Why the study?
High on-treatment platelet reactivity is linked to ischemic events in CAD, but data regarding its association with HCV infection are lacking.
Does Hepatitis C Virus infection increase on-treatment platelet reactivity and worsen clinical outcomes in patients with acute coronary syndrome on dual antiplatelet therapy?
Does Hepatitis C Virus infection increase on-treatment platelet reactivity and worsen clinical outcomes in patients with acute coronary syndrome on dual antiplatelet therapy?
HCV infection in ACS patients on dual antiplatelet therapy is associated with higher on-treatment platelet reactivity, more severe coronary artery disease, and worse long-term cardiovascular and bleeding outcomes.
HCV-associated platelet reactivity in ACS is hypothesis-generating; prospective validation required before clinical implications.
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. This post hoc analysis aims to assess high on‐treatment platelet reactivity, severity of CAD, and long‐term outcomes of patients with acute coronary syndrome (ACS) who were infected with HCV. Methods and Results Patients with ACS who were infected with HCV (n=47) were matched to patients with ACS and without HCV (n=137) for age, sex, diabetes mellitus, hypertension, and renal function. HCV‐infected patients with ACS had higher levels of platelet reactivity (ADP 10 –light transmittance aggregometry, 56±18% versus 44±22% [ P =0.002]; arachidonic acid–light transmittance aggregometry, 25±21% versus 16±15% [ P =0.011]) and higher rates of high on‐treatment platelet reactivity on clopidogrel and aspirin compared with patients without HCV. Moreover, HCV‐infected patients with ACS had higher rates of multivessel disease (53% versus 30%; P =0.004) and 3‐vessel disease (32% versus 7%; P <0.001) compared with patients without HCV. At long‐term follow‐up, estimated rates of major adverse cardiovascular events (cardiac death, nonfatal myocardial infarction, and ischemia‐driven revascularization) were 57% versus 34% ( P =0.005) in HCV‐ and non–HCV‐infected patients with ACS, respectively. In addition, thrombolysis In Myocardial Infarction (TIMI) major bleeding rates were higher in HCV‐infected patients (11% versus 3%; P =0.043) compared with noninfected patients. Multivariable analysis demonstrated that HCV infection was an independent predictor of high on‐treatment platelet reactivity, severity of CAD, and long‐term outcome. Conclusions In this hypothesis‐generating study, patients with ACS and HCV infection showed increased on‐treatment platelet reactivity, more severe CAD, and worse prognosis compared with patients without HCV.
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Scudiero et al. (2020) studied this question.
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