title: Recovery of coronary function and morphology during regression of left ventricular hypertrophy.
abstract: OBJECTIVE
  To investigate changes in coronary morphology and haemodynamic function during regression of established left ventricular hypertrophy (LVH) following surgical unloading.
  
  
  METHODS
  LVH was induced in guinea-pigs by aortic banding and sham operated animals served as controls. We examined the degree of LVH, coronary haemodynamic function and contemporaneous vessel morphology 42 days post-operation. Identically treated animals were debanded and the same parameters measured after 1, 3 and 6 weeks to assess haemodynamic and morphological changes as hypertrophy regressed.
  
  
  RESULTS
  Banding resulted in an aortic pressure gradient of 41+/-9 mmHg and increases in heart/body weight ratio (46%), myocyte size (26%) and a doubling of arteriolar wall thickness, all P<0.01. These changes were accompanied by a reduction in coronary reserve (38%) and significantly (P<0.01) decreased maximal response to acetylcholine (70%), sodium nitroprusside (87%), adenosine (70%) and reactive hyperaemia (52%). Surgical debanding normalised the systemic haemodynamics and removed the aortic gradient after 7 days. There was some limited improvement in coronary structure and, to a lesser extent, function despite the continued presence of significant LVH. This had completely regressed to normal levels 23 days after debanding and was accompanied by normalisation of coronary structure and function, although systolic impedance to flow remained significantly increased. After 44 days, debanding resulted in complete cardiac morphological and functional recovery.
  
  
  CONCLUSIONS
  Left ventricular haemodynamic unloading can result in complete normalisation of LVH, coronary morphology and haemodynamic function. Although morphological and functional recovery were closely correlated, recovery of coronary morphology and function slightly preceded that of the myocardium in this aortic banded/debanded model.
authors.affiliation: Academic Cardiology Unit, National Heart and Lung Institute, Imperial College School of Medicine, St. Mary's Campus, 10th floor QEQM Wing, South Wharf Road, London W2 1NY, UK. m.kingsbury@ic.ac.uk
authors.forename: Martyn
authors.initials: M
authors.lastname: Kingsbury
authors.forename: Almut
authors.initials: A
authors.lastname: Mahnke
authors.forename: Mark
authors.initials: M
authors.lastname: Turner
authors.forename: Desmond
authors.initials: D
authors.lastname: Sheridan
mesh_terms: D000109:Acetylcholine; D000241:Adenosine; D000818:Animals; D003331:Coronary Vessels / Q000473:pathology*; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D006168:Guinea Pigs; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000473:pathology* / Q000601:surgery; D008026:Ligation; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000473:pathology; D009599:Nitroprusside; D010477:Perfusion; D012086:Reoperation; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D000241:Adenosine; D000109:Acetylcholine