Journal of the Neurological Sciences 339 (2014) 164–168

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Blood pressure variability and stroke outcome in patients with internal carotid artery occlusion Laura Buratti a, Claudia Cagnetti a, Clotilde Balucani a,b, Giovanna Viticchi a, Lorenzo Falsetti c, Simona Luzzi a, Simona Lattanzi a, Leandro Provinciali a, Mauro Silvestrini a,⁎ a b c

Neurological Clinic, Marche Polytechnic University, Ancona, Italy Department of Neurology, SUNY Downstate Medical Center, Brooklyn, NY, USA Internal and Subintensive Medicine, Ospedali Riuniti, Ancona, Italy

a r t i c l e

i n f o

Article history: Received 11 November 2013 Received in revised form 8 February 2014 Accepted 11 February 2014 Available online 18 February 2014 Keywords: Blood pressure Carotid stenosis Ischemic stroke Hypertension Treatment Risk factors

a b s t r a c t Purpose: The aim of this study was to evaluate the relationship between arterial blood pressure (BP) variability during the acute phase and the 3-month outcome in ischemic stroke patients with internal carotid artery (ICA) occlusion. Methods: At least 10 BP measurements during the first 48 h after stroke onset were obtained in 89 patients with ICA occlusion. BP profile was described using various parameters: average of recordings, maximum (max), minimum (min), difference between max and min (max − min), standard deviation (SD) and coefficient of variation (CV) for both systolic and diastolic BP. Outcome at 3 months was defined using the modified Rankin Scale (mRS) score corrected for baseline stroke severity. Results: Fifty-five patients had a good and 34 a poor outcome. Max values, max − min, SD and CV of both systolic and diastolic BP resulted significantly higher in patients with poor outcome compared to those with good outcome (p b 0.05, multivariate adjusted model). Conclusions: In a cohort of acute ischemic stroke patients with ipsilateral ICA occlusion BP variability, assessed in the acute phase, was associated with poor clinical outcome. These preliminary exploratory findings are worthy of further study to be conducted to confirm or confute the role of BP variability in predicting stroke outcome. In order to obtain more comprehensive information, it would also be appropriate to consider the possibility of acquiring data related to the pathophysiology of stroke and to cerebral hemodynamic changes. © 2014 Elsevier B.V. All rights reserved.

1. Introduction An elevated blood pressure (BP), which often declines spontaneously, is seen on presentation in most patients with acute ischemic stroke [1,2]. Most studies, although not all, have found that high BP in the acute phase of stroke is associated with a poor outcome [3,4]. Observational and interventional studies of management of acute post-stroke hypertension yield conflicting results [5–7] and yet there is no reliable evidence to guide the management of BP during the acute phase of stroke. Whether high BP in acute stroke is a physiological and protective reaction or a harmful generalized stress response and whether it should be lowered or not, remains an unsolved issue in acute stroke management [8]. ⁎ Corresponding author at: Clinica Neurologica, Università Politecnica delle Marche, Azienda Ospedaliero-Universitaria Ospedali Riuniti, Via Conca 1, 60020 Ancona, Italy. Tel.: +39 071 596 4530; fax: +39 071 887 262. E-mail address: [email protected] (M. Silvestrini).

http://dx.doi.org/10.1016/j.jns.2014.02.007 0022-510X/© 2014 Elsevier B.V. All rights reserved.

In the lack of definitive evidence about the most appropriate approach, there is a general consensus to avoid BP reduction in the first hours after an ischemic stroke unless very critical levels are reached [9]. Previous research suggested that proper BP management in acute stroke may need to take into account the underlying etiology [10,11]. Consistently, while there is evidence about the negative impact of high BP in patients with lacunar stroke [12], some pathophysiological observations have suggested the possible detrimental effect of lowering BP in patients with persistent large-vessel occlusion [13]. Furthermore, recent observations suggested that fluctuations or “variability” of BP in the first hours after stroke onset may be more relevant for prognosis than high BP per se [11,14]. A precise definition of this last aspect could have implication for a better management especially during the acute phase. The aim of this study was to investigate how different components of BP, including BP variability, assessed in acute ischemic stroke patients relate to a 3-month clinical outcome. For this investigation, we selected patients with internal carotid artery (ICA) occlusion, intrinsically more vulnerable to BP fluctuations and in which BP reduction may precipitate chronically impaired cerebral perfusion.

L. Buratti et al. / Journal of the Neurological Sciences 339 (2014) 164–168

2. Methods We prospectively evaluated consecutive patients with acute ischemic stroke ipsilateral to an ICA occlusion. The study was approved by the ethics committee of the Marche Polytechnic University. All participants and/or caregivers gave their informed written consent according to the Declaration of Helsinki. Inclusion criteria were clinical and neuroimaging diagnosis of acute ischemic stroke in the presence of an ipsilateral ICA occlusion as evidenced by a Carotid Duplex ultrasound test performed within the first hours after admission to the hospital and defined as no detectable patent lumen at gray-scale ultrasound and no flow with spectral, power, and color Doppler ultrasound [15]. In each patient enrolled in the study the diagnosis of ICA occlusion was confirmed by repeating a Carotid Duplex ultrasound test within 24 h from the enrollment. In a subgroup of patients, a follow-up vascular imaging MR or CT angiography within 72 h from admission, according to the standard of care and independently from our study, was performed. The only exclusion criterion was heart failure defined as the left ventricular ejection fraction below 50%. This was an observational study and the study procedure did not interfere with the clinical management of any of the acute stroke patients enrolled. Each patient received the best standard care available at our institution and according to the current guidelines [9]. Specifically, with respect to the treatment of acute hypertension post-stroke, a treatment algorithm based on national guidelines has been followed in all cases [16]. In all patients, supine BP was measured in the non-paralyzed arm using a manually standard mercury sphygmomanometer every 4 h from the time of admission to the stroke unit until 48 h since the onset of the stroke. The BP profile was described using various parameters for each systolic (SBP) and diastolic blood pressure (DBP) value: average of all recordings (mean), maximum (max), minimum (min), difference between max and min (max − min), standard deviation (SD) and coefficient of variation (CV) [10]. As per study protocol, we recorded the following variables: patients' demographics, stroke lesion hemispheric side, stroke subtype according to the Oxford Classification [17]: total anterior (TACS) or partial anterior circulation stroke (PACS), medications before stroke occurrence, vascular risk factors including history of prior stroke and heart disease, and stroke severity at baseline defined by the National Institute of Health Stroke Scale (NIHSS) [18] score. The clinical outcome measure was assessed using the modified Rankin Scale (mRS) score at 3 months [19]. Two certified blinded assessors measured the mRS score in all subjects. We used a baseline severity-adjusted dichotomization to define functional outcome for improving study power [10,20,21]. Poor outcome was defined as a 3-month mRS score of 2 to 6 if the baseline NIHSS score was ≤ 7 points, a 3-month mRS score of 3 to 6 if the NIHSS score was 8 to 14 points, and a 3-month mRS score of 4 to 6 if the NIHSS score was ≥ 15 points. Post-hoc power analysis showed, for a sample of 89 subjects in a MANOVA model with 12 response variables, two groups and an α set of 0.05, a power of 0.85 and an effect size (f2) of 0.25. In order to identify the possible influence of BP variability in the acute phase on 3-month functional disability (mRS score), the dataset was subdivided into two different outcome groups including patients with good and poor outcome, respectively. Differences in baseline characteristics of the sample between the outcome groups were evaluated with chi-squared test for dichotomous variables and with t-test for independent samples for continuous variables. Ordinal variables were compared with the nonparametric median test. The differences between the two outcome groups for average (mean), maximum (max), minimum (min), difference between max and min (max − min), standard deviation (SD) and coefficient of

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variation (CV) for both systolic BP (SBP) and diastolic BP (DBP) were analyzed with a t-test for independent samples. The difference among groups was also evaluated with a multivariate, unadjusted model. In order to predict functional outcome from baseline hemodynamic variables, the multivariate/adjusted model was set up to evaluate differences between outcome groups accounting for age, sex, hypertension, diabetes, smoking, dyslipidemia, side and ischemic lesion subtype according to the Oxford classification of stroke (TACS/PACS) [19]. We also performed a multivariate analysis to evaluate whether SBP variability was associated with the 3-month functional outcome independently of other BP components. For this analysis, only SBP indices (SBP max, mean, min, CV, max − min and SD) were included, adjusting for the same covariates used in the previous model. In order to internally validate the outcome measure (mRS weighted by baseline NIHSS score) we also performed a multivariate model accounting of mRS score (binary: ≤2 for good outcome or N 2 for poor outcome) at 3 months as outcome variable and baseline NIHSS score as covariate, maintaining all the covariates and risk factors used in the multivariate adjusted model. Statistical analysis was performed with the SPSS 13.0 package for Windows systems, and power analysis was performed with G*Power 3.1 for Windows systems.

3. Results During the study period, 103 patients with acute ischemic stroke and ipsilateral ICA occlusion were considered for enrolment in the study. Four were excluded due to the presence of heart failure. Out of 99 included, 10 were lost at follow-up. In all subjects, the initial ultrasound-based diagnosis of ICA occlusion was confirmed by the second Carotid Duplex ultrasound test. Reliability of diagnostic ultrasound accuracy was further confirmed by the results of CT or MRI angiography performed in 54% of patients (36 and 12 patients respectively). The final analysis included 89 patients. Time from stroke onset to admission to the hospital ranged from 7 to 9 h (mean: 8.1 ± 1.3 SD). None of these patients were treated with intravenous thrombolysis, all patients being admitted outside the approved treatment time window. At least 10 BP measurements were taken for each patient during the first 48 h after stroke onset (41–37 h after enrolment). At 3 months fifty-five patients had a good outcome and 34 had a poor outcome. Comparisons of baseline characteristics between the two groups are reported in Table 1. No significant difference was found between the two groups, including median value of baseline NIHSS scores (9.5 vs. 8; p = 0.222, median test). Median NIHSS score resulted significantly different at the 3-month evaluation (3 vs. 8, p b 0.001, median test). Blood pressure measurements are reported in Table 2. Student's t-test for independent samples and multivariate unadjusted model showed that values of mean DBP, SBP and DBP max values, max − min values, SD and CV of SBP and DBP were significantly higher in the poor outcome group compared to those with good outcome. Mean DBP was no longer significantly different, while the difference

Table 1 Comparisons of baseline characteristics according to a 3-month functional outcome based on mRS score corrected for entry NIHSS score. Characteristics

Good outcome

Poor outcome

p

Age, years ± SD Male TACS Side: right Entry NIHSS (median) Three-month NIHSS (median) Hypertension Diabetes Dyslipidemia Smoking

67.25 ± 9.86 63.6% 30.9% 50.9% 8 3 65.5% 30.9% 32.7% 25.5%

69.85 ± 8.39 58.8% 35.3% 52.9% 9.5 6 52.9% 26.5% 35.3% 26.5%

0.205 0.661 0.816 0.999 0.222 b0.001 0.270 0.811 0.821 0.999

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Table 2 Comparisons of BP parameters (mm Hg) according to a 3-month functional outcome based on mRS score corrected for entry NIHSS score (t-test for independent variables). BP parameters

Good outcome

Poor outcome

p

SBPmean SBPmax SBPmin SBPmax − SBPSD SBPCV DBPmean DBPmax DBPmin DBPmax − DBPSD DBPCV

135.47 ± 10.48 143.0 ± 15.88 129.18 ± 10.35 13.82 ± 8.16 4.99 ± 2.54 0.036 ± 0.016 82.46 ± 9.48 84.91 ± 10.43 79.54 ± 9.63 5.36 ± 5.34 2.11 ± 1.93 0.025 ± 0.023

139.38 ± 14.36 151.62 ± 13.63 127.94 ± 13.43 23.68 ± 7.42 8.13 ± 2.48 0.059 ± 0.019 86.69 ± 9.57 93.82 ± 9.77 78.23 ± 10.58 15.59 ± 8.86 5.92 ± 3.34 0.069 ± 0.042

0.434 b0.05 0.516 b0.0001 b0.0001 b0.0001 b0.05 b0.0001 0.550 b0.0001 b0.0001 b0.0001

min

min

Values are mean ± SD. mRS: modified Rankin Scale. NIHSS: National Institute of Health Stroke Scale. BP: blood pressure. DBP: diastolic blood pressure. SBP: systolic blood pressure. SD: standard deviation. CV: coefficient of variation.

between the two groups in SBP and DBP max values, max − min values, SD and CV continued to be significant (p b 0.0001) in the final multivariate adjusted model (Table 3). The multivariate/adjusted model results, which included only SBP, supported the full model. SBP max, max − min, SD and CV values were significantly higher in patients with poor outcome with respect to those with good outcome (mean ± SD): 154.25 ± 19.94 vs. 146.85 ± 22.96, p b 0.05; 24.19 ± 10.27 vs.15.11 ± 11.82, p b 0.0001; 8.15 ± 3.34 vs. 5.23 ± 3.84, p b 0.0001; 0.058 ± 0.02 vs. 0.037 ± 0.03, p b 0.0001, respectively. SBP mean and min values did not significantly differ between the two groups. In the model that included baseline NIHSS score as covariate and the binary (≤2 for good outcome or N2 for poor outcome) 3-month mRS score as outcome, results were similar to those obtained with the model based on the outcome defined by the 3-month mRS score corrected for baseline NIHSS score. The only difference was the presence of a significantly higher value of mean DBP in patients with unfavorable with respect to those with favorable outcome. Results are shown in Table 4.

4. Discussion In the present study, we sought to explore the relationship between BP variability in the first hours after stroke onset, and the 3-month outcome in a specific group of acute ischemic stroke patients with ipsilateral ICA occlusion. We found an association between measures of BP variability and clinical outcome. In particular, patients with a 3-month poor clinical outcome showed significantly higher values of SBP and DBP max values, max − min, SD and CV in comparison with patients with a good outcome. SBP variability indices remained significantly associated to the 3-month functional outcome even when analyzed independently from DBP variability indices. This finding supports the hypothesis of an independent role of both systolic and diastolic BP variability in affecting patients' outcome. The concept that BP variability may be more harmful than hypertension per se is a relatively recent notion [14]. Different studies have already reported the assessment of visit-to-visit BP variability to be a reliable predictor of stroke recurrence [22] as well as of the extent of target organ damage [23–26]. On the other hand, the effect of BP variability during the first hours after stroke onset on outcome has been investigated in a limited number of studies [5,27,28]. Recently, a direct relationship between BP variability in the subacute phase and the outcome in a large population of stroke patients independently of the stroke subtype has been described [10]. During the acute phase of stroke, cerebral autoregulation is impaired and blood flow becomes completely dependent on systemic BP. For this reason, fluctuations in BP may be detrimental for ischemic territories, particularly in the presence of an anatomic or functional compromise of small cerebral vessels [27,29]. Despite these pathophysiologic considerations, the correct management of BP in the acute and subacute phases of stroke remains controversial. Results from clinical studies have supported contradictory results on the effects of increased BP [5–7]. These controversies are probably due to the fact that while an increased BP may have positive effects on perfusion in the ischemic penumbra [30], it may also contribute to the development of edema and hemorrhagic transformation [31]. On the other hand, low BP or BP fluctuation could increase infarct size and, as a result, lead to a poor outcome [32]. In stroke patients with ipsilateral ICA occlusion, the dependence of cerebral perfusion on BP may be even more important since the mechanisms of autoregulation might be already compromised before stroke in order to maintain adequate cerebral perfusion distally to arterial occlusion [33]. In this respect, it is possible that BP fluctuations can be

Table 3 Comparisons of BP parameters (mm Hg) according to a 3-month functional outcome based on mRS score corrected for entry NIHSS score (multivariate adjusted model). BP parameters

Good outcome (95% confidence interval)

Poor outcome (95% confidence interval)

p

SBPmean SBPmax SBPmin SBPmax − SBPSD SBPCV DBPmean DBPmax DBPmin DBPmax − DBPSD DBPCV

136.75 (132.76–140.76) 144.73 (139.78–149.67) 129.45 (125.55–133.45) 15.28 (12.75–17.80) 5.29 (4.47–6.11) 0.038 (0.032–0.044) 82.71 (79.55–85.87) 84.96 (81.57–88.35) 80.09 (76.84–83.36) 4.86 (2.55–7.16) 2.09 (1.24–2.94) 0.025 (0.014–0.036)

140.09 (135.36–144.81) 152.22 (146.39–158.06) 127.87 (123.27–132.47) 24.35 (21.37–27.33) 8.21 (7.24–9.18) 0.059 (0.053–0.063) 86.32 (82.58–90.05) 93.37 (89.37–97.37) 78.02 (74.17–81.87) 15.35 (12.63–18.07) 5.99 (4.99–6.99) 0.071 (0.058–0.083)

0.222 b0.05 0.552 b0.0001 b0.0001 b0.0001 0.096 b0.0001 0.348 b0.0001 b0.0001 b0.0001

min

min

mRS: modified Rankin Scale. NIHSS: National Institute of Health Stroke Scale. BP: blood pressure. DBP: diastolic blood pressure. SBP: systolic blood pressure. SD: standard deviation. CV: coefficient of variation.

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Table 4 Comparisons of BP parameters (mm Hg) according to a 3-month functional outcome based on mRS score not corrected for entry NIHSS score (multivariate adjusted model, using NIHSS as covariate). BP parameters

mRS b 2 (95% confidence interval)

mRS ≥ 2 (95% confidence interval)

p

SBPmean SBPmax SBPmin SBPmax − SBPSD SBPCV DBPmean DBPmax DBPmin DBPmax − DBPSD DBPCV

136.65 (132.63–140.69) 144.62 (139.64–149.61) 129.38 (125.44–133.31) 15.25 (12.69–17.79) 5.26 (4.43–6.09) 0.038 (0.032–0.043) 82.56 (79.39–85.73) 84.79 (81.39–88.18) 79.99 (76.71–83.27) 4.80 (2.48–7.12) 2.05 (1.20–2.90) 0.024 (0.014–0.035)

140.47 (135.55–145.39) 152.62 (146.54–158.70) 128.14 (123.34–132.94) 24.48 (21.37–27.59) 8.31 (7.30–9.32) 0.060 (0.053–0.067) 86.91 (83.04–90.78) 94.02 (89.87–98.16) 78.45 (74.45–82.45) 15.57 (12.73–18.40) 6.14 (5.09–7.18) 0.072 (0.059–0.085)

0.183 b0.05 0.656 b0.0001 b0.0001 b0.0001 0.05 b0.0001 0.507 b0.0001 b0.0001 b0.0001

min

min

mRS: modified Rankin Scale. NIHSS: National Institute of Health Stroke Scale. BP: blood pressure. DBP: diastolic blood pressure. SBP: systolic blood pressure. SD: standard deviation. CV: coefficient of variation.

more harmful when the occurrence of stroke ipsilateral to an ICA occlusion is linked to a hypoperfusion mechanism rather than to a thromboembolic event. Unfortunately, in our study, the stroke mechanism was not defined in all study subjects. In our cohort, the presence of a clear watershed distribution of the ischemic lesion was documented in a very low percentage (about 10%) of patients that were similarly distributed in the group with poor or good outcome. Due to its pathophysiologic relevance, this aspect deserves further investigations. Different studies have demonstrated a significant link between impaired cerebral hemodynamic status ipsilateral to a carotid steno-occlusive disease and the risk of developing cerebrovascular events [34,35] or functional negative consequences including cognitive impairment [36,37]. A metaanalysis of data from the United Kingdom Transient Ischemic Attack trial, the European Carotid Surgery Trial and the North American Symptomatic Carotid Artery Trial revealed a significant negative relationship between SBP and risk for stroke recurrence among patients with 70% or greater stenosis in both carotid arteries on medical treatment [38]. These results on secondary prevention of stroke confirm the presence of a critical hemodynamic condition in patients with carotid stenoocclusive disease. About 20% of patients with TIA or stroke have significant stenosis or occlusion of at least one carotid artery [39]. This is frequently associated with stenosis of the vertebral arteries, carotid siphons, and intracranial cerebral arteries [40,41]. Our study has important limitations: despite the standardized and consistently adopted algorithm used for treating acute post-stroke hypertension, our study was purely observational and did not intervene in the clinical management of patients. The relatively low number of patients included in our study did not allow us to explore the possible effect of the antihypertensive drug regimens on BP variability and finally on clinical outcome. Furthermore, the antihypertensive therapy in patients with a diagnosis of hypertension before stroke was extremely variable. Several studies have demonstrated that different pharmacological treatments could affect cerebral hemodynamics differently [42,43] and their preferential use in certain patients may have affected functional outcomes. In the present study, we did not systematically evaluate the cerebral hemodynamic status using the transcranial Doppler-based cerebrovascular reactivity test. This, in addition to the lack of an MR imaging in all included patients did not allow us to define the cerebral hemodynamic impairment the presence and extent of small vessel disease and their relationship with BP variability and clinical outcome. Finally, it is possible that BP variability is caused by stroke severity and thus the resulting link between BP variability and functional outcomes may be confounded. In this respect, we used a baseline severity-adjusted dichotomization to define functional

outcome to improve the power of the study [10,20,21]. However, since this approach has not been yet fully validated, we also repeated the analysis and substantially confirmed our findings by using a more traditional approach considering as the outcome measure the dichotomized 3-month mRS score (≤2 and N2). In conclusion: in consecutive acute ischemic stroke patients with large artery occlusion BP variability in the acute phase — and not high BP per se — was associated with poor late clinical outcome. Thus, BP variability may provide an important prognostic factor of clinical outcome in stroke patients and targeting this variability may be a crucial clinical goal. Future efforts should be directed at confirming this finding as a predictor of poor outcome in different populations, determining which representation of BP variability in acute ischemic stroke better predicts poor outcome and evaluating the potential benefit of targeting BP variability more than blood pressure reduction per se. Conflict of interest None declared. References [1] Britton M, Carlsson A, de Faire U. Blood pressure course in patients with acute stroke and matched controls. Stroke 1986;17:861–4. [2] Okumura K, Ohya Y, Maehara A, Wakugami K, Iseki K, Takishita S. Effects of blood pressure levels on case fatality after acute stroke. J Hypertens 2005;23:1217–23. [3] Dandapani BK, Suzuki S, Kelley RE, Reyes-Iglesias Y, Duncan R. Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995;26:21–4. [4] Skalidi SJ, Manios ED, Stamatelopoulos KS, Barlas G, Michas F, Toumanidis ST, et al. Brain edema formation is associated with the time rate of blood pressure variation in acute stroke patients. Blood Press Monit 2013;18:203–7. [5] Stead LG, Gilmore RM, Vedula KC, Weaver AL, Decker WW, Brown Jr RD. Impact of acute blood pressure variability on ischemic stroke outcome. Neurology 2006;66:1878–81. [6] Tuttolomondo A, Di Sciacca R, Di Raimondo D, Pedone C, La Placa CS, Pinto SA, et al. Effects of clinical and laboratory variables and of pretreatment with cardiovascular drugs in acute ischaemic stroke: a retrospective chart review from the GIFA study. Int J Cardiol 2011;151:318–22. [7] Leonardi-Bee J, Bath PM, Phillips SJ, Sandercock PA, IST Collaborative Group. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke 2002;33:1315–20. [8] Fischer U, Rothwell PM. Blood pressure management in acute stroke. Stroke 2011;42:2995–8. [9] Furie KL, Kasner SE, Adams RJ, Albers GW, Bush RL, Fagan SC, et al. American Heart Association Stroke Council, Council on Cardiovascular Nursing, Council on Clinical Cardiology, Interdisciplinary Council on Quality of Care and Outcomes Research. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011;42:227–76. [10] Kang J, Ko Y, Park JH, Kim WJ, Jang MS, Yang MH, et al. Effect of blood pressure on 3month functional outcome in the subacute stage of ischemic stroke. Neurology 2012;79:2018–24.

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Blood pressure variability and stroke outcome in patients with internal carotid artery occlusion.

The aim of this study was to evaluate the relationship between arterial blood pressure (BP) variability during the acute phase and the 3-month outcome...
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