Hong-Wei Tan1, Li Li, Wei Zhang, Zhi-Yong Ma, Xue-Zhen Zhong, Jing-Jing Li, Ying Wang. 1. Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health; Department of Cardiology, QiLu Hospital, Shandong University, Jinan, China.
Abstract
BACKGROUND: Hypertension is an important risk factor for myocardial infarction and stroke. Accumulating data support the association of blood pressure and impairment of fibrinolysis in hypertensive patients. Fibrinolysis plays a pivotal role in atherogenesis, but there are few studies that focus on evaluating the effect of calcium channel antagonists on fibrinolysis in hypertensive patients, and the results are controversial. The aim of this study was therefore to investigate the effects of cilnidipine on fibrinolysis in Chinese hypertensive patients. METHODS: This study was an open-label, paired trial that included 43 patients with mild-to-moderate hypertension. After a 2-week placebo washout period, patients were treated with cilnidipine 5mg daily for 8 weeks. Venous blood was taken before and after treatment between 8am and 9am, after an overnight fast. Plasma tissue plasminogen activator (tPA) antigen and plasminogen activator inhibitor type 1 (PAI-1) antigen were measured by ELISA and plasma angiotensin II was measured by radioimmunoassay. RESULTS: After treatment with cilnidipine for 8 weeks, plasma tPA antigen level increased significantly (from 12.12 +/- 6.77 ng/mL pre-treatment to 16.12 +/- 11.89 ng/mL post-treatment, p < 0.05), and the PAI-1 antigen level remained unaffected. There were no significant changes in plasma angiotensin II. Systolic and diastolic blood pressures were significantly decreased without changes in heart rate. CONCLUSIONS: These data suggest that in hypertensive patients, a population with impaired fibrinolysis, cilnidipine may improve the fibrinolytic balance, and that cilnidipine is effective in treating hypertension without causing reflex tachycardia.
RCT Entities:
BACKGROUND:Hypertension is an important risk factor for myocardial infarction and stroke. Accumulating data support the association of blood pressure and impairment of fibrinolysis in hypertensivepatients. Fibrinolysis plays a pivotal role in atherogenesis, but there are few studies that focus on evaluating the effect of calcium channel antagonists on fibrinolysis in hypertensivepatients, and the results are controversial. The aim of this study was therefore to investigate the effects of cilnidipine on fibrinolysis in Chinese hypertensivepatients. METHODS: This study was an open-label, paired trial that included 43 patients with mild-to-moderate hypertension. After a 2-week placebo washout period, patients were treated with cilnidipine 5mg daily for 8 weeks. Venous blood was taken before and after treatment between 8am and 9am, after an overnight fast. Plasma tissue plasminogen activator (tPA) antigen and plasminogen activator inhibitor type 1 (PAI-1) antigen were measured by ELISA and plasma angiotensin II was measured by radioimmunoassay. RESULTS: After treatment with cilnidipine for 8 weeks, plasma tPA antigen level increased significantly (from 12.12 +/- 6.77 ng/mL pre-treatment to 16.12 +/- 11.89 ng/mL post-treatment, p < 0.05), and the PAI-1 antigen level remained unaffected. There were no significant changes in plasma angiotensin II. Systolic and diastolic blood pressures were significantly decreased without changes in heart rate. CONCLUSIONS: These data suggest that in hypertensivepatients, a population with impaired fibrinolysis, cilnidipine may improve the fibrinolytic balance, and that cilnidipine is effective in treating hypertension without causing reflex tachycardia.
Authors: Marco Pahor; Lonneke V Franse; Steven R Deitcher; William C Cushman; Karen C Johnson; Ronald I Shorr; Kandice Kottke-Marchant; Russell P Tracy; Grant W Somes; William B Applegate Journal: Circulation Date: 2002-01-29 Impact factor: 29.690
Authors: D K Kim; J W Kim; S Kim; H C Gwon; J C Ryu; J E Huh; J A Choo; Y Choi; C H Rhee; W R Lee Journal: Arterioscler Thromb Vasc Biol Date: 1997-11 Impact factor: 8.311