title: [Does cardiac resynchronization therapy improve nitric oxide concentration in exhaled gas?].
abstract: OBJECTIVE
  Cardiac resynchronization therapy (CRT) is widely known to improve cardiac function in patients with chronic heart failure, especially those with increased intraventricular conduction delay. However, whether vascular endothelial cell function is improved remains unknown. Capability of nitric oxide (NO) production is a good marker to evaluate endothelial cell function. Therefore, NO output was measured in exhaled air in patients with chronic heart failure after CRT.
  
  
  METHODS
  Six patients with chronic heart failure and dilated cardiomyopathy (mean age 62.0 +/- 11.3 years, left ventricular ejection fraction 22.8 +/- 11.6%) received CRT. Pacing leads were lodged at the right atrium, the apex of the right ventricle and at the mid portion of the postero-lateral branch of the coronary sinus. One month after CRT, endtidal NO concentration was evaluated with and without pacing using the chemiluminescence method.
  
  
  RESULTS
  Left ventricular ejection fraction improved from 22.8% to 28.8% after the procedure. Endtidal NO was significantly (p = 0.038) increased from 64.7-13.2 ppb without pacing to 69.1-14.1 ppb with pacing. Respiratory rate (with pacing: 19.7-5.7 n/min, without pacing: 20.3-4.8 n/min), tidal volume (with pacing: 523.2-122.7 ml, without pacing: 516.2-160.3 ml) and minute ventilation were not changed.
  
  
  CONCLUSIONS
  CRT did not affect respiratory rate, tidal volume or minute ventilation, so increased endtidal NO did not result from enhanced production from tracheal and/or bronchial epithelial cells. Therefore, endtidal NO increased because chronic heart failure increased pulmonary perfusion and so raised vascular shear stress. CRT for patients with dilated cardiomyopathy can improve vascular endothelial cell function.
authors.affiliation: Division of Cardiology, Gunma Prefectural Cardiovascular Center, Kameizumi Ko 3-12, Maebashi, Gunma 371-0004.
authors.forename: Tomoya
authors.initials: T
authors.lastname: Hiratsuji
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Adachi
authors.forename: Naoki
authors.initials: N
authors.lastname: Isobe
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tada
authors.forename: Takuji
authors.initials: T
authors.lastname: Toyama
authors.forename: Shigeto
authors.initials: S
authors.lastname: Naito
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hoshizaki
authors.forename: Shigeru
authors.initials: S
authors.lastname: Oshima
authors.forename: Koichi
authors.initials: K
authors.lastname: Taniguchi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology / Q000628:therapy*; D005260:Female; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000032:analysis*; D013318:Stroke Volume
chemical_list: D009569:Nitric Oxide