Introduction: Early stent thrombosis (EST) may be life threatening complication of percutaneous coronary intervention (PCI) as it is associated with acute coro-nary syndrome and sudden death. Even with the huge advances in stent manufacturing technologies and an-tiplatelet therapy (APT), the incidence of EST is not negligible. This may be due to the increasing number of patients, as well as the higher complexity of coronary lesions, treated with PCI.
Objective: We report a case of a patient with recurrent EST presenting with acute myocardial infarction, ai-ming to reconsider the clinical significance of this con-dition.
Methods: A 64-year-old male with a history of hyper-tension and dyslipidaemia, was admitted for acute-on-nset chest pain and dyspnea at rest. Given the clinical status, the rising pattern of cardiac troponin, the dia-gnosis of acute non ST-elevation myocardial infarction established. Coronary angiography revealed 3 vessel coronary artery disease with critical lesion of mid right coronary artery (RCA), proximal and distal left circum-flex artery (LCX), mid left anterior descending artery (LAD) at the level of bifurcation of the first diagonal artery (D1). During coronary angiography the patient presented severe cutaneous allergic reaction that led to temporization of myocardial revascularization.
Results: After Heart Team discussion, a staged PCI approach was chosen. First PCI with drug eluting stent (DES) in the RCA was performed, followed by PCI with 2 DES in the LCX. 6 days later the patient was re-admitted with infero-lateral ST elevation myo-cardial infarction (STEMI). Angiography revealed EST in the LCX. Thrombectomy and PCI with a 3rd DES in the LCX were performed. After 2 months PCI with two DES at the level of bifurcation LAD-D1 (Culotte technique) was performed. Two weeks later the patient was re-admitted with anterior ST-elevation myocardial infarction. Echocardiography showed sever left ventri-cular (LV) dysfunction and angiography revealed EST at the level of LAD-D1. Thrombectomy was performed with complete flow restoration. Genetic testing show-ed a tendency for thrombophilia with no resistance to antiplatelet therapy, but serology did not confirm the diagnosis of thrombophilia. The patient was treated with sever antiplatelet regimen with triple therapy for 3 months then prolonged dual APT. Despite recurrent STEMI in 2 territories and LV dysfunction, the patient had a good outcome being asymptotic with complete recovery of LV function at follow ups, mainly because of early revascularization of STEMI.
Conclusions: Even though considered uncommon, EST is a serious and possible fatal complication of PCI. The management and decision of antithrombotic regi-mens in these patients may be challenging, knowing that no trials have been performed in this particular group that show superiority of more potent APT, such as oral anticoagulation or switching to prasugrel or ti-cagrelor or higher-dose clopidogrel.