Jianwen Liang1, Jian Shi1,2, Wenbin Wei1, Guifu Wu1,3. 1. Department of Cardiology, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, China. 2. Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Shenzhen, China. 3. Guangdong Innovative Engineering and Technology Research Center for Assisted Circulation, Shenzhen, China.
Abstract
BACKGROUND: Vascular injury is a landmark of hypertension and enhanced external counterpulsation (EECP) has been identified as a noninvasive treatment to restore the capacity of endothelial cells. However, the effect of EECP on blood pressure lowering in hypertension and the potential mechanism remain unknown. METHODS: We measured the ambulatory blood pressure (AMBP) and flow-mediated endothelial dilation (FMD) in the essential hypertensive patients who were randomly assigned to the EECP group (n = 20) or control group (n = 20). We also evaluated in vitro function of endothelial progenitor cells (EPCs). Furthermore, multivariate analysis was performed to determine the actual correlation between EPC function and FMD. RESULTS: Compared with the control, EECP group exhibited decreased systolic [(133.2 ± 4.9) mmHg vs. (139.3 ± 6.4) mmHg, P < 0.05] and diastolic [(83.4 ± 4.5) mmHg vs. (89.5 ± 7.6) mmHg, P < 0.05] blood pressure and increased FMD value [(8.87 ± 2.46%) vs. (7.51 ± 2.32%), P < 0.01]. In addition, the migration [(47.3 ± 6.4)/hpf vs. (33.4 ± 5.1) hpf, P < 0.05] and adhesion [(45.1 ± 5.5)/hpf vs. (28.4 ± 3.9) hpf, P < 0.05] functions of EPCs in the EECP group were improved significantly, whereas no change was observed in the control. Both migration [odds ratio (OR) = 0.47, 95% confidence interval (CI) = 0.27-0.64, P < 0.05] and adhesion (OR = 0.44, 95% CI = -0.0034 to 0.0012, P < 0.05) of EPCs correlated with FMD. After multivariate analysis, the migration (β = 3.37, 95% CI = 1.67-5.33, P < 0.05) and adhesion (β = 3.98, 95% CI = 1.12-6.43, P < 0.05) functions still independently correlated to FMD. CONCLUSION: The present study demonstrates for the first time that EECP decreases both systolic and diastolic blood pressure and increases FMD value in hypertension. The fall in endogenous EPCs repair capacity might be an important mechanism of hypertensive vascular injury and could be restored by EECP.
BACKGROUND: Vascular injury is a landmark of hypertension and enhanced external counterpulsation (EECP) has been identified as a noninvasive treatment to restore the capacity of endothelial cells. However, the effect of EECP on blood pressure lowering in hypertension and the potential mechanism remain unknown. METHODS: We measured the ambulatory blood pressure (AMBP) and flow-mediated endothelial dilation (FMD) in the essential hypertensive patients who were randomly assigned to the EECP group (n = 20) or control group (n = 20). We also evaluated in vitro function of endothelial progenitor cells (EPCs). Furthermore, multivariate analysis was performed to determine the actual correlation between EPC function and FMD. RESULTS: Compared with the control, EECP group exhibited decreased systolic [(133.2 ± 4.9) mmHg vs. (139.3 ± 6.4) mmHg, P < 0.05] and diastolic [(83.4 ± 4.5) mmHg vs. (89.5 ± 7.6) mmHg, P < 0.05] blood pressure and increased FMD value [(8.87 ± 2.46%) vs. (7.51 ± 2.32%), P < 0.01]. In addition, the migration [(47.3 ± 6.4)/hpf vs. (33.4 ± 5.1) hpf, P < 0.05] and adhesion [(45.1 ± 5.5)/hpf vs. (28.4 ± 3.9) hpf, P < 0.05] functions of EPCs in the EECP group were improved significantly, whereas no change was observed in the control. Both migration [odds ratio (OR) = 0.47, 95% confidence interval (CI) = 0.27-0.64, P < 0.05] and adhesion (OR = 0.44, 95% CI = -0.0034 to 0.0012, P < 0.05) of EPCs correlated with FMD. After multivariate analysis, the migration (β = 3.37, 95% CI = 1.67-5.33, P < 0.05) and adhesion (β = 3.98, 95% CI = 1.12-6.43, P < 0.05) functions still independently correlated to FMD. CONCLUSION: The present study demonstrates for the first time that EECP decreases both systolic and diastolic blood pressure and increases FMD value in hypertension. The fall in endogenous EPCs repair capacity might be an important mechanism of hypertensive vascular injury and could be restored by EECP.
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