title: Exercise-induced systolic dysfunction in patients  with non-obstructive hypertrophic cardiomyopathy  and mutations in the cardiac troponin genes.
abstract: OBJECTIVE
  The aim of this study was to investigate left ventricular (LV) function reserve in hypertrophic cardiomyopathy (HCM) patients with and without cardiac troponin gene mutations before transition to the dilated phase.
  
  
  METHODS
  LV ejection fraction (EF) was continuously evaluated in 52 patients with non-obstructive HCM during supine ergometer exercise using radionuclide ventricular function monitoring with a cadmium telluride detector (VEST). On the basis of genetic analysis, patients were divided into two groups: 10 with cardiac troponin gene mutations (group A) and 42 without these gene mutations (group B).
  
  
  RESULTS
  Exercise duration, peak exercise load, and heart rate during exercise did not differ between the two groups. The differences from baseline to peak exercise ofthe LV end-diastolic volume decreased similarly in the twogroups. In contrast, the difference of the LV end-systolicvolume in group A increased significantly compared withgroup B (17.7% (SD 12.7%) vs 3.4% (SD 13.2%);p=0.0031). Consequently, the difference of LVEF ingroup A decreased significantly in contrast with group B(-14.1% (SD 11.1%) vs -1.2% (SD 11.7%); p=0.0025).Additionally, the changes in LVEF and stroke volumedecreased significantly more in group A than in group B(-22.2% (SD 18.6%) vs -1.1% (SD 17.8%); p=0.0017and -12.9% (SD 21.7%) vs 12.3% (SD 24.4%);p=0.0042, respectively).
  
  
  CONCLUSIONS
  These results suggest that HCM patientswith cardiac troponin gene mutations may displayexercise-induced LV systolic dysfunction more frequentlythan HCM patients without this abnormality
authors.affiliation: Division of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan. kenjis@yu.incl.ne.jp
authors.forename: K
authors.initials: K
authors.lastname: Sakata
authors.forename: H
authors.initials: H
authors.lastname: Ino
authors.forename: N
authors.initials: N
authors.lastname: Fujino
authors.forename: M
authors.initials: M
authors.lastname: Nagata
authors.forename: K
authors.initials: K
authors.lastname: Uchiyama
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Konno
authors.forename: M
authors.initials: M
authors.lastname: Inoue
authors.forename: H
authors.initials: H
authors.lastname: Kato
authors.forename: Y
authors.initials: Y
authors.lastname: Sakamoto
authors.forename: T
authors.initials: T
authors.lastname: Tsubokawa
authors.forename: M
authors.initials: M
authors.lastname: Yamagishi
mesh_terms: D000328:Adult; D000368:Aged; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics* / Q000503:physiopathology; D004452:Echocardiography; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D013599:Systole / Q000502:physiology; D019210:Troponin I / Q000235:genetics*; D018487:Ventricular Dysfunction, Left / Q000235:genetics* / Q000503:physiopathology
chemical_list: D019210:Troponin I