title: Dissociation between changes in intramyocardial function and left ventricular volumes in the eight weeks after first anterior myocardial infarction.
abstract: OBJECTIVE
  We sought to examine the relation between regional changes in intramyocardial function and global left ventricular (LV) remodeling in the first 8 weeks after reperfused first anterior myocardial infarction (MI).
  
  
  BACKGROUND
  Because of limitations in imaging methods used to date, this relation has not been thoroughly evaluated.
  
  
  METHODS
  We studied 26 patients (21 men, 5 women; mean age 51 years) by magnetic resonance imaging (MRI) on day 5 +/- 2 (mean +/- SD) and week 8 +/- 1 after their first anterior MI. All patients had single-vessel left anterior descending coronary artery disease and although they had received reperfusion therapy, all had regional LV dysfunction and an initial ejection fraction (EF) < or = 50%. Short-axis magnetic resonance tagging was performed spanning the LV. Percent intramyocardial circumferential shortening (%S) on a topographic basis, LV mass index, LV end-diastolic volume index (LVEDVI), LV end-systolic volume index and LV ejection fraction (LVEF) were measured.
  
  
  RESULTS
  Left ventricular mass index tended to decrease, whereas the LVEDVI increased from 82 +/- 24 to 96 +/- 27 ml/m2 (p = 0.002). Left ventricular end-systolic volume index remained unchanged, whereas LVEF increased from 39 +/- 12% to 45 +/- 14% (p = 0.002). Apical %S improved from 9 +/- 6% to 13 +/- 5% (p < 0.0001), as it did in the midanterior (6 +/- 6% to 10 +/- 7%, p < 0.02) and midseptal regions (8 +/- 7% to 12 +/- 6%, p < 0.02). Early dysfunction in remote midinferior and basal lateral regions resolved by 8 weeks. By multivariate analysis, the only significant predictor of an increase in LVEDVI over the study period was peak creatine kinase (p = 0.04).
  
  
  CONCLUSIONS
  In the first 8 weeks after a large, reperfused anterior MI, %S improved in the apex, midanterior and midseptal regions and normalized in remote noninfarct-related regions, but LV end-diastolic volumes also increased. This increased LVEDVI correlated with infarct size by peak creatine kinase and was not related to changes in global and regional LV function.
authors.affiliation: Department of Medicine, Allegheny University of the Health Sciences, Pittsburgh, Pennsylvania 15212, USA. ckramer@pgh.auhs.edu
authors.forename: C M
authors.initials: CM
authors.lastname: Kramer
authors.forename: W J
authors.initials: WJ
authors.lastname: Rogers
authors.forename: T M
authors.initials: TM
authors.lastname: Theobald
authors.forename: T P
authors.initials: TP
authors.lastname: Power
authors.forename: G
authors.initials: G
authors.lastname: Geskin
authors.forename: N
authors.initials: N
authors.lastname: Reichek
mesh_terms: D000328:Adult; D015906:Angioplasty, Balloon, Coronary; D016022:Case-Control Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000401:mortality / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D009206:Myocardium / Q000473:pathology; D015912:Thrombolytic Therapy; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*