with clopidogrel in patients with STEMI after primary PCI. Other nonpharmacological or mechanical interventions during primary PCI, with the exception of newer-generation drug-eluting stents in the Swedish Coronary Angiography and Angioplasty Registry, have not affected rates of re-infarction. SUMMARY: Re-infarction remains a major cause of morbidity and mortality. Re-infarction rates are altered by pharmacological strategy and stent selection in primary PCI. The design of future trials to detect possible treatment differences in relatively low event rates will provide challenges, and may require more novel strategies such as administrative data collection for patient characteristics and key outcomes.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Thrombus formation, usually on a ruptured atherosclerotic plaque, is pivotal in the pathogenesis of ST segment elevation myocardial infarction (STEMI).

Leech-derived molecules this paper discusses, each with a full profile in the ASH compound registry:

Explore cómo esta investigación se conecta con la práctica clínica

More peer-reviewed studies in Desarrollo de fármacos.

• Novel Leech Antimicrobial Peptides — Hirunipins — Kumar et al. (2025)
• Medicinal Leech Genome Assembly — Anticoagulant Gene Catalog — Kvist et al. (2020)
• Effects of hirudotherapy on liver functions, lipid profile, and insulin sensitivity in rats with metabolic syndrome — Bilden A et al. (2026)
• Hirudotherapy in Medicine and Dentistry — Jha K et al. (2015)
• Medicinal leech therapy (hirudotherapy): a brief overview — Singh A (2010)
• HIRUDOTHERAPY IN PRESBYACUZIS PRAECOX IN CLEAN-UP WORKERS AFTER THE CHORNOBYL ACCIDENT DURING THE POST-CATASTROPHE YEARS — Zabolotnyi D, Mishchanchuk N (2019)
• Investigation of oxidant-antioxidant status in patients treated with hirudotherapy: an experimental study — Sarikan I, Savas H (2024)
• Leech therapeutic applications — Abdualkader A et al. (2013)
• Non-Occlusive Mesenteric Ischemia Due to Hirudotherapy: A Case Report — Akalın Ç, Ekmen N (2020)
• Leech therapy: a history — Hyson J (2005)

Browse all ASH-analysed research →