title: Postsystolic shortening in ischemic myocardium: active contraction or passive recoil?
abstract: BACKGROUND
  Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE).
  
  
  RESULTS
  In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4+/-1.2% to 5.9+/-0.9% (P<0.05), whereas postsystolic shortening increased from 1.1+/-0.3% to 4.2+/-0.7% (P<0.05). In hypokinetic and akinetic segments, LV pressure-segment length and LV stress-segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2+/-1.0% (P<0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (r=0.83, P<0.01).
  
  
  CONCLUSIONS
  Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.
authors.affiliation: Institute for Surgical Research and Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway.
authors.forename: Helge
authors.initials: H
authors.lastname: Skulstad
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
authors.forename: Stig
authors.initials: S
authors.lastname: Urheim
authors.forename: Stein Inge
authors.initials: SI
authors.lastname: Rabben
authors.forename: Marie
authors.initials: M
authors.lastname: Stugaard
authors.forename: Erik
authors.initials: E
authors.lastname: Lyseggen
authors.forename: Halfdan
authors.initials: H
authors.lastname: Ihlen
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000503:physiopathology; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000503:physiopathology; D004285:Dogs; D015150:Echocardiography, Doppler / Q000379:methods*; D005260:Female; D006439:Hemodynamics; D007700:Kinetics; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015203:Reproducibility of Results; D013314:Stress, Mechanical; D013599:Systole; D017725:Ventricular Pressure