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ABSTRAK
Proses inflamasi yang terjadi akibat cedera saat Intervensi Koroner Perkutan (IKP) berkaitan dengan progresivitas penyakit jantung koroner dan memiliki hubungan erat dengan proses trombosis. HsCRP sebagai penanda fase akut inflamasi dihubungkan dengan perubahan faktor prokoagulasi dan dapat merubah struktur dan fungsi bekuan fibrin. Fibrin clot strength sebagai gambaran aktivitas trombosit dan fibrinogen telah menjadi faktor risiko baru terhadap kejadian iskemik berulang pasca IKP. Penelitian ini bertujuan untuk mencari hubungan antara High Sensitivity C-Reactive Protein (HsCRP) dengan Fibrin Clot Strength (Kekuatan Bekuan Fibrin) pasca IKP elektif. Studi ini melibatkan 50
ix
ABSTRACT
Impact of injury during Percutaneous Coronary Intervention (PCI) on inflammation process are associated with progression of coronary disease and also thrombosis process. High Sensitivity C-Reactive Protein (HsCRP), one of the acute phase protein may be linked to procoagulant changes and altered structure and function of the fibrin plaque. Fibrin clot strength represents a function of maximal dynamic properties of fibrin and platelet bonding and becomes novel risk factor for ischemic events after PCI. This study was aimed to find correlation between High Sensitivity C-Reactive Protein (HsCRP) and Fibrin Clot Strength after electif PCI. We included 50 patients with stable angina undergone stenting in Haji Adam Malik General Hospital Medan. Subjects divided into 3 groups based on the value of hsCRP. Thrombosis profile was mentioned by thromboelastogram (TEG). The result of this research exhibit that the highest tertile of hsCRP had significantly higher fibrin clot strength (11.39 ± 0.65 vs 8.67 ± 0.59, p = 0.011). HsCRP also had correlation with TEG-α, TEG-K, TEG-MA, dan TEG-G (p = 0.040, p = 0.012, p = 0.004, p = 0.004). Platelet was associated with the value of fibrin clot strength and leucocyte connected with hsCRP. In conclusion,
thrombotic risk associated with elevated hsCRP may be linked to increasement of fibrin clot strength. Patients stratification for inflammation and thrombotic risk is
