Abstract
BACKGROUND: The extent of acute aortic dissection (AAD) was correlated with inflammation positively. On the other side, inflammation was negatively correlated with mean platelet volume (MPV), which can reflect platelet (PLT) activation. The aim of this study was to clarify the relationship between the extent of dissection and PLT activation. METHODS: Between February 2010 and October 2013, 147 patients with acute aortic dissection (AAD) were divided into Group 1 (Stanford A, n = 59) and Group 2 (Stanford B, n = 88). Platelet count, MPV and platelet size distribution width (PDW) were measured to assess PLT activation. Additionally, the severity of inflammation was assessed via serum C-reactive protein (CRP), white blood cell (WBC) count and the neutrophil percent (Neut%). Computerized tomography (CT) was employed to analyze the extent of AAD. Volume tear index (VTI) was calculated as the false lumen (FL) volume divided by body surface area (BSA). RESULTS: PLT count was significantly lower in group 1 than in group 2 (137.24 ± 31.04 × 10(9)/L vs 171.43 ± 27.57 × 10(9)/L, P < 0.001). The MPV/PLT ratio and PDW were significantly higher in the group 1 respectively(0.08 ± 0.02 vs 0.06 ± 0.02, P < 0.001; 22.65 ± 1.87 fl vs 20.69 ± 1.97 fl, P < 0.001). The CRP was significantly higher in group 1 than in group 2 (36.40 ± 8.89 mg/L vs 28.97 ± 8.48 mg/L, P < 0.001). VTI was significantly higher in group 1 than in group 2 (250.12 ± 27.82 vs 198.79 ± 24.52, P < 0.001). There was a significant negative correlation between VTI and PLT count (r = -0.673, P < 0.001), CRP and PLT count (r = -0.640, P < 0.001), respectively. There was a significant positive correlation between VTI and CRP (r = 0.670, P < 0.001), VTI and PDW (r = 0.601, P < 0.001), respectively. CONCLUSIONS: PLT activation and inflammation in AAD appear to be closely correlated with the extent of dissection, which possibly induced by the tear of aortic wall. Elimination of the false lumen is the goal of traditional surgery. Suppression of the PLT activation might be future targets of therapy in the prevention of systemic inflammation in AAD patients.