BACKGROUND: The time course and characteristics of persistent regional dysfunction after ischemia remain unclear. Velocity vector imaging (VVI) allows accurate quantification of regional myocardial function. The aim of this study was to characterize the time course of regional diastolic and systolic abnormality after recovery from different durations of ischemia by VVI. METHODS: 72 rats underwent brief left coronary occlusion (3, 5, 10 and 15 min, respectively) followed by reperfusion for 4-8h. Hemodynamic measurements and VVI were performed at various time points. Regional systolic and diastolic functions were estimated from peak diastolic and systolic circumferential strain rate (SR-d and SR-s) of the left ventricle, respectively. RESULTS: Both SR-d and SR-s were significantly decreased in the ischemic segment during occlusion compared to non-ischemic segment. With the increase in occlusive time, the duration of reduced SR-d and SR-s after reperfusion was prolonged. Both SR-d and SR-s returned to pre-occlusion values in less than 30 min after reperfusion in the 3 min and 5 min ischemia groups. However, in the 10- and 15-min ischemia groups, SR-d did not fully recovered even at 240 min after reperfusion despite complete recovery of SR-s. The left ventricular hemodynamics during occlusion were significantly changed in all groups and returned to baseline immediately after reperfusion. CONCLUSION: The persistence of diastolic regional dysfunction is longer than systolic regional dysfunction after a relative longer ischemic event, suggesting that recent myocardial ischemic insult mimicking variant angina may be recognized with the evaluation of regional diastolic function.
BACKGROUND: The time course and characteristics of persistent regional dysfunction after ischemia remain unclear. Velocity vector imaging (VVI) allows accurate quantification of regional myocardial function. The aim of this study was to characterize the time course of regional diastolic and systolic abnormality after recovery from different durations of ischemia by VVI. METHODS: 72 rats underwent brief left coronary occlusion (3, 5, 10 and 15 min, respectively) followed by reperfusion for 4-8h. Hemodynamic measurements and VVI were performed at various time points. Regional systolic and diastolic functions were estimated from peak diastolic and systolic circumferential strain rate (SR-d and SR-s) of the left ventricle, respectively. RESULTS: Both SR-d and SR-s were significantly decreased in the ischemic segment during occlusion compared to non-ischemic segment. With the increase in occlusive time, the duration of reduced SR-d and SR-s after reperfusion was prolonged. Both SR-d and SR-s returned to pre-occlusion values in less than 30 min after reperfusion in the 3 min and 5 min ischemia groups. However, in the 10- and 15-min ischemia groups, SR-d did not fully recovered even at 240 min after reperfusion despite complete recovery of SR-s. The left ventricular hemodynamics during occlusion were significantly changed in all groups and returned to baseline immediately after reperfusion. CONCLUSION: The persistence of diastolic regional dysfunction is longer than systolic regional dysfunction after a relative longer ischemic event, suggesting that recent myocardial ischemic insult mimicking variant angina may be recognized with the evaluation of regional diastolic function.