monitoring blood pressure in patients with acute stroke

Monitoring Blood Pressure in Patients withAcute StrokeDoes it Have a Positive Value?

Gastone Leonetti,1,2 Cesare Cuspidi,3 Marco Stramba-Badiale2 and Alberto Zanchetti2,4

1 Medical and Surgical Faculty, University of Milan, Milan, Italy2 S. Luca Hospital, IRCCS, Milan, Italy3 Institute of Internal Medicine and Treatment, University of Milan, Milan, Italy4 Center of Clinical Pharmacology and Hypertension, University of Milan, Milan, Italy

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351. Cerebral Circulation and Blood Pressure after Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 362. Acute Stroke Blood Pressure and Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363. Acute Stroke and 24-Hour Blood Pressure Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374. Current Practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375. Therapy for Lowering Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

Abstract Elevated blood pressure is a well recognised risk factor for cardiovascular events and the positive results ofpharmacological intervention trials have confirmed this relationship in primary and secondary prevention.However, our knowledge of the role of blood pressure in the acute phase of stroke is very limited and contro-versial. Indeed, in some studies no correlation has been found between elevated blood pressure in the earlyphase of stroke and prognosis, while in other studies of patients with hypertension elevated BP was associatedwith either a better or worse prognosis. In the limited number of studies that have involved ambulatory bloodpressure monitoring (ABPM) the trend has been toward a negative prognostic impact from elevated 24-hoursystolic blood pressure. In addition, studies in patients on ABPM after stroke have shown that there are differentpatterns of night-time blood pressure, and that these are related to the type of cerebral infarction or its location,which could, in part, explain the differences in results so far obtained in studies.

In the meantime, in the absence of data from interventional studies, the American Heart Association hassuggested conservative blood pressure levels (>220mm Hg systolic or >120mm Hg diastolic blood pressure)before starting the pharmacological reduction of blood pressure. The recent Seventh Report of the Joint NationalCommittee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (the JNC 7 Report)suggests decreasing blood pressure in the acute phase of stroke toward 160/100mm Hg. It is possible that withthe advent of specialist stroke units, which could allow the better characterisation and follow up of patients withacute stroke, it is time to start placebo-controlled intervention trials to investigate the clinical problem ofmanaging elevated blood pressure in the early phase of stroke.

REVIEW ARTICLE High Blood Press Cardiovasc Prev 2003; 10 (1): 35-401120-9879/03/0001-0035/$30.00/0

© Italian Society of Hypertension 2003. All rights reserved.

Elevated blood pressure is a well recognised risk factor forcerebrovascular events,[1] a relationship confirmed in interventio-nal primary prevention studies in both adult and elderly popula-tions.[2] The benefits of antihypertensive therapy in the secondary

prevention of cerebrovascular disease has also been assessed ina number of trials, however results have been conflicting, thoughtwo recent reports[3,4] have demonstrated a significant reductionin the recurrence of stroke events with this approach. However,

the current understanding of the role of blood pressure (in partic-ular, of hypertension) in the acute phase of stroke is still verylimited and controversial. This is of concern as arterial hyperten-sion (systolic blood pressure ≥140mm Hg and diastolic bloodpressure ≥90mm Hg) is present in about 75% of patient withischaemic stroke and about 80% of patients with parenchymalintracerebral haemorrhage (PICH).[5-8]

The International Stroke Trial[9] involved a large number ofpatients with ischaemic stroke (17 398 patients) of which 80%had high blood pressure with a mean systolic blood pressure of160mm Hg. In spite of this, research into improving the outcomefor patients with acute stroke has largely focused on antithrom-botic and neuroprotective drug strategies and health servicereorganisation, with the establishment of specialist stroke unitsfor the care of patients in the acute phase of stroke. Therapy withantiplatelet and thrombolytic drugs has been shown to reducecombined death and dependences,[10-12] while anticoagulationand neuroprotection have appeared ineffective and hazardous.[13]

Blood pressure elevation is frequently found in patients with is-chaemic stroke and PICH and in this paper we review the currentknowledge on this clinical relationship to answer to the questionof “to treat or not to treat”.[14,15]

1. Cerebral Circulation and Blood Pressure after Stroke

The clinical decision to treat elevated blood pressure is veryimportant because cerebral autoregulation, which normallymaintains a constant perfusion over a wide range of systemicblood pressures, becomes dysfunctional[16-20] during the acutephase of stroke and perfusion tends to be passively dependent onblood pressure. In addition, the natural history for blood pressureis to start falling within hours of stroke onset[21] and to settle overthe first weeks after stroke.[5-8] In 1981 Wallace and Levy[22]

published a paper that showed spontaneous and marked reduc-tions in systolic and, to a minor extent, diastolic blood pressurevalues in patients with all kinds of stroke (from ischaemic stroke,to parenchimal haemorrage, to hypertensive infarct, etc.) duringa 10-day control period after acute stroke, while there were nosignificant changes in the control group. The pattern of systolicand diastolic blood pressure profiles during the 10-day periodwas similar in patients with or without hypertension and with orwithout antihypertensive treatment.

The debate regarding “to treat or not to treat” blood pressureelevation[14,15] in patients in the early phase of acute stroke de-rives from two different interpretations of this haemodynamicpattern. On the one hand, initially elevated blood pressure maybe beneficial as it increases blood flow to ischaemic penumbra

(the periclot area) and could be regarded as a physiological com-pensatory mechanism for impaired perfusion pressure; on theother hand, sustained elevation in blood pressure may be harmfulas it increases the likelihood of cerebral oedema[16] and thehaemorrhagic transformation of ischaemic infarct.

2. Acute Stroke Blood Pressure and Outcome

After reviewing the available observational studies it is dif-ficult to say which of the two hypotheses is clinically more rele-vant; indeed, data (derived from observational studies) on theprognostic relevance of blood pressure levels following acutestroke are conflicting (see table I). In some studies no correlationbetween blood pressure values and short-term prognosis wasfound,[23-28] while in other studies[29-37] a negative correlationwas found: high blood pressure values were associated with apoor prognosis. Finally, other authors have found that patientswith the best outcome had the highest blood pressure during thefirst 24 hours after stroke[38-41] and this was also more frequentin those who had a lacunar stroke.[41] Differences in the designof the studies assessing prognostic significance of blood pressureafter acute stroke may explain some of the conflicting results.Some studies: (i) involved only patients with cerebral haemor-rhage (four studies); (ii) admitted only a highly selective groupof patients, i.e. those hospitalised in a specialist stroke unit (fourstudies); (iii) some patients continued or started antihypertensivetherapy (four studies); (iv) many patients were investigated aweek or more after the acute event, when the acute blood pressurechanges following the stroke had resolved (four studies); and(v) there were also confounding factors related to observer biasand inter-observer errors in recording blood pressure, in the tim-ing of blood pressure measurements and, finally, blood pressurevalues were often derived from retrospective review of medicalnotes (four studies).

Twenty-four-hour ambulatory blood pressure monitoring(ABPM) may help overcome some of these problems as it reducesthe influence of the blood pressure response to hospitalisation,the measurement variability and the observer bias of casual read-ings. We and other authors[42-46] have found that there is a positive

Table I. High blood pressure and prognosis in acute stroke: observationalstudies

References

No correlation 23-28

Negative correlation: high blood pressure = worseprognosis

29-37

Positive correlation: high blood pressure = betterprognosis

38-41

36 Leonetti et al.

© Italian Society of Hypertension 2003. All rights reserved. High Blood Press Cardiovasc Prev 2003; 10 (1)

relationship between 24-hour ABPM performed within 24–48hours of stroke onset, and short- or middle-term prognosis. Thesestudies provide evidence that elevated 24-hour systolic bloodpressure in the acute stroke period is associated with increasingrisk of death and disability;[42-46] however, Lip et al.[47] found thatthe mortality rates 6 months after stroke were not correlated with24-hour blood pressure levels.

3. Acute Stroke and 24-Hour Blood Pressure Profile

The question remains: “how can we explain these divergentresults between blood pressure levels and prognosis?” Even whenwe use very accurate methods to measure blood pressure, alongwith a significantly greater number of measurements than arecommonly performed, and very similar timings for blood pres-sure monitoring, the difference in outcome can be significant.

In patients with acute stroke we may oversimplify mattersby defining blood pressure levels with only one or a few (24-hour,day-time and night-time mean) values because this does not takeinto account other aspects or attributes, for instance the 24-hourblood pressure profile, independently from the absolute 24-hourblood pressure values. This idea was investigated by Lip et al.[47]

in the West Birmingham Stroke Project and they confirmed that24-hour systolic and diastolic blood pressure values were higherin haemorrhagic than in ischaemic or transient ischaemic attacks.Lip et al.[47] also found that the 24-hour blood pressure profileshowed differences in night-time blood pressure falls which wereslightly reduced in patients with transient ischaemic attack, al-most completely abolished in patients with atherothromboticstroke, while ‘reverse dipping’ (i.e. a blood pressure elevationduring the night) was found in patients with haemorrhagicstroke.

These differences in haemodynamic patterns of 24-hourblood pressure may be very important because some hyperten-sion studies have consistently reported that patients with a re-duced or ‘reversed’ fall in night-time blood pressure (‘non-dipper’or ‘reverse-dipper’) experience greater organ damage,[48-50] in-cluding progressive cerebrovascular disease,[51] when comparedwith patients with a normal night-time blood pressure fall.

Twenty-four-hour blood pressure monitoring has high-lighted other differences in blood pressure profiles according tothe stroke types and right- or left-side hemispheric location. In-deed, Sanders and Klingelhofer[52] found that night-time bloodpressure falls were greater in patients after haemodynamic strokeand smaller in atherothrombotic stroke than in normotensive andhypertensive controls. In addition, the percentage of patients withreduced or ‘reverse’ dipping was significantly higher in patientswith atherothrombotic stroke compared with those with haemo-

dynamic stroke and controls. Sanders and Klingelhofer[53] alsoinvestigated the effect of left and right hemispheric brain infarc-tion on variability in circadian blood pressure profiles and onsome cardiovascular measurements as the result of the asymmet-ric damage of sympathetic nervous system. They found a minorfall in night-time systolic and diastolic blood pressure in patientwith right-sided infarct. Right-side infarct was also associatedwith a higher serum noradrenaline concentrations (546 vs 405ng/L), more frequent QT prolongation (53% vs 35%), and morecardiac arrhythmias (67% vs 20%).

The advent of 24-hour ABPM has allowed the better evalu-ation of blood pressure changes and the highlighting of differentpatterns of night-time blood pressure falls according to stroketype (ischaemic and haemorrhagic) and their location. It is pos-sible that these changes in 24-hour ABPM may explain, in part,the different results from studies on the relationship betweenblood pressure and prognosis.

4. Current Practice

The current published guidelines[54-58] are not based on hardevidence and vary in their recommendations as to how to manageblood pressure in patients with acute stroke who have not re-ceived thrombolytic therapy.

The American Heart Association (AHA) guidelines for thetreatment of blood pressure in patients with acute stroke suggestthat antihypertensive agents should be administered to patientswith ischaemic stroke when their systolic blood pressure is above220mm Hg, diastolic blood pressure is above 120mm Hg, orwhen they have a mean arterial pressure above 130mm Hg, whilethe corresponding values for systolic and distolic blood pressureare 180mm Hg and 105mm Hg, respectively,[54] in patients withPICH. However, according to Joint National Committee guide-lines in acute stroke, control of blood pressure at intermediatelevels (of approximately 160/110mm Hg) is appropriate.[59] Inaddition, in a statement by the International Society of Hyperten-sion, it was suggested that a modest (5–10%) reduction in bloodpressure produces minimal or no measurable changes in cerebralblood flow, while a large (>15%) decrease in blood pressure canreduce cerebral perfusion.[60] It is worthwhile to underline againthat the relative recommendations are based on pathophysiolog-ical considerations or individual case reports, not on the resultsof systematic overviews or large intervention studies of bloodpressure manipulation in patients with acute stroke.[61]

Current guidelines recommend glyceryl trinitrate, sodiumnitroprusside, and labetalol, as agents for lowering blood pres-sure, but do not provide supporting trial data. A recent reviewfrom the Blood Pressure in Acute Stroke Collaboration[61] iden-

Blood Pressure in Acute Stroke 37


tified five randomised intervention trials aimed at altering bloodpressure within 2 weeks of acute haemorrhagic or atherothrom-botic stroke. However, the authors concluded that “none of thedrugs evaluated in the five trials significantly affected outcomeand the limited amount of data made it impossible to assess therelationship between changes in blood pressure and clinical out-come”.

5. Therapy for Lowering Blood Pressure

A number of different drug classes can be used to lowerblood pressure in stroke and each has potential advantages anddisadvantages; however, study data are few and inconclusivewhen considering whether lowering blood pressure in patientswith acute stroke is beneficial.

Among the different drug classes, the calcium antagonistsare the most extensively investigated with 25 randomised con-trolled studies in patients with ischaemic stroke. Overall, the cal-cium antagonists did not alter functional outcome whether givenintravenously or orally, or within 6–12 hours or later.[62] In par-ticular, nicardipine was found either to reduce or to have no effecton cerebral perfusion, despite blood pressure reductions in bothstudies.[62]

For other drug classes there are either no studies or a singlestudy which does not allow any conclusion.

6. Conclusion

There is no doubt that a transient rise in blood pressure isvery common in patients with acute stroke, in particular in pa-tients with PICH, and in these patients blood pressure may reachvalues above normal levels, levels currently treated in patientswith or without a history of previous cerebrovascular accident.

There are no conclusive results on the relationship betweenblood pressure levels and the incidence of death, recurrent stroke,or disability, although there is a positive trend toward a correla-tion with the functional outcome. These contrasting results maybe due either to differences in the protocols of the studies and, inparticular, in the method (time and frequency) of blood pressuremeasurements. Indeed, the advent of 24-hour blood pressuremonitoring has shown a more constant relationship between sys-tolic blood pressure and functional outcome in patients with acutestroke when blood pressure is monitored in the first 24–48hours.

In addition, 24-hour blood pressure profiles have shown thatthere are differences in the night-time blood pressure fall, fromreduced, to absent and to ‘reverse’ dipping, because of stroke type(from transient ischaemic attack, to atherothromboembolic, to

haemorrhagic stroke) or the right or left hemispheric location ofthe infarct.

In patients with hypertension, changes in the pattern of night-time blood pressure falls are associated with different cerebro-vascular prognosis and, we believe, the discrepancies observedwhen only casual blood pressure was evaluated could be due todifferences in the 24-hour blood pressure profile independentfrom absolute blood pressure values.

There is general agreement on the need for evidence-baseddata for the management of blood pressure in the acute phase ofstroke, i.e. if it is better not to treat or to intervene to regulateblood pressure levels. The advent of specialist stroke units, wherepatients are monitored and their progress followed by trainedspecialists, represents the ideal setting for the implementation ofa pilot study into the feasibility of comparing casual and 24-hourblood pressure before and during antihypertensive treatments.

At the present time intervention aimed at increasing bloodpressure in patients in acute stroke seems less justified.

Acknowledgements

The authors received no funding that assisted in the preparation of thismanuscript, nor do they have any potential conflicts of interest directlyrelevant to the content of this review.

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Correspondence and offprints: Dr Gastone Leonetti, Divisione diRiabilitazione Cardiologica e Malattie dell’Apparato Cardiovascolare,IRCCS, Ospedale San Luca, Via Spagnoletto, Milan, 20149, Italy.E-mail: [email protected]

40 Leonetti et al.


monitoring blood pressure in patients with acute stroke

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