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Angiogenic effects of long-term enhanced external counterpulsation in a dog model of myocardial infarction

¹Cardiology and the Key Lab on Assisted Circulation of the Health Ministry of China, The First Affiliated Hospital/Sun Yat-sen University, Guangzhou, People’s Republic of China; ²Cardiology and ³Cardiac Surgery, Harvard Medical School/Beth Israel Deaconess Medical Center, Boston, Massachusetts; and ⁴Cardiology, State University of New York at Stony Brook, Stony Brook, New York

Submitted 6 December 2004 ; accepted in final form 17 August 2005

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 -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; -actin, 11.8 ± 5.3 vs. 3.4 ± 1.2, P < 0.05). The positive-stained area per squared micrometer also increased significantly (-actin, 6.6 x 10³ ± 2.9 x 10³ µm² vs. 0.6 x 10³ ± 0.5 x 10³ µm², P < 0.05; vWF, 5.7 x 10³ ± 1.9 x 10³ µm² vs. 1.7 x 10³ ± 1.4 x 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.

angiogenesis; collateral circulation; growth factors; infarction; ventricular function

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