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Platelet reactivity in Hepatitis C virus infected patients on dual antiplatelet therapy for acute coronary syndrome

Session Poster Session 7

Speaker Fernando Scudiero

Congress : ESC Congress 2019

  • Topic : coronary artery disease, acute coronary syndromes, acute cardiac care
  • Sub-topic : Coronary Artery Disease: Pharmacotherapy
  • Session type : Poster Session
  • FP Number : P6406

Authors : F Scudiero (Florence,IT), R Valenti (Florence,IT), R Marcucci (Florence,IT), GD Sanna (Sassari,IT), AM Gori (Florence,IT), A Migliorini (Florence,IT), R Vitale (Florence,IT), B Giusti (Florence,IT), E De Vito (Florence,IT), G Corda (Sassari,IT), R Paniccia (Florence,IT), G Parodi (Sassari,IT)

Authors:
F Scudiero1 , R Valenti1 , R Marcucci1 , GD Sanna2 , AM Gori1 , A Migliorini1 , R Vitale1 , B Giusti1 , E De Vito1 , G Corda2 , R Paniccia1 , G Parodi2 , 1Careggi University Hospital (AOUC), Cardiovascular and Thoracic Department - Florence - Italy , 2University of Sassari, Clinical and Interventional Cardiology - Sassari - Italy ,

Citation:

Background. Coronary artery disease (CAD) has been recognized as a serious and potentially life-threatening complication of Hepatitis C Virus (HCV) infection. High on treatment platelet reactivity has been associated with high risk of ischemic events in patients with CAD, but data regarding the association with HCV infection are still lacking. 

Purpose. We sought to assess platelet reactivity on dual anti-platelet therapy and long-term outcome of acute coronary syndrome (ACS) patients infected with HCV.

Methods. ACS patients infected with HCV were matched to ACS patients without HCV for age, sex, diabetes, hypertension and renal function. Primary and secondary study endpoints were the proportion of patients with high on treatment platelet reactivity (HTPR) and long-term outcomes, respectively. 

Results. HCV-infected ACS patients had higher levels of platelet reactivity (ADP10-LTA: 56% ± 18% vs. 44% ± 22%; p = 0.002; Arachidonic Acid-LTA: 25% ± 21% vs. 16% ± 15%; p = 0.011) and higher rate of HTPR on clopidogrel and aspirin compared with non-HCV patients. Multivariable analysis demonstrated HCV-infection to be an independent predictor of HTPR. At follow-up, estimated major adverse clinical events (MACE: cardiac death, non fatal myocardial infarction and any revascularization) were 57% vs. 37%, p=0.006 in HCV-infected ACS and non-HCV, respectively. Also, TIMI major bleeding rates were higher in HCV-infected subjects (11% vs. 3%; p=0.043) as compared with non-infected patients.

Conclusions. ACS patients with HCV infection have increased on treatment platelet reactivity, higher rate of HTPR, MACE and bleedings as compared with non-HCV patients.

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