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The Association between Multi-Vessel Coronary Artery Disease and High On-Aspirin Platelet Reactivity
Arthur Shiyovich1, Liat Sasson2, Eli Lev2
1Department of Cardiology, Rabin Medical Center, Beilinson Hospital, Petah-Tikva, and "Sackler" Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. arthur.shiyovich@gmail.com.
Insights
Multi-vessel coronary artery disease (MV-CAD) is linked to high on-aspirin platelet reactivity (HAPR). Patients with MV-CAD show significantly higher rates of HAPR compared to single-vessel disease, indicating a potential risk factor.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Medicine
Background:
- Multi-vessel coronary artery disease (MV-CAD) is associated with poorer clinical outcomes than single-vessel CAD (SV-CAD).
- Understanding factors influencing treatment efficacy in CAD is crucial for patient management.
Purpose of the Study:
- To investigate the association between MV-CAD and high on-aspirin platelet reactivity (HAPR).
- To assess HAPR in patients with stable CAD receiving aspirin therapy.
Main Methods:
- Analysis of prospectively enrolled patients with stable CAD on aspirin therapy.
- Coronary angiography used to define MV-CAD and SV-CAD.
- Platelet function testing (VerifyNow) to determine HAPR (ARU >550).
Main Results:
- 507 patients analyzed; 44% had MV-CAD.
- HAPR rate was significantly higher in MV-CAD (14.8%) versus SV-CAD (3.5%) (p < 0.001).
- MV-CAD independently predicted HAPR (OR=1.8, p=0.014), with a dose-response observed.
Conclusions:
- A significant association exists between MV-CAD and HAPR.
- MV-CAD is an independent predictor of HAPR in patients on aspirin.
- Further research into HAPR mechanisms and therapeutic strategies for MV-CAD patients is warranted.
Background:
Multi-vessel coronary artery disease (MV-CAD) is correlated with worse clinical outcomes compared with single-vessel CAD (SV-CAD). The aim of this study was to evaluate the association between MV-CAD and high on-aspirin platelet reactivity (HAPR) in patients with stable CAD treated with aspirin.
Methods:
The current study is an analysis of prospectively enrolled randomly selected patients with known stable CAD, who were taking aspirin (75-100 mg qd) regularly for at least one month, and had undergone coronary angiography at least 3 months prior to the enrollment to the study.
Exclusion Criteria:
acute coronary syndrome at the time of platelet function testing, active malignancy, acute infection, active inflammatory/rheumatic disease, major surgery in the past 6 months, chronic liver failure, treatment with oral anticoagulation, non-adherence with Aspirin and thrombocytopenia (<100 K/micl). Blood was drawn from the participants and sent for platelet function testing (VerifyNow, Instrumentation Laboratory Company, Bedford, Massachusetts, United States). MV-CAD was defined as >50% stenosis in ≥2 separate major coronary territories per coronary angiography. HAPR was defined as aspirin reaction units (ARU) >550.
Results:
Overall, 507 patients were analyzed; age 66.7 ± 11.2, 17.9% women, 223 (44%) had MV-CAD. The rate of HAPR was significantly higher among patients with MV-CAD vs. SV-CAD (14.8% vs. 3.5%, p < 0.001, respectively). Furthermore, a "dose response"-like association was found between the number of stenotic coronary arteries and the rate of HAPR (3.5%, 13.5 and 17.3% for SV-CAD, 2-vessel and 3-vessel disease, respectively). In a multivariate analysis adjusted for potential confounders, MV-CAD was found to be a strong independent predictor of HAPR [OR = 1.8 (95%CI: 1.05-4.7), p = 0.014].
Conclusions:
A significant association between MV-CAD and HAPR was found. Additional studies designed to investigate the mechanisms of HAPR and different therapeutic options for this subset of patients are warranted.
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