Abstract

We have read the article published by Kamisli et al. [1] with a great interest. They have examined the mean platelet volume (MPV) and platelet counts in patients with vertebral artery dissections and carotid artery dissections and they compared them with controls. They found a significantly higher MPV values only in the vertebral artery dissection group. On the other hand, they did not find a significant difference in platelet count between the dissection and control groups. Although the sample volume is small, this is the first study in this subject. On the other hand, we want to offer minor criticism of this study from a methodological perspective. First, the authors did not indicate the time which elapsed between blood sampling and analysis. They used ethylenediaminetetraacetic acid (EDTA) anticoagulated tubes for sample collection. However, MPV increases over time in EDTA-anticoagulated samples and this increase was shown to be proportional with the delay in time between sample collection and laboratory analysis. With impedance counting, the MPV increases over time as platelets swell in EDTA, with increases of 7.9 % within 30 min having been reported and an overall increase of 13.4 % over 24 h, although the majority of this increase occurs within the first 6 h [2]. The recommended optimal measuring time of MPV is maximum 120 min after venipuncture. For reliable MPV measurement, the potential influence of anticoagulant on the MPV must be carefully controlled by standardizing the time delay between sampling and analysis (\2 h). This situation is not clear in study. Second, there are significant associations of MPV with smoking, obesity and metabolic syndrome [3]. They did not mention about the body mass index of patients and controls, smoking status, proportion of patients and controls with metabolic syndrome. These situations are not clear in the study. Recently, it has been demonstrated that blood flow through the false lumen is a powerful activator of the coagulation and fibrinolytic systems. Because, there is intense thrombin generation and fibrinolysis and platelet activation in acute aortic dissection patients in the acute phase [4]. This appears to be major mechanism of increased MPV, an indicator of platelet reactivity. Platelet volume is mainly determined in the bone marrow. It is supposed that the large platelets are caused by a reduced fragmentation of megakaryocytes. MPV has been shown to inversely correlate with the total platelet count, which could even suggest the consumption of small platelets and a compensatory production of larger reticulated platelets [5]. Although, they did not find a significant difference in platelet count between the dissection and control groups, this may be due to small sample size. Activated platelets make thrombi at the injury site in dissections [6]. As a result, consumption of small platelets in dissection site and a compensatory production of larger reticulated platelets may be another reason of higher MPV.

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