title: Three-dimensional in-vivo dimensions of 'He's triangle' during acute left ventricular ischemia.
abstract: OBJECTIVE
  Changes in the dimensions of 'He's triangle' (formed by mitral leaflet segments subtending two associated chordae tendineae) derived from data obtained in in-vitro mitral valve models have been proposed to provide a mechanistic explanation for mitral leaflet malcoaptation. The in-vivo dynamics of He's triangle, however, have not been hitherto determined.
  
  
  METHODS
  Radio-opaque markers were placed in 13 sheep to delineate the mitral annulus and four (of an infinite number of possible) He's triangles formed by: (i) the anterior mitral leaflet (AML), first- (CT1) and second-order (CT2) chordae tendineae emanating from the anterior papillary tip (APT1) as well as from the posterior papillary tip (PPT1), respectively; and (ii) the posterior mitral leaflet (PML), CT1 and CT2 emanating from other loci on the anterior as well as the posterior papillary tips (APT2 and PPT2), respectively. Immediately postoperatively (anesthetized, open-chest), three-dimensional end-systolic marker positions were measured before and during circumflex coronary artery occlusion sufficient to produce mitral regurgitation, as verified by echocardiography.
  
  
  RESULTS
  During ischemia, three leaflet segments constituting one side of three He's triangles elongated: The AML attached to APT1 and to PPT1 by 1.5+/-1.2 mm (p <0.001) and 1.3+/-0.8 mm (p <0.001), respectively, and the posterior leaflet attached to APT2 by 1.4+/-1.9 mm (p = 0.02). Apart from a 0.9+/-1.1 mm (p = 0.02) increase in the length of CT2 attached to APT2, the length of the seven other CT1 and CT2 remained relatively unchanged during acute left ventricular ischemia.
  
  
  CONCLUSIONS
  With acute posterolateral ischemia, the lengths of CT1 and CT2 remained relatively constant, but the AML and PML lengths were not constant as the AML and PML 'unfurled' during acute left ventricular ischemia. These geometric changes may provide further insight into the mechanisms of acute ischemic mitral regurgitation, though it is not clear how they will be clinically helpful.
authors.affiliation: Department of Cardiothoracic Surgery, Stanford University School of Medicine, California 94305-5247, USA.
authors.forename: D T
authors.initials: DT
authors.lastname: Lai
authors.forename: F A
authors.initials: FA
authors.lastname: Tibayan
authors.forename: T A
authors.initials: TA
authors.lastname: Timek
authors.forename: D
authors.initials: D
authors.lastname: Liang
authors.forename: G T
authors.initials: GT
authors.lastname: Daughters
authors.forename: N B
authors.initials: NB
authors.lastname: Ingels
authors.forename: D C
authors.initials: DC
authors.lastname: Miller
mesh_terms: D000208:Acute Disease; D000818:Animals; D002815:Chordae Tendineae / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology; D021621:Imaging, Three-Dimensional; D008297:Male; D008943:Mitral Valve / Q000473:pathology* / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology; D010210:Papillary Muscles / Q000473:pathology* / Q000503:physiopathology; D012756:Sheep; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology