GRETTA NIKEN PURBOSARI, 051515153007 (2017) PERUBAHAN KADAR sST2 SETELAH PEMBERIAN TERAPI ACE INHIBITORS PADA PASIEN GAGAL JANTUNG (Penelitian Dilaksanakan di IRNA SMF Kardiologi dan Kedokteran Vaskular RSUD Dr. Soetomo Surabaya). Thesis thesis, Universitas Airlangga.

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Abstract

Background: In heart failure, mechanical stretch of myocardium is increased, resulted from neurohormonal activation as a compensation mechanism. sST2 is a cardiac marker expressed on fibroblast and cardiomyocyte as a response in myocardial mechanical stretch. sST2/1L33 complex stimulates myocytes fibrosis and hypertrophy, eventually leads to cardiac remodeling. ACE Inhibitors significantly prevent cardiac remodeling in heart failure patients by reducing mechanical stretch via several mechanisms. Objectives: To analyze the effect of ACE inhibitors therapy on sST2 level, as a cardiac marker, on inpatients with heart failure. Methods: This is an observational prospective study using one group pretest-posttest design. Conducted from July to November 2017 after ethical clearance approval from Dr. Soetomo Teaching Hospital‟s ethical comittee was issued. Patients who met all inclusion criterias was asked to signed the consent, 3 ml of blood was drew by nurse in charge before ACE inhibitor was administered and 3 days after. Serum level of sST2 were measured using ELISA and the results were statistically tested using Wilcoxon Test. Results: 3 of total 31 patients were dropped out due to death. From 28 patients analyzed, there was a decrease with mean of 45.6% in sST2 level found in 25 patients. sST2 of 18 patients decreased more than 15.5%, indicating there was a clinically significant physiological change. sST2 level before ACE Inhibitors therapy were significantly higher than on the fourth day, 222.8 (16.0-1397.2) ng/mL vs 91.5 (11.6-1319.5) ng/mL, with p=0.001. Conclusion: ACE Inhibitors therapy significantly decreased sST2 level in patients with heart failure.

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