摘要
Background: Unstable atherosclerotic plaques activate blood cells which may adhere to the coronary endothelium causing vessel occlusion. However, it is unknown if different clinical syndromes associated with plaque rupture induce similar blood cell activation and adhesion to the endothelium. Methods: We studied changes in adhesion molecule expression of platelets(GPIIb/IIIa), neutrophils -CD18, CD11b and L-selectin -and monocytes(CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina(UA). Generation of superoxide(SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta(Ao) and coronary sinus(CS) before and 15 min after PTCA(n=13) and within the first 48 h of UA(n=12). Results: PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA. Conclusions: The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.
Background: Unstable atherosclerotic plaques activate blood cells which may adhere to the coronary endothelium causing vessel occlusion. However, it is unknown if different clinical syndromes associated with plaque rupture induce similar blood cell activation and adhesion to the endothelium. Methods: We studied changes in adhesion molecule expression of platelets(GPIIb/IIIa), neutrophils -CD18, CD11b and L-selectin -and monocytes(CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina(UA). Generation of superoxide(SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta(Ao) and coronary sinus(CS) before and 15 min after PTCA(n=13) and within the first 48 h of UA(n=12). Results: PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA. Conclusions: The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.
