Treating Hypertension in Acute Ischemic Stroke
2009; Lippincott Williams & Wilkins; Volume: 54; Issue: 4 Linguagem: Inglês
10.1161/hypertensionaha.109.134486
ISSN1524-4563
Autores Tópico(s)Neurological Disorders and Treatments
ResumoHomeHypertensionVol. 54, No. 4Treating Hypertension in Acute Ischemic Stroke Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBTreating Hypertension in Acute Ischemic Stroke J. David Spence J. David SpenceJ. David Spence From the Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute, University of Western Ontario, London, Ontario, Canada. Originally published3 Aug 2009https://doi.org/10.1161/HYPERTENSIONAHA.109.134486Hypertension. 2009;54:702–703Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 3, 2009: Previous Version 1 Persistence of the controversy over whether hypertension should be treated in acute ischemic stroke is a testament to the power of tradition and authority in medicine. It also probably reflects the tendency of physicians to be unduly influenced by the most recent adverse events that they remember in their own patients.1Concern about worsening of stroke with excessive lowering of blood pressure has been based to a large extent on inappropriate historical hypotensive therapies that cannot be controlled, such as "sublingual" nifedipine or intramuscular hydralazine.2 As I pointed out with Del Maestro in 1985,3 there are some circumstances in which severe hypertension must be treated in acute ischemic stroke. Two examples I have seen are aortic dissection picking off a renal and a carotid origin, with sudden severe renovascular hypertension, hypertensive encephalopathy in the territory of the patent carotid artery, and ischemia in the territory of the occluded internal carotid, and severe hypertension with acute pulmonary edema in the setting of myocardial ischemia, with acute embolic stroke from the myocardial infarction. The question, therefore, is not whether hypertension should be treated in the setting of acute cerebral ischemia but when and how.Since the publication of the National Institutes of Health trial of recombinant tissue plasminogen activator for acute stroke,4 treating hypertension in acute stroke has become more common, because tissue plasminogen activator is contraindicated with blood pressures >185 mm Hg systolic or 110 mm Hg diastolic.5 Guidelines suggest various approaches for the lowering of blood pressure, including intravenous labetalol, nitroglycerine paste, intravenous nicardipine, and, in extreme cases, intravenous nitroprusside.5,6Two articles in this issue of Hypertension shed some light on this problem. Geeganage and Bath7 performed a metaregression analysis of 37 acute ischemic stroke trials involving blood pressure reduction in 9008 patients. They found a U-shaped relationship between blood pressure reduction and outcomes, with the lowest risk of death or dependency at the end of follow-up in patients with blood pressure reductions of ≈14 to 15 mm Hg. Large falls in blood pressure or increases in blood pressure were associated with a higher risk of poor outcomes. Similarly, the authors of the Virtual International Stroke Trial Archive collaboration8 recently found that high systolic pressures, a small drop in systolic pressure, and large variability in systolic pressure were associated with poor outcomes.The authors of a Spanish multicenter observational study of blood pressure changes in acute ischemic stroke9 reported that age determined the effects of blood pressure change on outcome. Systolic blood pressures >180 mm Hg (in the emergency department and after 24 hours) doubled the risk of poor outcomes (modified Rankin score at 3 months), and systolic blood pressures 28 mm Hg gave a 21.7-fold increase in the risk of poor outcomes.High blood pressure during acute stroke aggravates cerebral edema. Because the brain is enclosed by a rigid skull and compartments in the brain are determined by the falx, corpus callosum, and the tentorium of the posterior fossa, cerebral edema results in a progressive reduction in perfusion pressure (systemic blood pressure minus venous and tissue pressure), strangulation of the salvageable penumbra, and progressive infarction. This is why early hemicraniectomy has such dramatic effects in malignant middle cerebral artery syndrome, with a number needed to treat of only 2 to prevent death or severe disability.10 Thus, it would be expected that, in patients with very high pressures, blood pressure reduction would improve outcomes. On the other hand, excessive blood pressure reduction reduces blood flow in the ischemic penumbra, also leading to worse outcomes.Reasons why the elderly would fare worse with blood pressure reduction could include pseudohypertension and hypertensive arteriolar hypertrophy from long-standing hypertension. Approximately 4% of elderly patients have a very significant (≈30 mm Hg) difference between their diastolic cuff pressure and intra-arterial pressure.11–13 Such patients would, therefore, have much lower pressures than measured, when their pressures are treated, and would be expected to have worsening of ischemia in the salvageable penumbra.Elderly patients are also much more likely to have long-standing hypertension and, therefore, to have hypertensive hypertrophy in their cerebral arterioles. This would render them more intolerant to drops in blood pressure. The Figure is a cartoon illustrating the principle described many years ago by Strandgaard et al.14 Long-standing hypertension leads to arteriolar hypertrophy, so autoregulation of cerebral blood flow (CBF) is shifted to the right: patients with long-standing hypertension withstand higher pressures and do not tolerate blood pressures as low as those patients without hypertensive arteriolar hypertrophy. In a sense, this is the mirror image of the cerebral hyperperfusion syndrome that is rarely seen after carotid revascularization.15,16Download figureDownload PowerPointFigure. Loss of CBF regulation during acute ischemic stroke. In physiological conditions, CBF is autoregulated over a wide range of perfusion pressures, from ≈50- to 150-mm Hg mean arterial pressure. This is shifted to the right in long-standing hypertension because of arteriolar hypertrophy. During acute ischemia, CBF becomes pressure passive, resulting in a marked reduction of CBF if pressure drops too low. The threshold at which this becomes a problem will be higher for patients with long-standing hypertension whose CBF autoregulation is shifted to the right.Blood pressure treatment in acute stroke is, thus, a double-edged sword. Autoregulation is lost in the ischemic region (Figure), so higher pressures aggravate cerebral edema17,18 and thereby cause progressive ischemia; blood pressure that is too low aggravates ischemia in the salvageable penumbra. Mean arterial pressures at ≈120 mm Hg (representing blood pressures ≈160/100 or 180/90 mm Hg) are probably on the autoregulation plateau for most patients and may represent a reasonable target for blood pressure in acute stroke; this might be shifted up for patients with long-standing hypertension and down a bit for patients with no history of hypertension. Blood pressure should be reduced carefully and only with short-acting intravenous drugs that can be controlled (preferably by infusion rather than bolus injections or by nitrate paste, which can be wiped off if pressures are dropping too low).2,19 In elderly patients, it may be wise to measure intra-arterial pressure to really know what the pressure is and the effect of treatment. Randomized trial results that tell us when and how to treat hypertension will be most welcome. In the meantime, we need to be thoughtful, careful, and wise.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to J. David Spence, Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute, University of Western Ontario, 1400 Western Rd, London, Ontario, Canada N6G 2V2. E-mail [email protected] References 1 Choudhry NK, Anderson GM, Laupacis A, Ross-Degnan D, Normand SL, Soumerai SB. Impact of adverse events on prescribing warfarin in patients with atrial fibrillation: matched pair analysis. BMJ. 2006; 332: 141–145.CrossrefMedlineGoogle Scholar2 Spence JD, Paulson OB, Strandgaard S. Hypertension and stroke. In: Messerli FH, ed. The ABCs of Antihypertensive Therapy. New York, NY: Lippincott Williams & Wilkins; 2000: 279–296.Google Scholar3 Spence JD, Del Maestro RF. Hypertension in acute ischemic strokes: treat. Arch Neurol. 1985; 42: 1000–1002.CrossrefMedlineGoogle Scholar4 The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995; 333: 1581–1587.CrossrefMedlineGoogle Scholar5 Adams HP Jr, Del ZG, Alberts MJ, Bhatt DL, Brass L, Furlan A, Grubb RL, Higashida RT, Jauch EC, Kidwell C, Lyden PD, Morgenstern LB, Qureshi AI, Rosenwasser RH, Scott PA, Wijdicks EF. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups-the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007; 38: 1655–1711.LinkGoogle Scholar6 Spence JD. New treatment options for hypertension during acute ischemic or hemorrhagic stroke. Curr Treat Options Cardiovasc Med. 2007; 9: 242–246.CrossrefMedlineGoogle Scholar7 Geeganage CM, Bath PMW. Relationship between therapeutic changes in blood pressure and outcomes in acute stroke: a meta-regression. Hypertension. 2009; 54: 775–781.LinkGoogle Scholar8 Sare GM, Ali M, Shuaib A, Bath PM. Relationship between hyperacute blood pressure and outcome after ischemic stroke: data from the VISTA collaboration. Stroke. 2009; 40: 2098–2103.LinkGoogle Scholar9 Leira R, Millán M, Díez-Tejedor E, Blanco M, Serena J, Fuentes B, Rodríguez-Yañez M, Castellanos M, Lago A, Dávalos A, Castillo J; for the TICA Study, Stroke Project, Cerebrovascular Diseases Group of the Spanish Neurological Society. Age determines the effects of blood pressure lowering during the acute phase of ischemic stroke: the TICA Study. Hypertension. 2009; 54: 769–774.LinkGoogle Scholar10 Vahedi K, Hofmeijer J, Juettler E, Vicaut E, George B, Algra A, Amelink GJ, Schmiedeck P, Schwab S, Rothwell PM, Bousser MG, van der Worp HB, Hacke W. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007; 6: 215–222.CrossrefMedlineGoogle Scholar11 Spence JD, Sibbald WJ, Cape RD. Pseudohypertension in the elderly. Clin Sci Mol Med. 1978; 55 (suppl 4): 399s–402s.MedlineGoogle Scholar12 Spence JD. Pseudohypertension. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. New York, NY: Raven Press; 1995: 1929–1937.Google Scholar13 Spence JD. Pseudo-hypertension in the elderly: still hazy, after all these years (comment). J Hum Hypertens. 1997; 11: 621–623.CrossrefMedlineGoogle Scholar14 Strandgaard S, Olesen J, Skinhoj E, Lassen NA. Autoregulation of brain circulation in severe arterial hypertension. BMJ. 1973; 1: 507–510.CrossrefMedlineGoogle Scholar15 Moulakakis KG, Mylonas SN, Sfyroeras GS, Andrikopoulos V. Hyperperfusion syndrome after carotid revascularization. J Vasc Surg. 2009; 49: 1060–1068.CrossrefMedlineGoogle Scholar16 Rothwell PM, Howard SC, Spence JD. Relationship between blood pressure and stroke risk in patients with symptomatic carotid occlusive disease. Stroke. 2003; 34: 2583–2590.LinkGoogle Scholar17 Ayata C, Ropper AH. Ischaemic brain oedema. J Clin Neurosci. 2002; 9: 113–124.CrossrefMedlineGoogle Scholar18 Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke. Stroke. 1999; 30: 287–292.CrossrefMedlineGoogle Scholar19 Spence JD. Treating hypertension in acute stroke: a better arrow for the quiver. Hypertension. 2006; 47: 1051.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Versaci F, Andò G, Chiocchi M and Romeo F (2019) Long-term benefit of renal denervation on blood pressure control in a patient with hemorrhagic stroke, SAGE Open Medical Case Reports, 10.1177/2050313X19870972, 7, (2050313X1987097), Online publication date: 1-Jan-2019. Hasegawa Y, Nakagawa T, Matsui K and Kim-Mitsuyama S (2017) Renal Denervation in the Acute Phase of Ischemic Stroke Provides Brain Protection in Hypertensive Rats, Stroke, 48:4, (1104-1107), Online publication date: 1-Apr-2017. Spence J and Hammond R (2016) Hypertension and Stroke Hypertension and the Brain as an End-Organ Target, 10.1007/978-3-319-25616-0_3, (39-54), . Tziomalos K, Giampatzis V, Bouziana S, Spanou M, Papadopoulou M, Kostaki S, Dourliou V, Papagianni M, Savopoulos C and Hatzitolios A (2014) Elevated Diastolic But Not Systolic Blood Pressure Increases Mortality Risk in Hypertensive But Not Normotensive Patients With Acute Ischemic Stroke, American Journal of Hypertension, 10.1093/ajh/hpu234, 28:6, (765-771), Online publication date: 1-Jun-2015. Yeh K, Tsai T, Chai H, Leu S, Chung S, Chua S, Chen Y, Lin H, Yuen C and Yip H (2012) Comparison of acute versus convalescent stage high-sensitivity C-Reactive protein level in predicting clinical outcome after acute ischemic stroke and impact of erythropoietin, Journal of Translational Medicine, 10.1186/1479-5876-10-6, 10:1, Online publication date: 1-Dec-2012. Furlan N, Bazan S, Braga G, Castro M, Franco R, Gut A, Bazan R and Martin L (2018) Association between blood pressure and acute phase stroke case fatality rate: a prospective cohort study, Arquivos de Neuro-Psiquiatria, 10.1590/0004-282x20180059, 76:7, (436-443) Spence J (2019) Blood Pressure Gradients in the Brain: Their Importance to Understanding Pathogenesis of Cerebral Small Vessel Disease, Brain Sciences, 10.3390/brainsci9020021, 9:2, (21) October 2009Vol 54, Issue 4 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.109.134486PMID: 19652079 Originally publishedAugust 3, 2009 PDF download Advertisement SubjectsCerebrovascular Disease/Stroke
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