title: Myocardial strain analysis in acute coronary occlusion: a tool to assess myocardial viability and reperfusion.
abstract: BACKGROUND
  This study proposes 2 new echocardiographic indices with potential application in acute coronary artery occlusion to differentiate between viable and necrotic myocardium and to identify reperfusion. We investigated whether the ratio between systolic lengthening and combined late and postsystolic shortening (L-S ratio) could identify viable myocardium and whether systolic myocardial compliance, calculated as systolic lengthening divided by systolic pressure rise, could identify necrotic myocardium.
  
  
  RESULTS
  In anesthetized dogs, we measured left ventricular (LV) pressure and long-axis strain by Doppler echocardiography (SDE) and sonomicrometry. The left anterior descending coronary artery was occluded for 15 minutes with 3-hour reperfusion (n=6), for 4 hours with 3-hour reperfusion (n=6), or for 4 hours with no reperfusion (n=6). Myocardial work was quantified by pressure-segment length analysis, necrosis by triphenyltetrazolium chloride staining, and edema by water content. L-S ratio and systolic compliance were calculated by SDE. The L-S ratio ranged between 0.00 and 1.00 and was well correlated with regional myocardial work (r=0.77, P<0.0001). In entirely passive myocardium, the L-S ratio approached 1 and was similar in viable (0.88+/-0.02) and necrotic (0.81+/-0.03) myocardium. Compliance, however, was reduced in necrotic myocardium owing to edema (0.07+/-0.01%/mm Hg) but was preserved in viable myocardium (0.15+/-0.01%/mm Hg, P<0.05). Reperfusion of viable myocardium caused a reduction of the L-S ratio after 15 minutes (0.57+/-0.06, P<0.05), reflecting recovery of function. Reperfusion of necrotic myocardium caused no change in the L-S ratio, but compliance was further reduced within 15 minutes (0.03+/-0.01%/mm Hg, P<0.05).
  
  
  CONCLUSIONS
  Myocardial L-S ratio and compliance by SDE identified active contraction and necrosis, respectively. These indices should be tested clinically for assessment of myocardial viability and reperfusion.
authors.affiliation: Institute for Surgical Research, Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway.
authors.forename: Erik
authors.initials: E
authors.lastname: Lyseggen
authors.forename: Helge
authors.initials: H
authors.lastname: Skulstad
authors.forename: Thomas
authors.initials: T
authors.lastname: Helle-Valle
authors.forename: Trond
authors.initials: T
authors.lastname: Vartdal
authors.forename: Stig
authors.initials: S
authors.lastname: Urheim
authors.forename: Stein Inge
authors.initials: SI
authors.lastname: Rabben
authors.forename: Anders
authors.initials: A
authors.lastname: Opdahl
authors.forename: Halfdan
authors.initials: H
authors.lastname: Ihlen
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000000981:diagnostic imaging*; D004285:Dogs; D025401:Echocardiography, Stress / Q000379:methods* / Q000592:standards; D009200:Myocardial Contraction; D017202:Myocardial Ischemia; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D014022:Tissue Survival