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Blood pressure and early neurological deterioration in acute ischemic stroke

Kjeldsen, Sverre E.a,b; Berge, Eivinda

doi: 10.1097/HJH.0000000000000689
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aDepartment of Cardiology, Oslo University Hospital

bInstitute for Clinical Medicine, University of Oslo, Oslo, Norway

Correspondence to Sverre E. Kjeldsen, MD, PhD, Department of Cardiology, Oslo University Hospital Ullevål, University of Oslo, N-0407 Oslo, Norway Tel: +47 22 11 91 00; fax: +47 22 11 91 81; e-mail: sverrkj@online.no

Early neurological deterioration is an indicator of poor outcome after acute ischemic stroke [1]. The condition can be caused by different mechanisms, for example progression of thrombus, development of cerebral edema and hemorrhagic transformation [2]; it affects up to a quarter of all acute stroke patients and raises the risk of death or disability two to three-fold [3].

In this issue of Journal of Hypertension, Chung et al.[4] report their data on the association between blood pressure (BP) and the development of early neurological deterioration. In their retrospective study, they observed a consecutive series of patients hospitalized for acute ischemic stroke within 24 h of onset. The primary outcome was the development of early neurological deterioration according to predefined criteria within the first 72 h of stroke onset. For systolic blood pressure (SBP) and diastolic blood pressure (DBP) variability, they used the difference between the maximum and minimum recordings, the standard deviation and the coefficient of variation. They also studied effects of maximum and mean SBP and DBP. Of 1161 patients, 210 (18%) developed early neurological deterioration. All BP parameters (except for the difference between maximum and minimum SBP) were linearly and significantly associated with early neurological deterioration, independent of mean BP and clinical variables. After adjustments for confounders, the odds for early neurological deterioration increased with 14–21% with an increase of one standard deviation in any of the BP parameters. The authors conclude that high BP and high BP variability were independently and linearly associated with the development of neurologic deterioration in acute ischemic stroke.

BP may contribute to the development of early neurological deterioration and poor outcome by affecting cerebral perfusion. For example, reduced cerebral haemodynamic reserve [5] and absence of collateral blood supply seem to be associated with early neurological deterioration, whereas the presence of collateral blood flow seems to be associated with early spontaneous neurological improvements in acute ischemic stroke [6]. Not only mean BP but also BP variability seems to be an independent negative prognostic variable. Visit-to-visit BP variability is a risk factor for vascular events during long-term follow-up [7,8], and increased BP variability in the acute phase of intracerebral haemorrhage has been shown to be a predictor of poor prognosis in the long term [9]. There are also studies on the association between BP variability in the acute phase of ischemic stroke and lesion growth measured by diffusion-weighted MRI [10], early neurological deterioration [11], symptomatic haemorrhagic transformation [12], poor functional outcome [10] and death [13]. Other studies have also shown the importance of BP for prognosis after ischemic stroke. In one study, an inverted J-shaped relationship was observed between a decrease in BP and prognosis [14], and another study demonstrated an increased risk in the high BP group [15].

In the Scandinavian Candesartan Acute Stroke Trial (SCAST) of patients with acute ischemic stroke or intracerebral haemorrhage, we did not see a beneficial effect of lowering of systolic BP by about 5 mmHg with active treatment with candesartan vs. placebo started within 30 h of onset of symptoms [16], but a nonrandomized comparison using observational data from the whole study population showed less early neurological deterioration in patients with small to moderate fall in SBP from day 1 to day 2, compared with the patients with a rise or with a large fall in SBP [16]. This analysis also showed that patients with the highest SBP at baseline were at highest risk of early adverse events [17]. This is consistent with the results of previous studies [18,19]. These results are also supported by a population-based study, which suggested that optimal outcome after acute stroke is determined both by initial BP levels and also the magnitude of BP change over the first 24–48 h [20].

In the analysis of SCAST, we also observed that patients with an increase in SBP from day 1 to day 2 had an increased risk of early adverse events [17]. The reason for this association cannot be elucidated from this analysis [17], but it is possible that this association was not caused by the increase in BP per se, but rather that the increase in BP was a marker for other disease, such as edema development, hemorrhagic transformation, pain or infection. It is important to note that the same may be true for the association between BP variability in the acute phase and outcome after stroke; increased BP variability may be a consequence of the underlying severity of the neurological damage and not necessarily the cause of it, as suggested by Chung et al.[4]. Still, the study of Chung et al.[4] makes an important contribution to our understanding of the role of BP and BP variability in the acute phase of stroke. Future prospective and even larger studies should aim at understanding in more detail the underlying pathophysiology of BP and BP variability in acute ischemic stroke and continue to test meaningful interventions that may favour patient treatment.

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ACKNOWLEDGEMENTS

Conflicts of interest

S.E.K. was a member of the SCAST Steering Committee and has received honoraria for lectures and participation in advisory boards from Bayer, Merck Sharp and Dome, Novartis, Serodus and Takeda within the past 2 years. E.B. was coordinating investigator in SCAST.

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