title: Exercise training early after acute myocardial infarction reduces stress-induced hypoperfusion and improves left ventricular function.
abstract: OBJECTIVE
  Exercise training might exert its beneficial effects on myocardial perfusion by inducing coronary vascular adaptations or enhancing collateralization. We evaluated whether long-term exercise-based cardiac rehabilitation started early after ST-elevation acute myocardial infarction (STEMI) improves myocardial perfusion and left ventricular (LV) function.
  
  
  METHODS
  Forty-six patients with recent STEMI and residual inducible hypoperfusion were randomized into two groups: 25 enrolled in a 6-month outpatient exercise-based cardiac rehabilitation programme (group T) and 21 discharged with generic instructions for maintaining physical activity and correct lifestyle (group C). All patients underwent cardiopulmonary exercise test and dipyridamole rest gated myocardial perfusion single photon emission computed tomography within 1 week after STEMI and at 6-month follow-up.
  
  
  RESULTS
  At follow-up, group T showed an improvement in peak oxygen consumption, oxygen pulse and in the slope of increase in ventilation over carbon dioxide output (all p < 0.01) associated with a reduction of stress-induced hypoperfusion (p < 0.01) and an improvement in resting and post-stress wall motion score indexes (both p < 0.01), resting and post-stress wall thickening score indexes (both p < 0.05) and resting and post-stress LV ejection fraction (both p < 0.05). On the contrary, no changes in cardiopulmonary indexes, myocardial perfusion and LV function parameters were observed in group C at follow-up.
  
  
  CONCLUSIONS
  Exercise training started early after STEMI reduces stress-induced hypoperfusion and improves LV function and contractility. Exercise-induced changes in myocardial perfusion and function were associated with the absence of unfavourable LV remodelling and with an improvement of cardiovascular functional capacity.
authors.affiliation: Department of Clinical Medicine, Cardiovascular and Immunological Sciences, University of Naples Federico II, Naples, Italy.
authors.forename: Francesco
authors.initials: F
authors.lastname: Giallauria
authors.forename: Wanda
authors.initials: W
authors.lastname: Acampa
authors.forename: Francesca
authors.initials: F
authors.lastname: Ricci
authors.forename: Alessandra
authors.initials: A
authors.lastname: Vitelli
authors.forename: Giorgio
authors.initials: G
authors.lastname: Torella
authors.forename: Rosa
authors.initials: R
authors.lastname: Lucci
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Del Prete
authors.forename: Emilia
authors.initials: E
authors.lastname: Zampella
authors.forename: Roberta
authors.initials: R
authors.lastname: Assante
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Rengo
authors.forename: Dario
authors.initials: D
authors.lastname: Leosco
authors.forename: Alberto
authors.initials: A
authors.lastname: Cuocolo
authors.forename: Carlo
authors.initials: C
authors.lastname: Vigorito
mesh_terms: D000208:Acute Disease; D055426:Cardiac-Gated Single-Photon Emission Computer-Assisted Tomography; D003326:Coronary Circulation; D004562:Electrocardiography; D005080:Exercise Test; D005081:Exercise Therapy; D005260:Female; D006352:Heart Ventricles; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000534:rehabilitation*; D055414:Myocardial Perfusion Imaging; D012307:Risk Factors; D013312:Stress, Physiological; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology* / Q000628:therapy; D016276:Ventricular Function / Q000502:physiology*