Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.

Abstract

Postsystolic shortening and thickening of ischemic and postischemic myocardium are wellrecognized phenomena, but their significance is controversial. To discover whether postsystolic shortening and thickening might represent an active process and to establish their place as possible predictors of functional recovery during and after recovery from ischemia, we examined correlations in severely ischemic dyskinetic myocardial segments in 14 open-chest anesthetized dogs (90 minutes' ischemia, n=9; 180 minutes' ischemia, n=5) between the magnitudes of postsystolic shortening and thickening during ischemia and either the magnitudes of systolic shortening and thickening in the same segments before coronary occlusion or the magnitudes of shortening and thickening at 30-60 minutes and at 2-3 weeks after reperfusion. We found positive correlations between preocclusion shortening and postsystolic shortening (r=0.44, n=33 myocardial segments; p<0.02) and between preocclusion thickening and postsystolic thickening (r= 0.73, n=13 segments; p<0.01), both measured at 5 minutes after onset of ischemia. Strong correlations were found also between postsystolic shortening and thickening measured immediately before reperfusion and systolic shortening and thickening measured after recovery at 2-3 weeks (r= 0.73, n = 28; p<0.001 for shortening; r= 0.79, n = 12; p<O.Ol for thickening). Significant but less-exact correlations were found between postsystolic shortening and thickening measured immediately before reperfusion and early recovery of shortening and thickening at 30-60 minutes after reperfusion (during the "stunned myocardium" period). Postsystolic shortening and thickening persisted early after reperfusion in dogs that had had 90 minutes of ischemia, and this predicted further significant return of function at 2-3 weeks. However, dogs that had had 180 minutes of ischemia did not have postsystolic shortening or thickening during early recovery and showed no further return of function at 2-3 weeks. The magnitudes of postsystolic shortening and thickening immediately before reperfusion were better predictors of late return of function than the histological appearance of the ischemic segments at 2-3 weeks or the magnitude of their blood flow during ischemia (15 ± 3 ,pm microspheres). From correlations made immediately before reperfusion with those at functional recovery after reperfusion, we conclude that postsystolic shortening and thickening of dyskinetic myocardial segments are markers of their potential for recovery. Correlations between preocclusion shortening and thickening and the postsystolic changes at 5 minutes after occlusion further suggest that postsystolic shortening and thickening represent active contraction; probably because of delay in relaxation caused by acute ischemia. Persistence of the postsystolic changes after reperfusion shows that prolonged contraction continues into the postischemic period. (Circulation 1988;78:994-1007) From the Coronary-Care Unit and Surgical Laboratory, Green t is well known that ...

Tissue Doppler Imaging Differentiates Transmural From Nontransmural Acute Myocardial Infarction After Reperfusion Therapy

“…Several studies have reported that PSS is consistently observed during severe ischemia. [27][28][29] The meaning of its persistence after reperfusion and the underlying mechanism, however, are a matter of debate. Mainly, it is not clear whether PSS represents an active delayed contraction (ie, identifying viable myocardium) or a passive elastic recoil.…”

Detection of Diastolic Abnormality by Dyssynchrony Imaging Correlation With Coronary Artery Disease in Patients Presenting With Visibly Normal Wall Motion

“…[3][4][5][6][7][8][9][10] It is frequently observed in patients with CAD presenting with LV asynergy. [23][24][25] Earlier studies have demonstrated the presence of abnormal diastolic function in patients with CAD without evidence of systolic wall motion abnormalities by radionuclide angiography or digitized cineangiography.…”

“…Both clinical [3][4][5] and animal studies [6][7][8][9][10] have demonstrated that PSS is related to myocardial ischemia.…”

Critical Myocardial Ischemia

“…9 Takayama et al investigated the significance of PSS before reperfusion and early recovery after reperfusion, and they demonstrated that the PSS of dyskinetic myocardium segments was a marker of their potential for recovery. 7 With the advent of tissue Doppler techniques, the detection of spatial and temporal heterogeneity of myocardial systolic strain has become feasible in the clinical setting. 8,10,11 However, tissue Doppler has an unavoidable limitation based on ultrasound angle dependency.…”