To the editor
We read with interest the study by Karabacak et al. [Citation1] that investigates for the first time mean platelet volume (MPV) in patients with hypertensive emergencies and urgencies. Although this study confirms the hypothesis of increased MPV in these patients, we believe that these findings should be critically reviewed taking into consideration the following methodological issues.
First, the definition of hypertensive emergencies in the current study differed from that of the previous [Citation2] and current [Citation3] guidelines of the European Society of Hypertension. Unlike the guidelines’ definitions, the authors included in this group patients with hypertensive crises and retinopathy or microangiopathy, which represent markers of subclinical target organ damage rather than impending or progressive organ damage characterising hypertensive emergencies. On the other hand, the authors did not include patients with elevated blood pressure (BP) and eclampsia. In addition, there is no information regarding the proportion of different organ damage associated with hypertensive emergencies and no sub-group analysis regarding MPV levels among patients with different organ damage.
Second, MPV was measured only during the hypertensive crisis in these patients, for whom no previous or future assessment of hypertension grade was performed. It would have been necessary to assess other MPV values immediately after BP control and after a period of antihypertensive treatment in the same patients or at least assess MPV values in an age- and sex-matched group of patients with well-defined grade 3 or resistant hypertension, in order to reach a safe conclusion regarding the possibly increased MPV during hypertensive urgencies or emergencies.
Third, another limitation of the present work is the lack of a well-defined normotensive control group. Office BP values were the only selection criterion for the normotensive control group, which could therefore have included patients with masked hypertension characterised by increased MPV as compared to true normotensive individuals [Citation4].
Fourth, blood sampling conditions, which are known to affect platelet activation (for example use of 18G syringe instead of 21G, collection of blood in Sodium Citrate rather than EDTA) [Citation5–7], are not clearly described by the authors, neither for the hypertensive individuals in the emergency room, nor for the normotensive control group in a probably quiter room.
In conclusion, the present study has opened the Pandora’s Box regarding platelet activation during hypertension crises. A recent study has described elevated levels of soluble P-selectin in hypertensive emergencies [Citation8]. Nevertheless, the most sensitive and reliable marker of platelet activation in several clinical settings including essential hypertension [Citation6, Citation9] is nowadays considered the measurement of monocyte-platelet aggregates (MPA) [Citation10]. Thus, well-designed studies using not only a widely accessible and rough marker of platelet activation, such as MPV but also more reliable markers such as MPA are warranted in order to confirm the hypothesis of increased platelet activation in hypertensive emergencies and urgencies.
Declaration of interest
The authors report no conflicts of interest
References
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