title: Attenuated progression of coronary artery disease after 6 years of multifactorial risk intervention: role of physical exercise.
abstract: BACKGROUND
  It was the aim of this study to assess the long-term effects of physical exercise and low-fat diet on the progression of coronary artery disease. At the beginning of the study, 113 male patients with coronary artery disease were randomized to an intervention group (n=56) or a control group (n=57); 90 patients (80%) could be reevaluated after 6 years.
  
  
  RESULTS
  Patients in the intervention group (n=40) showed a reduction in total serum cholesterol (6.03+/-1.03 versus 5.67+/-1.01 mmol/L; P<.03) and triglyceride levels (1.94+/-0.8 versus 1.6+/-0.89 mmol/L; P<.005) and maintained their initial body mass index (26+/-2 versus 27+/-2 kg/m2; P=NS), but results were not statistically different from the control group (n=50) (total serum cholesterol, 6.05+/-1.02 versus 5.79+/-0.88 mmol/L; triglycerides, 2.25+/-1.28 versus 1.85+/-0.96 mmol/L [both P=NS]; body mass index, 26+/-2 versus 28+/-3 kg/m2 [P<.0001]). In the intervention group, there was a significant 28% increase in physical work capacity (166+/-59 versus 212+/-89 W; P<.001), whereas values remained essentially unchanged in the control group (165+/-51 versus 170+/-60 W; P=NS; between groups, P<.05). In the intervention group, coronary stenoses progressed at a significantly slower rate than in the control group (P<.0001). Energy expenditure during exercise was assessed in a subgroup; patients with regression of coronary stenoses spent an average of 1784+/-384 kcal/wk (approximately 4 hours of moderate aerobic exercise per week). Multivariate regression analysis identified only physical work capacity as independently contributing to angiographic changes.
  
  
  CONCLUSIONS
  After 6 years of multifactorial risk intervention, there is significant and persistent improvement in lipoprotein levels and physical work capacity, which results in a significant retardation of disease progression. These beneficial effects appear to be largely due to chronic physical exercise.
authors.affiliation: Medizinische Universitätsklinik Heidelberg, Abteilung Innere Medizin III-Kardiologie, Germany. j.niebauer@ic.ac.uk
authors.forename: J
authors.initials: J
authors.lastname: Niebauer
authors.forename: R
authors.initials: R
authors.lastname: Hambrecht
authors.forename: T
authors.initials: T
authors.lastname: Velich
authors.forename: K
authors.initials: K
authors.lastname: Hauer
authors.forename: C
authors.initials: C
authors.lastname: Marburger
authors.forename: B
authors.initials: B
authors.lastname: Kälberer
authors.forename: C
authors.initials: C
authors.lastname: Weiss
authors.forename: E
authors.initials: E
authors.lastname: von Hodenberg
authors.forename: G
authors.initials: G
authors.lastname: Schlierf
authors.forename: G
authors.initials: G
authors.lastname: Schuler
authors.forename: R
authors.initials: R
authors.lastname: Zimmermann
authors.forename: W
authors.initials: W
authors.lastname: Kübler
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D006328:Cardiac Catheterization; D002784:Cholesterol / Q000097:blood; D017023:Coronary Angiography; D003327:Coronary Disease / Q000503:physiopathology*; D004041:Dietary Fats; D004734:Energy Metabolism; D015444:Exercise; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009538:Nicotine / Q000494:pharmacology; D012307:Risk Factors; D012907:Smoking / Q000503:physiopathology; D014280:Triglycerides / Q000097:blood
chemical_list: D004041:Dietary Fats; D014280:Triglycerides; D009538:Nicotine; D002784:Cholesterol