title: Serum cardiac troponin I is related to increased left ventricular wall thickness, left ventricular dysfunction, and male gender in hypertrophic cardiomyopathy.
abstract: BACKGROUND
  Serum cardiac troponin I (cTnI) is a sensitive and specific marker of myocardial injury. However, a systematic evaluation of cTnI in hypertrophic cardiomyopathy (HCM) patients has not been performed.
  
  
  OBJECTIVE
  The purpose of this study is to evaluate cTnI and determine its relationship to clinical features in HCM.
  
  
  METHODS
  We studied serum cTnI in 162 consecutive HCM patients.
  
  
  RESULTS
  Serum cTnI ranged from 0.01 to 0.83 ng/mL (mean, 0.068 +/- 0.100 ng/mL) and was higher in male patients (P < .001), those with atrial fibrillation (P = .033), and left ventricular (LV) systolic dysfunction (P = .046). Serum cTnI values were also correlated with maximum LV wall thickness (r = 0.30, P < .001), LV end-systolic diameter (r = 0.20, P = .012), and E/Ea (peak early transmitral filling velocity/early diastolic mitral annulus velocity; r = 0.24, P = .004). Serum cTnI levels were not significantly different among New York Heart Association (NYHA) functional class and there was no difference between patients with or without LV outflow tract obstruction; although B-type natriuretic peptide (BNP) levels showed significant difference in those variables. Serum cTnI had very weak correlation with BNP values (r = 0.18, P = .023). Multivariate analysis revealed an independent relationship between cTnI and maximum LV wall thickness, E/Ea, and male gender.
  
  
  CONCLUSIONS
  In patients with HCM, serum cTnI was associated with important clinical indices such as maximum LV wall thickness, LV dysfunction, and male gender. Serum cTnI seemed to have clinical significance different from that of BNP and may not be reflecting cardiac load but the LV remodeling process in HCM.
authors.affiliation: Department of Medicine and Geriatrics, Kochi Medical School, Kochi, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Kubo
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kitaoka
authors.forename: Makoto
authors.initials: M
authors.lastname: Okawa
authors.forename: Shigeo
authors.initials: S
authors.lastname: Yamanaka
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Hirota
authors.forename: Eri
authors.initials: E
authors.lastname: Hoshikawa
authors.forename: Kayo
authors.initials: K
authors.lastname: Hayato
authors.forename: Naohito
authors.initials: N
authors.lastname: Yamasaki
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Matsumura
authors.forename: Nobufumi
authors.initials: N
authors.lastname: Yasuda
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Sugiura
authors.forename: Yoshinori L
authors.initials: YL
authors.lastname: Doi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D016009:Chi-Square Distribution; D002648:Child; D003430:Cross-Sectional Studies; D015150:Echocardiography, Doppler; D005260:Female; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011237:Predictive Value of Tests; D012044:Regression Analysis; D012737:Sex Factors; D019210:Troponin I / Q000097:blood*; D015854:Up-Regulation; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling; D055815:Young Adult
chemical_list: D015415:Biomarkers; D019210:Troponin I; D020097:Natriuretic Peptide, Brain