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Comparision Between Clopidogrel and Prasugrel On hs-CRP Levels Post Percutaneous Intervention
ashokari@gmail.com
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Received: ,
This article was originally published by Thieme Medical and Scientific Publishers Private Ltd. and was migrated to Scientific Scholar after the change of Publisher.
Abstract
Abstract
Aims: This study investigated the effect of clopidogrel versus prasugrel treatment on inflammatory activity as evidenced by high-sensitivity C-reactive protein (hs-CRP) levels among patients who underwent percutaneous intervention (PCI). The effect in clinical outcomes between both the treatment groups is also explored.
Methods: The study included 53 patients into two cohorts with 30 from clopidogrel group and 23 from prasugrel group who underwent PCI for coronary artery disease. Patients were assigned either to clopidogrel or prasugrel group based on mehraan bleeding risk score. Hs-CRP was measured on 15thfollowup day. The predefined primary composite endpoint was myocardial infarction, stroke, vascular complications or death from cardiovascular causes.
Results: In both treatment groups the changes in hs-CRP levels over time were identical (2.97±3.2 in clopidogrel vs. 4.47±4.1in prasugrel p:0.14). Clinical outcomes occurred in 3 cases in clopidogrel group and one patient had puncture site hematoma in prasugrel group (p: 0.72). In contrast no significant difference in hs-CRP was noted among those had adverse clinical outcomes (1.67±2.2 vs 3.12±3.3 p: 0.47). Baseline parameters height (158.3±7.7 vs 157.8±7.7p:0.80) weight (63.4±9.7 vs 63.8±9.6 p: 0.87) hypertension (17 vs 11 p: 0.58) diabetes (11 vs 8 p: 1.00) smokers (1 vs. 5 p: 0.06) are matched between both the groups. Clopidogrel group were elderly (63.1±9.6 vs 53.7±9.5 p: 0.001) and had higher systolic blood pressure (154.7±26.2 vs 138.7±18.7 p: 0.01). Clinical scenario like type of presentation (CSA 16 vs 9 p: 0.29) LV dysfunction (10 vs 10 p: 0.57) previousPCI (5 vs 4 p: 0.94) previous CABG (2 vs 0 p: 0.143) are identical in both groups. Lesion characteristics like calcification (15 vs 11 p:0.97) tortuosity(4 vs 3 p:0.94) angulation (2 vs 0p:0.49) ostial lesion ( 8 vs 5 p:0.75) thrombotic (0 vs 1 p:0.30) was similar in both the groups. Bifurcation lesion (6 vs 1 p:0.06) usage of Gp2B3A inhibitors(3 vs 0 p:0.06) was higher in clopidogrel group.
Conclusions: Antiplatelet prasugrel and clopidogrel significantly did not affect inflammation post PCI as assessed by hs-CRP which is an established inflammatory marker. No significant difference in clinical outcomes in the follow-up between both the groups. Neither hs-CRP level was elevated in those with adverse clinical events.
