INTRODUCTION/ OBJECTIVES: Polymorphonuclear leukocytes (PMNL) are involved in the pathogenesis of acute cerebral ischemia and atherosclerosis. Elastase is one of the proteolytic enzymes released by activated PMNL. We evaluated whether plasma levels of elastase-inhibitor complexes (EIC) are related to acute cerebral damage or with extension of carotid atherosclerosis in patients with stroke. METHODS: Plasma levels of EIC were determined in 44 patients during acute and chronic phases of stroke. We recorded in all patients vascular risk factors, clinical severity on admission, infarct volume, and extension of carotid atherosclerosis using B-mode ultrasound exam. RESULTS: EIC levels were not different between acute and chronic phases of stroke. Eleven patients (25%) had increased values of EIC. On multiple regression analysis diabetes, dislipemia, and coronary disease were predictors of abnormal EIC levels. EIC levels were not related to neurological severity on admission, infarct volume, or carotid atherosclerosis. CONCLUSION: EIC levels in stroke patients are associated to the presence of vascular risk factors and may reflect cellular inflammatory aspects of chronic vessel disease. However, whether elastase contributes to the development of carotid atherosclerosis in patients with stroke remains unknown.
INTRODUCTION/ OBJECTIVES: Polymorphonuclear leukocytes (PMNL) are involved in the pathogenesis of acute cerebral ischemia and atherosclerosis. Elastase is one of the proteolytic enzymes released by activated PMNL. We evaluated whether plasma levels of elastase-inhibitor complexes (EIC) are related to acute cerebral damage or with extension of carotid atherosclerosis in patients with stroke. METHODS: Plasma levels of EIC were determined in 44 patients during acute and chronic phases of stroke. We recorded in all patients vascular risk factors, clinical severity on admission, infarct volume, and extension of carotid atherosclerosis using B-mode ultrasound exam. RESULTS: EIC levels were not different between acute and chronic phases of stroke. Eleven patients (25%) had increased values of EIC. On multiple regression analysis diabetes, dislipemia, and coronary disease were predictors of abnormal EIC levels. EIC levels were not related to neurological severity on admission, infarct volume, or carotid atherosclerosis. CONCLUSION: EIC levels in strokepatients are associated to the presence of vascular risk factors and may reflect cellular inflammatory aspects of chronic vessel disease. However, whether elastase contributes to the development of carotid atherosclerosis in patients with stroke remains unknown.