title: Aerobic interval exercise training in the afternoon reduces attacks of coronary spastic angina in conjunction with improvement in endothelial function, oxidative stress, and inflammation.
abstract: BACKGROUND
  Coronary spasm plays an important role in the pathogenesis of ischemic heart disease. Endothelial function is impaired in patients with coronary spasm. Exercise training has been shown to improve endothelial function.
  
  
  OBJECTIVE
  We examined the effects of aerobic interval exercise training (AIT) on attacks in conjunction with endothelial function in patients with coronary spastic angina.
  
  
  METHODS
  The study participants were 26 patients with rest angina (19 men and 7 women, mean age 61.7±11.7 years) in whom coronary spasm was documented and no severe organic lesions were found. The numbers of attacks and of individuals with attacks were examined in conjunction with endothelial function, oxidative stress, inflammation, and insulin resistance before and after 3 successive days of AIT.
  
  
  RESULTS
  The number of attacks/patient and the ratio of patients with attacks/5 days decreased [from 2 (1, 7) to 0 (0, 2), P<0.001, and from 23/26 (88.5%) to 10/26 (38.5%), P<0.001] in conjunction with the improvement in endothelial function assessed by improved flow-mediated dilatation (4.8±2.7 vs. 6.9±2.8%, P<0.001), plasma levels of diacron-reactive oxygen metabolites (363±58 vs. 349±61 U.CARR, P=0.001), interleukin-6[1.63 (1.33, 2.22) vs. 1.39 (1.09, 2.02) pg/ml, P=0.012], high-sensitivity C-reactive protein [0.087 (0.041, 0.136) vs. 0.063 (0.028, 0.085) mg/dl, P=0.028], and homeostasis model assessment-insulin resistance [1.79 (1.41, 2.39) vs. 1.54 (1.17, 1.79) mg/dl µU/ml, P=0.005] after AIT.
  
  
  CONCLUSIONS
  AIT in the afternoon suppressed the attacks in conjunction with improvement in endothelial function, oxidative stress, inflammation, and insulin resistance in patients with coronary spastic angina.
authors.affiliation: Division of Cardiovascular Medicine, Kumamoto Kinoh Hospital, Kumamoto Aging Research Institute, Kumamoto City, Japan.
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Morikawa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Mizuno
authors.forename: Eisaku
authors.initials: E
authors.lastname: Harada
authors.forename: Daisuke
authors.initials: D
authors.lastname: Katoh
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Kashiwagi
authors.forename: Sumio
authors.initials: S
authors.lastname: Morita
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Shiro
authors.initials: S
authors.lastname: Uemura
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Saito
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology / Q000517:prevention & control*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002940:Circadian Rhythm; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D003329:Coronary Vasospasm / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005081:Exercise Therapy; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010865:Pilot Projects; D017382:Reactive Oxygen Species / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome; D014664:Vasodilation
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D002097:C-Reactive Protein