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Abstract 13917: Post-systolic Shortening in the Ischemic Myocardium is Attenuated in Multivessel Disease
Ist Teil von
Circulation (New York, N.Y.), 2015-11, Vol.132 (Suppl_3 Suppl 3), p.A13917-A13917
Ort / Verlag
by the American College of Cardiology Foundation and the American Heart Association, Inc
Erscheinungsjahr
2015
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
BackgroundPost-systolic shortening (PSS) is myocardial shortening that occurs after end-systole and is considered as a sensitive marker of myocardial ischemia. Empirically, PSS in patients with multivessel disease is smaller than that in those with single vessel disease. Although this seems to be due to a decrease of difference in contraction between the ischemic and the surrounding myocardium, no study has elucidated it. We investigated the relationship between PSS and the difference of contraction between the ischemic and surrounding myocardium in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (single vessel disease model) followed by left circumflex coronary artery (LCx) occlusion (multivessel disease model).MethodsIn 7 open-chest dogs, left ventricular short-axis images (GE Vivid E9) and hemodynamic data were acquired at 3 conditions(1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strains were analyzed in 6 segments by speckle tracking software. The amplitude of PSS (εPSS) and end-systolic strain (εES) were measured and the difference of εES between a segment perfused by the LAD and the average of the other 5 segments was calculated (ΔεES).ResultsIn the LAD segment, dyskinetic motion and PSS occurred during LAD occlusion but they were paradoxically attenuated during both LAD and LCx occlusion. εPSS significantly correlated with ΔεES (r=0.95, p<0.05). Although εPSS significantly decreased during both occlusion compared to LAD occlusion, εPSS corrected by ΔεES (εPSS/ΔεES) did not decrease (figure).ConclusionsPSS in the ischemic myocardium was attenuated when the surrounding myocardium also became ischemic. The difference of contraction between the ischemic and the surrounding myocardium at end-systole seems to be a determinant of the amplitude of PSS. A parameter εPSS/ΔεES may be useful for assessing ischemia in patients with multivessel disease.