Zhonghua xin xue guan bing za zhi · 2005
[Exploration on the relationship between thrombosis and stability of coronary atherosclerotic plaque in patients with unstable angina pectoris].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ma Shu-mei, Zou De-ling, Sun Zhi-jun, Yang Zhi-yong, Cao Qian, Sun Zhao-qing, Li Xiao-dong, Sun Ying-xian, Mizino Kyoichi
Аннотация
OBJECTIVE: To evaluate the correlation between thrombosis and stability of atherosclerotic plaque within criminal vessels in patients with unstable angina pectoris (UAP) by coronary angioscopy, to explore the clinical pathological basis for acute coronary syndromes (ACS).
METHODS: Sixty-eight patients with UAP were enrolled, the patients with post-infarction angina pectoris and variant angina pectoris were excluded. There were 48 males and 20 females, aged from 40 to 73 (average 62.4 +/- 8.6) years. The criminal vessels of there patients were observed by coronary angioscopy during percutaneous coronary intervention (PCI) therapy.
RESULTS: There were 68 criminal vessels in 68 patients. Atherosclerotic plaques were observed in all criminal vessels. Among criminal vessels, thrombi and intimae lesions were detected in 63 cases and 46 cases, respectively. Among 68 cases with atherosclerotic plaques, there were 48 cases of yellow plaques (70.5%), 18 cases of light yellow plaques (26.5%) and 2 cases of white plaques (2.94%). Sixty-three thrombi cases were mural and on-occlusive, which included 11 cases of red or mixed thrombi (17.5%) and 52 cases of white or pink thrombi (82.5%). All intimae lesions were accompanied by thrombosis, which included 11 cases of red or mixed thrombi (23.9%) and 35 cases of white or pink thrombi (76.1%).
CONCLUSION: The study has shown that the rupture of unstable yellow plaque and its thrombosis were the pathological basis of UAP. Therefore, stabilizing yellow plaque before its rupture may play critical role in prevention and treatment of ACS.
METHODS: Sixty-eight patients with UAP were enrolled, the patients with post-infarction angina pectoris and variant angina pectoris were excluded. There were 48 males and 20 females, aged from 40 to 73 (average 62.4 +/- 8.6) years. The criminal vessels of there patients were observed by coronary angioscopy during percutaneous coronary intervention (PCI) therapy.
RESULTS: There were 68 criminal vessels in 68 patients. Atherosclerotic plaques were observed in all criminal vessels. Among criminal vessels, thrombi and intimae lesions were detected in 63 cases and 46 cases, respectively. Among 68 cases with atherosclerotic plaques, there were 48 cases of yellow plaques (70.5%), 18 cases of light yellow plaques (26.5%) and 2 cases of white plaques (2.94%). Sixty-three thrombi cases were mural and on-occlusive, which included 11 cases of red or mixed thrombi (17.5%) and 52 cases of white or pink thrombi (82.5%). All intimae lesions were accompanied by thrombosis, which included 11 cases of red or mixed thrombi (23.9%) and 35 cases of white or pink thrombi (76.1%).
CONCLUSION: The study has shown that the rupture of unstable yellow plaque and its thrombosis were the pathological basis of UAP. Therefore, stabilizing yellow plaque before its rupture may play critical role in prevention and treatment of ACS.