title: Clinical assessment of left ventricular rotation and strain: a novel approach for quantification of function in infarcted myocardium and its border zones.
abstract: Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects (n = 15) and patients with myocardial infarction (n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 +/- 4.9 vs. 12.9 +/- 3.5 degrees and -13.9 +/- 10.7 vs. -23.8 +/- 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent (r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction.
authors.affiliation: Department of Cardiology and Institute for Surgical Research, Rikshospitalet University Hospital and University of Oslo, Oslo, Norway.
authors.forename: Thomas
authors.initials: T
authors.lastname: Helle-Valle
authors.forename: Espen W
authors.initials: EW
authors.lastname: Remme
authors.forename: Erik
authors.initials: E
authors.lastname: Lyseggen
authors.forename: Eirik
authors.initials: E
authors.lastname: Pettersen
authors.forename: Trond
authors.initials: T
authors.lastname: Vartdal
authors.forename: Anders
authors.initials: A
authors.lastname: Opdahl
authors.forename: Hans-Jørgen
authors.initials: HJ
authors.lastname: Smith
authors.forename: Nael F
authors.initials: NF
authors.lastname: Osman
authors.forename: Halfdan
authors.initials: H
authors.lastname: Ihlen
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
mesh_terms: D000328:Adult; D000368:Aged; D003198:Computer Simulation; D005260:Female; D020342:Finite Element Analysis; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D015588:Observer Variation; D013314:Stress, Mechanical; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000502:physiology*