Enhanced external counterpulsation (EECP) is an effective noninvasive treatment of coronary artery disease. Its mechanism of action remains unknown. An acute coronary occlusion dog model was created to explore the angiogenic effect of EECP. After coronary occlusion, 12 dogs were randomly assigned to either EECP ( n = 6) or control ( n = 6). Immunohistochemical studies of α-actin and von Willebrand factor (vWF) were used to detect newly developed microvessels. Systemic and local vascular endothelial growth factor (VEGF) were identified by ELISA and reverse transcriptase PCR analysis. There was a significant increase in the density of microvessels per squared millimeter in the infarcted regions of the EECP group compared with the control group (vWF, 15.2 ± 6.3 vs. 4.9 ± 2.1, P < 0.05; α-actin, 11.8 ± 5.3 vs. 3.4 ± 1.2, P < 0.05). The positive-stained area per squared micrometer also increased significantly (α-actin, 6.6 × 103 ± 2.9 × 103 μm2 vs. 0.6 × 103 ± 0.5 × 103 μm2, P < 0.05; vWF, 5.7 × 103 ± 1.9 × 103 μm2 vs. 1.7 × 103 ± 1.4 × 103 μm2, P < 0.05). Immunohistochemical staining and reverse transcriptase PCR analysis documented a significant increase in VEGF expression. These factors associated with angiogenesis corresponded to improved myocardial perfusion by 99mTc-sestamibi single-photon emission computed tomography. Angiogenesis may be a mechanism of action for the improved myocardial perfusion demonstrated after EECP therapy.
Beneficial effects of enhanced external counterpulsation (EECP) may not be mediated by changes in myocardial perfusion
