title: Physical training after percutaneous coronary intervention in patients with stable angina: effects on working capacity, metabolism, and markers of inflammation.
abstract: OBJECTIVE
  Physical activity is effective in primary and secondary prevention of cardiovascular disease. In this study, we tested the hypothesis that exercise training improves glucose and lipid metabolism, the inflammatory/anti-inflammatory balance, and the outcome of elective percutaneous coronary intervention (PCI) in patients with stable coronary disease.
  
  
  METHODS
  Sixty-two patients scheduled to undergo PCI for stable angina were randomized to intensive physical activity (n=33) consisting of home-based exercise on a bicycle ergometer or maintain their usual sedentary life (n=29). The training program started 2 months before PCI and terminated 6 months afterwards. Clinical examination, blood sampling (fasting glucose, glycated hemoglobin, lipid profile, apolipoprotein B, apolipoprotein A1, C-reactive protein, serum amyloid A, interleukin-6, interleukin-8, and interleukin-10), and maximal exercise tests were performed at inclusion, 1 week before PCI, and 3 and 6 months afterwards.
  
  
  RESULTS
  Fifty-six patients [28 per group, 45 men, mean age 63 (SD 7.8) years] completed the follow-up. According to self-reports, patients in the training group exercised more often and longer [4.9 (SD 1.1) vs. 0.6 (SD 1.3) days/week, 36 (SD 12) vs. 15 (SD 31) min/session, P<0.0001]. Improvement in maximal exercise capacity was significantly better in the training group [27 (SD 27) vs. 9 (SD 27) W, P=0.02]. Exercise had no significant effects on glucose and lipid metabolism, plasma cytokines, or acute-phase reactants.
  
  
  CONCLUSIONS
  A home-based training program significantly improved maximal exercise capacity but did not affect glucose or lipid metabolism or markers of inflammation.
authors.affiliation: Department of Geriatrics, Ospedale San Giovanni Battista, Torino, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Astengo
authors.forename: Asa
authors.initials: A
authors.lastname: Dahl
authors.forename: Thomas
authors.initials: T
authors.lastname: Karlsson
authors.forename: Lillemor
authors.initials: L
authors.lastname: Mattsson-Hultén
authors.forename: Olov
authors.initials: O
authors.lastname: Wiklund
authors.forename: Bertil
authors.initials: B
authors.lastname: Wennerblom
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D003327:Coronary Disease / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D004734:Energy Metabolism; D005081:Exercise Therapy; D017079:Exercise Tolerance; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006699:Home Care Services; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000378:metabolism; D013548:Sweden; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D015415:Biomarkers; D001786:Blood Glucose; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D018836:Inflammation Mediators; D016753:Interleukin-10; D015850:Interleukin-6; D016209:Interleukin-8; D008055:Lipids; D000685:Serum Amyloid A Protein; C505693:APOA1 protein, human; C508606:CXCL8 protein, human; C508609:IL10 protein, human; C508600:IL6 protein, human; C517652:hemoglobin A1c protein, human