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1 Institute for Surgical Research, Rikshospitalet, Oslo, Norway; Department of Cardiology, Rikshospitalet, Oslo, Norway
2 Department of Cardiology, Rikshospitalet, Oslo, Norway
3 Institute for Surgical Research, Rikshospitalet, Oslo, Norway
* To whom correspondence should be addressed. E-mail: stig.urheim{at}klinmed.uio.no.
Background and aims: Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to post-systolic shortening of ischemic apical segments that leads to reversal of early-diastolic apical flow. Methods: Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and the left atrium, and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by SDE were assessed from an apical view. Measurements were taken before and after 5 minutes of LAD occlusion. In 4 of the dogs we measured the pressure difference between LV apex and outflow tract. Results: At baseline peak early-diastolic flow velocities in the distal 1/3 of the left ventricle were directed towards apex (9.2 ± 1.6 cm/s). Following LAD occlusion the velocities reversed (-2.3 ± 0.4 cm/s, P<0.01), indicating that blood was ejected from the apex towards the base during early filling. This interpretation was confirmed by wall motion analysis, which showed post-systolic shortening of apical myocardial segments. The post-systolic shortening represented 9.7 ± 1.7 % (P<0.01) and 14.2 ± 2.4 % (P<0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. Conclusion: In the present model acute LAD occlusion resulted in reversal of early-diastolic apical flow and this was attributed to post-systolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined.
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