Z R Luo1, B Zheng. 1. Department of Cardiology, Fuzhou General Hospital of PLA, Fuzhou 350025.
Abstract
OBJECTIVE: To explore the action of platelet surface activity protein (platelet granule membrane protein CD63 and lysosome membrane protein CD62P), plasminogen activator inhibitor (PAI-1) and C-reactive protein (C-RP) in occurrence and development of unstable angina pectoris (UAP), and the effect of Puerarin on them. METHODS:Patients with UAP were randomly divided into the treated group (32 cases, treated with Puerarin) and the control group (27 cases, treated with Ticlid), the therapeutic course was 4 weeks for both groups. Changes of CD63, CD62P, PAI-1 and C-RP before and after treatment were observed. RESULTS: The levels of CD63, CD62P, PAI-1 and C-RP were higher in UAP patients than those in normal subjects and in the patients with stable angina pectoris (P < 0.05 or P < 0.01). These parameters were increased along with the aggravating of patients in Braunwald's degree. After 4-week treatment, the above-mentioned parameters lowered in both groups (P < 0.05 or P < 0.01), and comparison between the two groups showed no significant difference statistically. CONCLUSION: Platelet activation, plasminogen activator and C-RP play important roles in the occurrence and development of UAP. The obvious effect of Puerarin in anti-platelet activation, improving plasminogen activator and relieving inflammatory reaction was of great importance in preventing the occurrence and development of acute coronary syndrome clinically.
RCT Entities:
OBJECTIVE: To explore the action of platelet surface activity protein (platelet granule membrane protein CD63 and lysosome membrane protein CD62P), plasminogen activator inhibitor (PAI-1) and C-reactive protein (C-RP) in occurrence and development of unstable angina pectoris (UAP), and the effect of Puerarin on them. METHODS:Patients with UAP were randomly divided into the treated group (32 cases, treated with Puerarin) and the control group (27 cases, treated with Ticlid), the therapeutic course was 4 weeks for both groups. Changes of CD63, CD62P, PAI-1 and C-RP before and after treatment were observed. RESULTS: The levels of CD63, CD62P, PAI-1 and C-RP were higher in UAP patients than those in normal subjects and in the patients with stable angina pectoris (P < 0.05 or P < 0.01). These parameters were increased along with the aggravating of patients in Braunwald's degree. After 4-week treatment, the above-mentioned parameters lowered in both groups (P < 0.05 or P < 0.01), and comparison between the two groups showed no significant difference statistically. CONCLUSION: Platelet activation, plasminogen activator and C-RP play important roles in the occurrence and development of UAP. The obvious effect of Puerarin in anti-platelet activation, improving plasminogen activator and relieving inflammatory reaction was of great importance in preventing the occurrence and development of acute coronary syndrome clinically.