Analysis of NT-proBNP and uric acid due to left ventricle hypertrophy in the patients of aortic valve disease.
Aortic valve
Heart failure
Left ventricle hypertrophy
NT-proBNP
Uric acid
Journal
Pakistan journal of medical sciences
ISSN: 1682-024X
Titre abrégé: Pak J Med Sci
Pays: Pakistan
ID NLM: 100913117
Informations de publication
Date de publication:
Historique:
entrez:
19
3
2019
pubmed:
19
3
2019
medline:
19
3
2019
Statut:
ppublish
Résumé
To evaluate the concentration of N terminal proBNP (NT-proBNP) and partially the serum uric acid in the severe condition of aortic valve dysfunction for assessment of left ventricle hypertrophy. The study was conducted in the signal transduction lab department of biochemistry Quaid-I-Azam University, Islamabad from September 2013 to February 2017. NT-proBNP and serum uric acid were measured in one hundred patients of aortic valve dysfunction. The patients were divided into three main groups: 1) Aortic stenosis, 2) Aortic regurgitation, and 3) Aortic stenosis with Aortic regurgitation. The results were compared between disease and controls groups. High level of plasma NT-proBNP was detected in all the three disease groups of aortic valve (stenosis, p<0.001), (regurgitation, p<0.001) and (stenosis with regurgitation, p<0.001). In addition, non-significantly increased level of serum uric acid was also observed in left ventricle hypertrophy in all the three respective disease groups of aortic valve. Increased secretion of NT-proBNP during cardiac remodeling can be related to the severity of left ventricle hypertrophy due to aortic valve abnormality in all the disease groups of severe stenosis, severe regurgitation, and combine disease condition of severe stenosis and severe regurgitation. However, non-significant increase in uric acid concentration is also identified which may be due to one of the factors involved in left ventricle hypertrophy in all the three disease groups of aortic valve. The interaction of uric acid with NT-proBNP during cardiac remolding due to aortic valve dysfunction is still not clear.
Identifiants
pubmed: 30881420
doi: 10.12669/pjms.35.1.148
pii: PJMS-35-183
pmc: PMC6408659
doi:
Types de publication
Journal Article
Langues
eng
Pagination
183-188Déclaration de conflit d'intérêts
Conflict of Interest: The authors have no conflict of interest.
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