Significance of plasma levels of N-terminal Pro-B-type natriuretic peptide on left ventricular remodeling in non-obstructive hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the alpha-tropomyosin gene.
Hypertrophic cardiomyopathy (HC) is an inherited heart disease characterized by left ventricular (LV) remodeling. The present study was conducted to investigate the association of N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) levels with LV remodeling on magnetic resonance imaging and procollagen formation in 17 healthy controls and 24 patients with nonobstructive HC attributable to an identical Asp175Asn (aspartic acid to asparagine at codon 175) mutation in the alpha-tropomyosin gene. None of the patients had history of decompensated heart failure, and all patients had normal LV ejection fraction. Patients with HC had higher NT-pro-BNP levels compared with controls (median 60 pmol/L, range <40 to 359, vs <40 pmol/L; p <0.001), but 9 patients with HC had normal NT-pro-BNP levels (<40 pmol/L). In patients with HC, levels of NT-pro-BNP were correlated significantly with LV end-systolic volume index (r = 0.50, p <0.05), LV mass index (r = 0.47, p <0.05), proportion of hypokinetic segments (r = 0.50, p <0.05), and levels of serum aminoterminal propeptide of type III procollagen (r = 0.52, p <0.01). When patients with HC were divided into 3 groups on the basis of their NT-pro-BNP levels, there were statistically significant linear associations of LV end-systolic volume (test for linearity p = 0.034), LV mass index (p = 0.009), proportion of hypokinetic segments (p = 0.016), and levels of serum aminoterminal propeptide of type III procollagen (p = 0.020) with NT-pro-BNP levels over the 3 groups, suggesting a tight relation between LV remodeling and levels of NT-pro-BNP. In conclusion, in patients with nonobstructive HC attributable to an Asp175Asn mutation in the alpha-tropomyosin gene, elevated NT-pro-BNP levels are associated with incipient LV remodeling, suggesting that NT-pro-BNP could be used to diagnose insidious unfavorable LV remodeling in HC.
Magga
Jarkko
J
Department of Medicine, Kuopio University Hospital, Kuopio, Finland.
Sipola
Petri
P
Vuolteenaho
Olli
O
Risteli
Juha
J
Jääskeläinen
Pertti
P
Peuhkurinen
Keijo
K
Kuusisto
Johanna
J
D000328:Adult; D019943:Amino Acid Substitution; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood* / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009154:Mutation; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D011347:Procollagen / Q000097:blood; D013599:Systole / Q000502:physiology; D014335:Tropomyosin / Q000235:genetics; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*
D010446:Peptide Fragments; D011347:Procollagen; D014335:Tropomyosin; C109794:pro-brain natriuretic peptide (1-76); C041876:procollagen Type III-N-terminal peptide; D020097:Natriuretic Peptide, Brain