Value of Low Dose Dobutamine Doppler Tissue Imaging for Detecting Hibernating Myocardium

Summary: In order to assess the value of Doppler tissue imaging (DTI) in detecting viable hibernating myocardium, 20 patients with coronary artery disease and chronic left ventricular dysfunction underwent low dose dobutamine stress echocardiography and low dose dobutamine stress DTI. The results showed that among the 100 asynergic segments, 35 segments showed improvement after dobutamine infusion (group H) and no changes were observed in the remaining 65 segments (group N). The left ventricular echocardiographic score index decreased from 1.60±0. 35 to 1.44±0.36 ( n =20, P <0.01). During low dose dobutamine stress DTI, there was no difference in the values of velosity of S wave (V s) before dobutamine infusion between two groups. However, after dobutamine infusion, the values of V s and VR in group H were significantly higher than those in group N (V s:10.1±3.0 cm/s vs 7.3±2.2 cm/s, P <0.01; VR: 60 %±41 % vs 25 %±32 %, P <0.001). 95.7 % asynergic myocardial segments with VR≤0 had no viability while 86 % asynergic segments with VR>80 % were viable myocardium. It is concluded that the different reactions to dobutamine stress between hibernating and necrosis myocardium could be showed by DTI and it is more clinically significant when VR≤0 and VR>80 %.

Effect of pharmaceutical intervention on AT_1R, AT_2R, ERK and JNK activity in chronic hibernating myocardium in rabbits

Objective： To investigate in chronic hibernating myocardium in rabbits and the influence and significance of captopril, betaloc, valsartan in angiotensin Ⅱ subtype 1 receptor（AT1R）, angiotensin Ⅱ subtype 2 receptor（AT2R）, extracellular signal regulated kinase 1/2 （ERK1/2）, c-Jun N-terminal kinase（JNK）. Methods： The model of chronic hibernating myocardium（CHM） was established. The changes of AT1R, AT2R, ERK1/2, JNK in different groups were assessed by western blotting and immunohistochemistry. Results： The amount of AT1R decreased while AT2R increased in the CON group compared with in sham group, and both AT1R and AT2R decreased in drug groups compared with the CON group. The content of ERK had no change in each group, while that of ＂expression＂ p-ERK increased in CON group compared with in sham group, and was lower in drug intervention groups than in CON and sham groups. The contents of JNK and p-JNK decreased in CON and drug intervention groups compared with in sham group. The protein levels of JNK, p-JNK in drug intervention groups were lower than in the CON group. Three drugs can inhibit interstitial fibrosis and reduce apoptotic cells. The expression levels in the groups（with different doses） had statistical difference as well as between groups of captopril and other drugs; however the results between betaloc and valsartan had no significant difference. Conclusion： AT1R, AT2R may be the upper stream receptor of ERK and JNK and may participate in generation and evolution of CHM. Captopril, valsartan and betaloc may preserve CHM by inhibiting ATIR, AT2R and JNK activity.