title: The angiotensin II type 2 receptor and improved adjacent region function post-MI.
abstract: Angiotensin II type 2 receptor (AT2-R) overexpression in the mouse heart preserves left ventricular (LV) size and global LV function during post-MI remodeling. We hypothesized that CMR tagging would localize regional improvements in myocardial function during post-MI remodeling in AT2-R cardiac overexpressed transgenic mice (TG), which could explain the preservation of global LV function post-MI. Six male wild-type (WT) C57BL/6 mice and 10 TG mice were studied by CMR at baseline (day 0) and days 1, 7, and 28 post-MI. MI was induced by 1 hour occlusion of the LAD followed by reperfusion. On day 1 post-MI, gadolinium-DTPA was injected to assess infarct size. LV size and function was assessed by cine CMR. Mean % circumferential shortening (%CS) was calculated within infarcted, adjacent, and remote regions at each time point in WT and TG mice. Quantitative interstitial collagen and mean myocyte cross-sectional area was measured postmortem at day 28 post-MI. LV end-systolic volume was lower and ejection fraction higher at baseline in the TG group and these differences were maintained post-MI. Within infarcted and remote zones, although %CS was higher in TG mice at day 0, there was no difference by day 28 between groups. Within adjacent regions, while there was no difference at day 0 or 1 in TG vs. WT, %CS was significantly higher in TG mice by day 7, and these changes persisted out to day 28 post-MI. Regional interstitial collagen and myocyte size were similar between groups. Thus, myocardial tagging can detect regional differences in contractile function post-MI in TG mice, and AT2-R overexpression is associated with improved contractile function in adjacent noninfarcted myocardium.
authors.affiliation: Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, USA.
authors.forename: Christina M
authors.initials: CM
authors.lastname: Bove
authors.forename: Wesley D
authors.initials: WD
authors.lastname: Gilson
authors.forename: Christopher D
authors.initials: CD
authors.lastname: Scott
authors.forename: Frederick H
authors.initials: FH
authors.lastname: Epstein
authors.forename: Zequan
authors.initials: Z
authors.lastname: Yang
authors.forename: Joseph M
authors.initials: JM
authors.lastname: Dimaria
authors.forename: Stuart S
authors.initials: SS
authors.lastname: Berr
authors.forename: Brent A
authors.initials: BA
authors.lastname: French
authors.forename: Sanford P
authors.initials: SP
authors.lastname: Bishop
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Kramer
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D003094:Collagen / Q000032:analysis; D003287:Contrast Media; D004195:Disease Models, Animal; D019786:Gadolinium DTPA; D006352:Heart Ventricles / Q000473:pathology; D007091:Image Processing, Computer-Assisted; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology; D044139:Receptor, Angiotensin, Type 2 / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D003287:Contrast Media; D044139:Receptor, Angiotensin, Type 2; D000804:Angiotensin II; D003094:Collagen; D019786:Gadolinium DTPA