Impact of Acute Bronchiolitis on Cardiac Functions and Serum microRNA-122 and 499
Mona Abd El-Gelel Mohamed1 & Khalid Mahmoud Zayed1 Show affiliations
- Al-Azhar University, Egypt
American Journal of Infectious Diseases, Volume 12, Issue 1, pp. 11–19 · doi.org/10.3844/ajidsp.2016.11.19
Abstract
Bronchiolitis is an acute inflammatory injury of the bronchioles that is usually caused by a viral infection, most commonly Respiratory Syncytial Virus (RSV). This study aimed to verify the direct injurious effect of acute bronchiolitis on the myocardium and serum level of microRNA-122 and 499 (miR-122 and miR-499) of infected infants. Serum lactate dehydrogenase (LDH), creatine phosphokinase-isoenzyme MB (CK-MB) and cardiac troponin I (cTp I) were significantly elevated in mild to moderate group as well as severe group except cTp I which showed non-significant elevation in mild to moderate group, compared to control group. Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) was carried out to evaluate the serum level of miR-122 and miR-499. Sharp elevation in serum miR-122 was observed in severe cases, while miR-499 was statistically non-significant as compared to both normal and mild to moderate groups. The flow velocities across the pulmonary, tricuspid and mitral valves were recorded using standard echocardiographic techniques. Echocardiographic data showed significant reduction in pulmonary At/Et ratio in severe bronchiolitis group, compared to both normal and mild to moderate groups, respectively. Parallel reduction was also observed in tricuspid and mitral E/A ratios, compared to both normal and mild to moderate groups, respectively. Severe bronchiolitis causes cardiac dysfunction due to hypoxia, cardiac strain and pulmonary hypertension in addition to up-regulation of serum miRNA-122.
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Mohamed, M. A. E. & Zayed, K. M. (2016). Impact of Acute Bronchiolitis on Cardiac Functions and Serum microRNA-122 and 499. American Journal of Infectious Diseases, 12(1), 11–19. https://doi.org/10.3844/ajidsp.2016.11.19
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