Determining NAC mechanism in the prevention of early remodeling

Not Applicable

Conditions: Acute Myocardial Infarction.
Acute Myocardial Infarction

Registration Number: IRCT201102283449N5

Lead Sponsor: Tehran University of Medical Sciences

Brief Summary: Background: Ischemia following acute myocardial infarction provoked an increase in the level of main pro-fibrotic and inflammatory cytokine including transforming growth factor ß (TGF-ß) and tumor necrosis factor a (TNF-a) . NAC is hypothesized to have numerous therapeutic benefits in the management of cardiovascular diseases including post AMI cardiac remodeling. However, to the best of our knowledge, this is the first study evaluated NAC effect on TNF-a and TGF-ß levels in human subjects with AMI.<br /> Method: Following confirmation of STEMI, 88patients randomly administered NAC effervescent tablet 600 mg (Fluimucil®, Zambon, Swiss) or placebo twice daily for three days. For quantification of TGF-ß and TNF-a serum levels after 24 and 72 hours of NAC or placebo administration, peripheral venous blood (10 ml) samples were collected at these time points.<br /> Results: The comparison of biomarkers’ levels measured after 24 and 72 (hours between NAC and placebo groups did not show any statistically significant difference. The comparisons between levels of TGF-ß and TNF-a after 24 and 72 hours within NAC or placebo groups revealed that there was not any significant difference except for TGF-ß levels in placebo group that increased significantly with time past (p=0.042).<br /> Conclusion: The administration of NAC could prevent TGF-ß levels from increasing after 72 hours as compared with those received placebo. As TGF-ß had strong correlations with the ejection fraction as the marker of LV systolic function its late antagonism seems to be important. <br />

Detailed Description: Not available

Recruitment & Eligibility

Status: Complete

Sex: All

Target Recruitment: 80

Inclusion Criteria

Inclusion Criteria; Patients with criteria of first episode of ST-elevation AMI including typical chest pain with the duration of more than 30 minutes, >1-mm ST elevation in =2 adjacent limb leads or >2-mm ST elevation in =2 adjacent chest leads, and a raise in creatine kinase or in troponin T level 2 times the upper limit of normal were included in the study.
Exclusion Criteria; Patients with history of prior AMI, heart failure, atrial fibrillation, valvular dysfunction, and neoplastic, renal, liver, or thyroid diseases were excluded from the study. Moreover patients with current acute or chronic infections, autoimmune diseases, surgical procedures in the past 3 months; under treatment with anti-inflammatory drugs, supplements and antioxidants, subsequent MI, discharge or death during the study period were excluded.

Exclusion Criteria

Not provided

Study & Design

Study Type: interventional

Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
Tumor necrosis factor-alpha. Timepoint: 24 and 72 hours after administration of NAC or Placebo. Method of measurement: Elisa.;Transforming growth factor-beta. Timepoint: 24 and 72 hours after administration of NAC or Placebo. Method of measurement: Elisa.

Secondary Outcome Measures