The Effect of Ramipril in Suppressing ST2 Expression in Rheumatic Mitral Stenosis Patients

  • End date
    Aug 8, 2024
  • participants needed
  • sponsor
    Indonesia University
Updated on 23 August 2021
heart disease
mitral valve replacement
tricuspid valve repair
rheumatic heart disease


Objective propose: to investigate the effect of Ramipril in suppressing ST2 (suppression of tumorigenicity 2) in the cardiac mitral valve in patients with Rheumatic Heart Disease. We hypothesized that we hypothesized that ramipril will improve rheumatic mitral valve fibrosis through the downregulation of ST2.


The efficacy of secondary prevention is limited in the prevention of RHD progression. For this reason, new strategies and therapies are needed to prevent the progression of RHD. Neutralizing inflammatory cytokines or antagonizing their receptor function has been considered as a useful therapeutic strategy to treat autoimmune diseases. In this respect, new therapies targeting ST 2 and their receptors as studied in some autoimmune diseases may promise a new approach for patients with RHD. Angiotensin II induces the upregulation of Transforming growth factor (TGF-) and latter the binding of IL-33 to sST2 and not to the natural ligand (ST2L). The binding of IL-33 to sST2 will cause fibrogenesis even more. Thus, ACEI is hypothesized to attenuate this vicious cycle through the inhibition of Angiotensin II and consequently increase Bradykinin that furtherly inhibits fibrosis through the negative regulation of angiotensin II activity in Mitogen Activator Protein Kinase (MAPK) pathways through the suppression of the Ca2+ response and the Na+ transportACE inhibitor were agents with anti-fibrosis effects. The investigators keen to investigate the effect of Ramipril in suppressing ST2 expression as biomarkers of fibrosis in cardiac mitral valve in patients with Rheumatic Heart Disease in the National Cardiac Center Harapan Kita hospital Jakarta Indonesia. This study was designed as a randomized clinical trial. Patients with mitral stenosis valvular dysfunction due to rheumatic process planned for cardiac valve replacement surgery were given Ramipril or placebo for a minimum of 12 weeks (3 months). ST2 expression will be analyzed as the fibrosis biomarker in the mitral valve. This study will be conducted in the Department of Cardiology and Vascular Medicine, University Indonesia, National Cardiac Center Harapan Kita Hospital, Jakarta, Indonesia from June 2019

Condition Rheumatic Heart Disease, Rheumatic Fever, Heart disease, ACE inhibitor, VALVULAR HEART DISEASE, Mitral Stenosis, Heart Valve Disease, Cardiac Disease, Rheumatic Mitral Stenosis, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, angiotensin-converting enzyme inhibitor, angiotensin-converting enzyme inhibitors, ace inhibitors, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart, Fibrosis; Heart
Treatment placebos, Ramipril 5Mg Oral Capsule
Clinical Study IdentifierNCT03991910
SponsorIndonesia University
Last Modified on23 August 2021


Yes No Not Sure

Inclusion Criteria

Patients with mitral valve stenosis or a combination
aged more than 18 years
undergo cardiac valve replacement operation with or without a tricuspid valve repair
patients with systolic blood pressure (SBP) 100 mmHg and diastolic blood pressure (DBP) 60 mmHg
passed in medication phase without side effect minimum 4 weeks until operation schedule

Exclusion Criteria

Patients with congenital heart disease
patients with non-mitral valve surgery
patients with coronary artery bypass surgery
patients who refuse to join this study
adults aged over 65 years or older
pregnant women
patients with autoimmune disease
Patients with persistent hypotension (systolic blood pressure (BP) < 100 mm Hg)
severe aortic stenosis (aortic valve orifice < 0.75 cm2 )
chronic renal dysfunction with serum creatinine > 2.5 mg/ dL
known ACEI intolerance
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