title: Relationships between regional myocardial wall stress and bioenergetics in hearts with left ventricular hypertrophy.
abstract: This study utilized porcine models of postinfarction left ventricular (LV) remodeling [myocardial infarction (MI); n = 8] and concentric LV hypertrophy secondary to aortic banding (AoB; n = 8) to examine the relationships between regional myocardial contractile function (tagged MRI), wall stress (MRI and LV pressure), and bioenergetics ((31)P-magnetic resonance spectroscopy). Physiological assessments were conducted at a 4-wk time point after MI or AoB surgery. Comparisons were made with size-matched normal animals (normal; n = 8). Both MI and AoB instigated significant LV hypertrophy. Ejection fraction was not significantly altered in the AoB group, but significantly decreased in the MI group (P < 0.01 vs. normal and AoB). Systolic and diastolic wall stresses were approximately two times greater than normal in the infarct region and border zone. Wall stress in the AoB group was not significantly different from that in normal hearts. The infarct border zone demonstrated profound bioenergetic abnormalities, especially in the subendocardium, where the ratio of PCr/ATP decreased from 1.98 +/- 0.16 (normal) to 1.06 +/- 0.30 (MI; P < 0.01). The systolic radial thickening fraction and the circumferential shortening fraction in the anterior wall were severely reduced (MI, P < 0.01 vs. normal). The radial thickening fraction and circumferential shortening fraction in the AoB group were not significantly different from normal. The severely elevated wall stress in the infarct border zone was associated with a significant increase in chemical energy demand and abnormal myocardial energy metabolism. Such severe metabolic perturbations cannot support normal cardiac function, which may explain the observed regional contractile abnormalities in the infarct border zone.
authors.affiliation: Department of Medicine and Biomedical Engineering, University of Minnesota, 401 East River Road, Minneapolis, MN 55455, USA.
authors.forename: Julia
authors.initials: J
authors.lastname: Feygin
authors.forename: Qinsong
authors.initials: Q
authors.lastname: Hu
authors.forename: Cory
authors.initials: C
authors.lastname: Swingen
authors.forename: Jianyi
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000601:surgery; D003331:Coronary Vessels / Q000601:surgery; D004195:Disease Models, Animal; D004734:Energy Metabolism; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008026:Ligation; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010725:Phosphocreatine / Q000378:metabolism; D012107:Research Design; D013314:Stress, Mechanical; D013318:Stroke Volume; D013552:Swine; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate