title: Effect of cardiac resynchronization therapy on cardiac sympathetic nervous dysfunction and serum C-reactive protein level.
abstract: BACKGROUND
  Cardiac autonomic dysfunction is associated with a poor prognosis in patients with heart failure (HF). Systemic inflammation is elevated in patients with HF. We hypothesized that cardiac resynchronization therapy (CRT) improves cardiac sympathetic nervous dysfunction and systemic inflammation. To test our hypothesis, we evaluated cardiac sympathetic activity and serum levels of high sensitive C-reactive protein (hs-CRP) before and after CRT.
  
  
  METHODS
  Twenty-seven patients with chronic HF (19 men, eight women; mean age 67 ± 10 years) with nonischemic cardiomyopathy who underwent CRT were evaluated. Each patient was evaluated before and 6 months after CRT. Responders were defined as patients showing ≥15% absolute decrease in left ventricular end-systolic volume. Cardiac sympathetic activity was estimated with cardiac (123) I-metaiodobenzylguanidine (MIBG) scintigrams.
  
  
  RESULTS
  Patients were categorized as responders (n = 19) and nonresponders (n = 8) according to echocardiographic findings. In responders, the mean heart-to-mediastinum (H/M) ratio at the delayed phase in cardiac (123) I-MIBG scintigraphic findings was significantly increased (P<0.05) and serum levels of hs-CRP were decreased (P <0.01). Such improvements were not observed in nonresponders. Stepwise multiple regression analysis showed that the reduction in hs-CRP level was independently associated with the increase in the H/M ratio at delayed phase.
  
  
  CONCLUSIONS
  Our results demonstrated that cardiac sympathetic nervous dysfunction and systemic inflammation were improved in responder HF patients to CRT. Furthermore, the reduction in systemic inflammation was associated with the improvement in cardiac sympathetic nervous dysfunction.
authors.affiliation: Department of Internal Medicine 1             Department of Laboratory Examination and Diagnostics, Faculty of Medicine, Oita University, Oita, Japan.
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Shinohara
authors.forename: Naohiko
authors.initials: N
authors.lastname: Takahashi
authors.forename: Syotaro
authors.initials: S
authors.lastname: Saito
authors.forename: Norihiro
authors.initials: N
authors.lastname: Okada
authors.forename: Osamu
authors.initials: O
authors.lastname: Wakisaka
authors.forename: Kunio
authors.initials: K
authors.lastname: Yufu
authors.forename: Masahide
authors.initials: M
authors.lastname: Hara
authors.forename: Mikiko
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Tetsunori
authors.initials: T
authors.lastname: Saikawa
authors.forename: Hironobu
authors.initials: H
authors.lastname: Yoshimatsu
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism*; D058406:Cardiac Resynchronization Therapy; D002908:Chronic Disease; D005260:Female; D006321:Heart / Q000294:innervation* / Q000503:physiopathology; D006333:Heart Failure / Q000097:blood* / Q000000981:diagnostic imaging / Q000628:therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D016896:Treatment Outcome; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy
chemical_list: D002097:C-Reactive Protein