Context: Recent studies suggest that factors other than the degree of carotid stenosis are involved in ischemic stroke pathogenesis, especially modifications of plaque composition and related complications. Objective:...Context: Recent studies suggest that factors other than the degree of carotid stenosis are involved in ischemic stroke pathogenesis, especially modifications of plaque composition and related complications. Objective: To examine the role of carotid plaque rupture and thrombosis in ischemic stroke pathogenesis in patients undergoing carotid endarterectomy, excluding thosewith possible cardiac embolization or with severe stenosis of the circle of Willis. Design, Setting, and Patients: A total of 269 carotid plaques selected from an Interinstitutional Carotid Tissue Bank were studied by histology after surgical endarterectomy between January 1995 and December 2002. A total of 96 plaques were from patients with ipsilateral major stroke, 91 plaques from patients with transient ischemic attack(TIA), and 82 plaques from patients without symptoms. Main Outcome Measures: Differences in the frequency of thrombosis, cap rupture, cap erosion, in-flammatory infiltrate, and major cardiovascular risk factors between study groups. Results: A thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in 71(74.0%) of 96 patients with ipsilateral major stroke(and in all 32 plaques from patients operated within 2 months of symptom onset) compared with 32(35.2%) of 91 patients with TIA(P< .001) or 12(14.6%) of 82 patients who were without symptoms(P< .001). In addition, a fresh thrombus was observed in 53.8%of patients with stroke operated 13 to 24 months after the cerebrovascular event. An acute thrombus was associated with cap rupture in 64(90.1%) of 71 thrombosed plaques from patients with stroke and with cap erosion in the remaining 7 cases(9.9%). Ruptured plaques of patients affected by stroke were characterized by the presence of a more severe inflammatory infiltrate, constituted by monocytes, macrophages, and T lymphocyte cells compared with that observed in the TIA and asymptomatic groups(P=.001). There was no significant difference between groups in major cardiovascular risk factors. Conclusion: These results demonstrate a major role of carotid thrombosis and inflammation in ischemic stroke in patients affected by carotid atherosclerotic disease.展开更多
患者男性,76岁.高血压病史12年,吸烟史30年,已成烟10年.2007年1月因不稳定性心绞痛在左前降支和左回旋支近中段分别置入3 0 mm×33 mm Cypher支架和3 0mm×30 mm Endeavor支架（Cordis公司,美国）各1枚,释放压力均为16个大气压...患者男性,76岁.高血压病史12年,吸烟史30年,已成烟10年.2007年1月因不稳定性心绞痛在左前降支和左回旋支近中段分别置入3 0 mm×33 mm Cypher支架和3 0mm×30 mm Endeavor支架（Cordis公司,美国）各1枚,释放压力均为16个大气压（1个大气压=101.325 kPa）,未行后扫张（图1）.展开更多
Background: Acute myocardial infarction(MI) stems from a disruption of the plaque in the coronary artery. Based on postmortem examinations, such plaque disruption has been classified as either a rupture or an erosion....Background: Acute myocardial infarction(MI) stems from a disruption of the plaque in the coronary artery. Based on postmortem examinations, such plaque disruption has been classified as either a rupture or an erosion. Unfortunately, it has been difficult to clinically identify plaque ruptures and plaque erosions during the development of acute MI. To elucidate the relationships between clinical features and the morphological characteristics of the infarct- related lesions, we observed the culprit lesions in patients with acute MI by coronary angioscopy and intravascular ultrasound. Methods: We examined culprit lesions in 107 patients with acute MI using coronary angioscopy and intravascular ultrasound immediately before performing percutaneous coronary intervention. The lesions were then classified as plaque ruptures or nonruptured erosions, and their clinical features were compared. Results: Among the lesions studied, 44 were classified as plaque ruptures, 28 were classified as plaque erosions, and 35 were unclassified. Patients with nonruptured eroded plaques had more preinfarction angina before the onset of MI than those with ruptured plaques(53.6% vs 22.7% , P=.0074). They also had less ST- segment elevation MI(71.4% vs 93.2% , P=.0185), lower peak creatine kinase levels(2029± 1517 vs 4033± 2699 IU/L, P=.0009), less distal embolization after percutaneous coronary intervention(3.6% vs 36.4% , P=.0014), and less Q- wave MI 1 month after onset(40.7% vs 88.4% , P< .0001). Conclusion: Patients with eroded plaque lesions have smaller infarctions than those with ruptured plaque lesions, suggesting that an eroded plaque is less potently thrombogenic than a ruptured plaque.展开更多
文摘Context: Recent studies suggest that factors other than the degree of carotid stenosis are involved in ischemic stroke pathogenesis, especially modifications of plaque composition and related complications. Objective: To examine the role of carotid plaque rupture and thrombosis in ischemic stroke pathogenesis in patients undergoing carotid endarterectomy, excluding thosewith possible cardiac embolization or with severe stenosis of the circle of Willis. Design, Setting, and Patients: A total of 269 carotid plaques selected from an Interinstitutional Carotid Tissue Bank were studied by histology after surgical endarterectomy between January 1995 and December 2002. A total of 96 plaques were from patients with ipsilateral major stroke, 91 plaques from patients with transient ischemic attack(TIA), and 82 plaques from patients without symptoms. Main Outcome Measures: Differences in the frequency of thrombosis, cap rupture, cap erosion, in-flammatory infiltrate, and major cardiovascular risk factors between study groups. Results: A thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in 71(74.0%) of 96 patients with ipsilateral major stroke(and in all 32 plaques from patients operated within 2 months of symptom onset) compared with 32(35.2%) of 91 patients with TIA(P< .001) or 12(14.6%) of 82 patients who were without symptoms(P< .001). In addition, a fresh thrombus was observed in 53.8%of patients with stroke operated 13 to 24 months after the cerebrovascular event. An acute thrombus was associated with cap rupture in 64(90.1%) of 71 thrombosed plaques from patients with stroke and with cap erosion in the remaining 7 cases(9.9%). Ruptured plaques of patients affected by stroke were characterized by the presence of a more severe inflammatory infiltrate, constituted by monocytes, macrophages, and T lymphocyte cells compared with that observed in the TIA and asymptomatic groups(P=.001). There was no significant difference between groups in major cardiovascular risk factors. Conclusion: These results demonstrate a major role of carotid thrombosis and inflammation in ischemic stroke in patients affected by carotid atherosclerotic disease.
文摘患者男性,76岁.高血压病史12年,吸烟史30年,已成烟10年.2007年1月因不稳定性心绞痛在左前降支和左回旋支近中段分别置入3 0 mm×33 mm Cypher支架和3 0mm×30 mm Endeavor支架（Cordis公司,美国）各1枚,释放压力均为16个大气压（1个大气压=101.325 kPa）,未行后扫张（图1）.
文摘Background: Acute myocardial infarction(MI) stems from a disruption of the plaque in the coronary artery. Based on postmortem examinations, such plaque disruption has been classified as either a rupture or an erosion. Unfortunately, it has been difficult to clinically identify plaque ruptures and plaque erosions during the development of acute MI. To elucidate the relationships between clinical features and the morphological characteristics of the infarct- related lesions, we observed the culprit lesions in patients with acute MI by coronary angioscopy and intravascular ultrasound. Methods: We examined culprit lesions in 107 patients with acute MI using coronary angioscopy and intravascular ultrasound immediately before performing percutaneous coronary intervention. The lesions were then classified as plaque ruptures or nonruptured erosions, and their clinical features were compared. Results: Among the lesions studied, 44 were classified as plaque ruptures, 28 were classified as plaque erosions, and 35 were unclassified. Patients with nonruptured eroded plaques had more preinfarction angina before the onset of MI than those with ruptured plaques(53.6% vs 22.7% , P=.0074). They also had less ST- segment elevation MI(71.4% vs 93.2% , P=.0185), lower peak creatine kinase levels(2029± 1517 vs 4033± 2699 IU/L, P=.0009), less distal embolization after percutaneous coronary intervention(3.6% vs 36.4% , P=.0014), and less Q- wave MI 1 month after onset(40.7% vs 88.4% , P< .0001). Conclusion: Patients with eroded plaque lesions have smaller infarctions than those with ruptured plaque lesions, suggesting that an eroded plaque is less potently thrombogenic than a ruptured plaque.
