doi: 10.1161/CIRCULATIONAHA.107.723874
(Circulation. 2008;118:176-187.)
© 2008 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Acute Hypertensive Response in Patients With Stroke
Pathophysiology and Management
From the Zeenat Qureshi Stroke Research Center, University of Minnesota, Minneapolis.
Correspondence to Adnan I. Qureshi, MD, University of Minnesota, MMC 295, 420 Delaware St SE, Minneapolis, MN 55455.
Key Words: stroke • hypertension • blood pressure • cerebral infarction • cerebral ischemia • hemorrhage • thrombolysis
 |
Introduction |
|---|
 Top Introduction Definition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Acute hypertensive response is the elevation of blood pressure (BP) above normal and premorbid values that initially occurs within the first 24 hours of symptom onset in patients with stroke. This phenomenon was reported in >60% of patients presenting with stroke in a nationally representative study from the United States.1 With
980 000 patients2 admitted with stroke each year in the United States, the estimated annual prevalence of acute hypertensive response is more than half a million patients. With 15 million patients experiencing stroke worldwide each year,3 the acute hypertensive response may be expected in 10 million patients per year. The acute hypertensive response in stroke patients is managed by a diverse group of physicians, including emergency physicians, intensivists, internists, primary care physicians, neurologists, neurosurgeons, and cardiologists. Previous audits suggest that antihypertensive agents and management strategies vary considerably and are not always consistent with recommended guidelines.4 Data from 1181 acute ischemic stroke patients enrolled in the Project for Improvement of Stroke Care Management suggested that administration of antihypertensive medication within 24 hours in 56% of the patients was inconsistent with guidelines provided by the American Stroke Association (ASA).5 The present review article summarizes the current concepts pertaining to treatment of the acute hypertensive response derived from recent guidelines provided by professional organizations and "best available" evidence derived from experimental and clinical studies and discusses incorporation of these concepts into clinical practice. Randomized trials, nonrandomized controlled studies, and selected observational studies were identified with multiple searches on Medline from 1980 to 2007 by cross-referencing the key words of stroke, acute hypertension, antihypertensive agents, acute stroke, and hypertension. Pertinent articles identified from bibliographies of selected articles were also reviewed. Treatment targets and strategies were identified by review of existing guidelines from professional organizations. |
Definition of Acute Hypertensive Response |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
The 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement6 and the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)7 define hypertension on the basis of the presence of consistent BP
140/90 mm Hg (multiple readings on separate days). This definition of hypertension is a threshold for the use of long-term antihypertensive treatment that is supported by evidence derived from randomized trials and clinic- or population-based data that demonstrate reduction in cardiovascular events with this threshold for treatment. The same definition cannot be applied in the case of acute hypertensive response, because the above-mentioned ascertainment criteria and rationale are not valid. The executive summary of the ISH statement8 on management of BP in acute stroke stated that high BP (>140/90 mm Hg) is very common early after ischemic stroke (occurring in 75% of cases) and intracerebral hemorrhage (ICH; >80%) and is independently associated with a poor functional outcome. To maintain consistency with the ISH statement, acute hypertensive response is defined as "systolic BP 140 mm Hg or diastolic BP of 90 mm Hg demonstrated on 2 recordings taken 5 minutes apart within 24 hours of symptom onset." This definition predominantly serves to provide a uniform standard for measuring prevalence and not for setting treatment thresholds for antihypertensive treatment, which may vary depending on stroke subtype and other considerations. |
Prevalence of Acute Hypertensive Response |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
The reported prevalence of the acute hypertensive response depends on patient selection, study design, referral patterns, and the definition used. In a systematic review of 18 studies,9 52% of patients with stroke were reported to have an acute hypertensive response at the time of admission. The criteria used to define high BP varied considerably: Systolic BP criteria ranged from 150 to 200 mm Hg and diastolic BP criteria from 90 to 115 mm Hg. In one of the largest studies in the United States using the National Hospital Ambulatory Medical Care Survey,1 systolic BP
140 mm Hg was observed in 63% of the 563 704 adult stroke patients, diastolic BP 90 mm Hg in 28%, and mean arterial pressure (MAP) 107 mm Hg in 38%. In the International Stroke Trial,10 17 398 patients were randomized within 48 hours of stroke onset (median time 20 hours) from 467 hospitals in 36 countries. Mean systolic BP at enrollment was 160.1 mm Hg, and 82% of patients had high BP based on the WHO definition of hypertension (systolic BP >140 mm Hg). |
Characteristics of Acute Hypertensive Response |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
The acute hypertensive response in stroke is characterized by its high prevalence, self-limiting nature, and prognostic significance. With the definition of hypertension provided by the WHO6 and JNC 7,7 the age-, sex-, and ethnicity-adjusted rates were 61% among stroke patients and 14% in the US population in 1999 to 2000.1,11 New-onset high BP in patients without a previous history of hypertension has been observed in 20% of patients with stroke12 and 8% of the general population.11 A crude comparison suggests that these proportions are higher than expected on the basis of premorbid hypertension among stroke patients. There is also spontaneous reduction of BP (by an average of 20/10 mm Hg) within 10 days after the acute event without any specific antihypertensive therapy.13 Among the 1455 patients from the Glycine Antagonist in Neuroprotection International Trial14 evaluated within 6 hours of symptom onset, MAP declined gradually over the next 60 hours regardless of initial MAP value, with a prominent reduction observed within 10 hours of the first measurement. The prognostic significance is highlighted in a systematic review of 18 studies9 that demonstrated that patients with stroke and high initial BP were at a 1.5- to 5.0-fold increased risk of death or dependency and clinical deterioration.
|
Underlying Causes of Acute Hypertensive Response |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
In at least a portion of these patients, the acute hypertensive response is merely a reflection of inadequately treated or undetected chronic hypertension15; however, spontaneous reduction in the initial BP over the next few days in most patients13,14 supports the role of other transient and stroke-specific mechanisms. Spontaneous reduction of BP after vessel recanalization in patients with ischemic stroke also implies stroke-specific mechanisms.16 Stroke involves transient or permanent damage to the areas involved in the brain regulation of cardiovascular functioning, including BP. The parasympathetic and sympathetic nervous systems are lateralized to the left and right cerebral hemispheres, respectively.17 Prefrontal18 and insular19 cortices provide inhibitory and excitatory input, respectively, through pathways that connect to the nuclei in the brainstem, particularly in nucleus tractus solitarius and ventrolateral medulla.20 Further modulation is provided by cingulated cortex, amygdala, and hypothalamus. Because of the widespread distribution of these areas, most stroke lesions involve these areas to a varied extent.
Increased sympathoadrenal tone21 with subsequent release of renin and vasoconstriction of arterioles results from (1) direct injury to inhibitory or modulatory brain regions or (2) indirect effects of reduced parasympathetic activity,22 which leads to impaired cardiac baroreceptor sensitivity in patients with stroke.23 Although direct injury is the most likely explanation, an indirect effect of muscle paralysis24 or the release of neurotransmitters such as nitric oxide25 during ischemia may be contributing factors to altered activity of these nuclei. Other stress responses to hospitalization, headache, urinary retention, or concomitant infection26 may lead to abnormal autonomic activity and raised levels of circulating catecholamines27 and inflammatory cytokines12 and subsequently may contribute to the hypertensive response. Presumably, these abnormal autonomic responses normalize over a few hours owing to spontaneous or therapeutic recanalization and resolution of the ischemia and perhaps because of other neural compensatory mechanisms.28
An increase in systemic BP associated with increased intracranial pressure (ICP), particularly in the presence of brainstem compression,29–31 has particular relevance for patients with intracerebral and subarachnoid hemorrhages. Elevated ICP can result in a systemic BP increase32; however, the elevation in systemic BP does not appear to demonstrate a clear relationship to the presence of cerebral ischemia,32,33 ICP values, transtentorial herniation,32,33 or response to hyperosmotic treatment.32,33 This suggests that the primary cause of the acute hypertensive response is damage or compression of specific regions in the brain that mediate autonomic control. Hypertensive responses to other factors mentioned above are exaggerated and additive because of impaired parasympathetic activity and baroreceptor sensitivity.
|
Cerebrovascular Physiology and Implications for Treatment |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Under normal circumstances, changes in precapillary arteriolar diameter (<400 µm) maintain constant cerebral blood flow in the capillary bed between MAPs of 60 and 150 mm Hg.34 A fast dynamic response to changes in pressure pulsations is followed by a slow static response that restores cerebral blood flow after the initial dynamic response has settled35 by myogenic (mechanogenic) and metabolic (chemogenic) mechanisms.36 With decreasing BP, there is vasodilation of arterioles until maximal vasodilation occurs, and subsequently, there is reduction of blood flow. With increasing BP, there is progressive vasoconstriction of arterioles until the BP exceeds the upper limit of autoregulation, followed by breakthrough vasodilation, increase in cerebral blood flow,36 blood-brain barrier dysfunction, and cerebral edema.
In chronic hypertension, the lower end of the autoregulation curve is shifted toward high pressure,37 presumably because vessel wall thickening and luminal narrowing limit the capacity of the resistance vessels for dilation. In acute stroke, autoregulation may be impaired in regions surrounding an acute lesion and even in the hemisphere contralateral to the lesion because of dilation of cerebral resistance vessels in an attempt to increase blood flow in response to tissue ischemia and acidosis.38 More recently, it has been shown that autoregulation is impaired for rapid changes (dynamic autoregulation) in systemic BP even when it is preserved for controlled changes.39 Other conditions, such as cerebral vasospasm in subarachnoid hemorrhage,40 also cause arteriolar constriction, which shifts the autoregulatory range toward higher values.
In the presence of elevated ICP, MAPs >60 mm Hg may not be adequate to maintain constant cerebral blood flow in the capillary bed. Ascertainment of the difference between MAP and ICP is recommended as an index of cerebral perfusion pressure. The standard, global measure of cerebral perfusion pressure can underestimate the localized pressure and perfusion changes in focal stroke lesions but is still useful in the absence of another, more sensitive measure. The Brain Trauma Foundation41 recommends maintenance of a cerebral perfusion pressure >70 mm Hg to enhance perfusion to ischemic regions of the brain after severe traumatic injury. In stroke, such treatment thresholds have been extrapolated from global cerebral perfusion data derived from traumatic brain injury patients in the absence of any other pertinent data.
|
Management of Acute Hypertensive Response in Stroke Subtypes |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Despite the high prevalence of acute hypertensive responses observed in all stroke subtypes, differences in underlying pathophysiology mandate different management strategies (Figure).7,42–47 BP responses can be categorized as (1) spontaneous decline without medication; (2) no clear decline, or even an elevation, despite administration of antihypertensive medication; (3) modest decline with antihypertensive medication (
10% to 15% from baseline value); and (4) intense decline with antihypertensive medication (20% from baseline value). The studies presented below are confounded by overlap of the 4 categories of responses in varying proportions and require interpretation with this understanding. Another important issue in management is the identification of intravascular volume depletion (dehydration)48 in these patients, which may result in a natural hypertensive or hypotensive response or an exaggerated hypotensive response to antihypertensive medication.49,50 Early identification and appropriate fluid repletion before pharmacological intervention ensures a controlled response to treatment.
|
Based on recommendations of the ASA, Stroke Council,
Based on recommendations of JNC 7 |
Patients With Acute Ischemic Stroke |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Ischemic stroke results from occlusion of an artery with subsequent reduction in regional cerebral blood flow, demarcated into regions of severe reduction (core) and moderate reduction (penumbra).51 The penumbra remains viable for hours because some degree of blood flow is sustained through collateral supply; however, it is theoretically vulnerable to further ischemic injury with systemic BP reduction52 because of impaired regional autoregulation,38 particularly during rapid BP reduction. Conversely, in an experimental model of focal cerebral ischemia and reperfusion, BP reduction reduced infarct size and deficits.53 Therefore, a period of vulnerability to progression of ischemic deficits may exist after which there may be benefit from BP reduction. A higher rate of death or dependency was observed in patients with initially high or low systolic BP (U-shaped relationship) among 17 398 ischemic stroke patients randomized in the International Stroke Trial.10 The relationship appeared to be mediated in part by increased rates of early recurrence and death that resulted from presumed cerebral edema in patients with high BP and increased coronary heart disease events in those with low BP. Recent data suggest that wide fluctuations (not initial values) of BP in the first few hours in patients with acute ischemic stroke may be associated with an increased risk of death at 90 days.14,54
The Low Dose Beta Blockade in Acute Stroke (BEST) study55 (Table 1
42,47,55–60) revealed greater mortality among patients in whom β-blocker therapy was begun within 48 hours of symptom onset. An analysis of data from the Intravenous Nimodipine West European Stroke Trial (INWEST) found a significant correlation between diastolic BP reduction with nimodipine and worsening of neurological status (within 24 hours of symptom onset).61 Patients with a diastolic BP reduction 20% or a diastolic BP drop to 
60 mm Hg had a significantly higher risk of death or dependency at 21 days. A subsequent meta-analysis58 evaluating the use of oral or intravenous calcium channel blockers initiated at 6 hours to 5 days after symptom onset in acute ischemic stroke patients found that intravenous administration, higher doses, and administration within 12 hours of symptom onset were associated with an increased risk of poor outcomes. The effect may be mediated in part by alterations of regional cerebral blood flow.62 This susceptibility varies with stroke subtype and evolution stage, showing higher tolerance to BP lowering in patients with total anterior circulation infarction63 and in those treated after 12 hours of symptom onset.58
|
|
New data suggest that the increased risk of poor outcomes is probably limited to patients treated very aggressively or to specific antihypertensive agents (Table 1
). The Acute Candesartan Cilexetil Evaluation in Stroke Survivors (ACCESS)47 trial initiated treatment with either the angiotensin receptor antagonist candesartan or placebo in patients with ischemic stroke and a BP measurement 200/100 mm Hg 6 to 24 hours after admission or 180/105 mm Hg at 24 to 36 hours. The target reduction in BP was 10% to 15% within 24 hours. If patients in the candesartan group displayed a hypertensive profile on day 7 (mean daytime BP >135/85 mm Hg), candesartan was increased or an additional antihypertensive drug was added. In placebo-treated patients with a hypertensive profile on day 7, candesartan was begun. Both the cumulative 12-month mortality rate (2.9% versus 7.2%) and the incidence of vascular events (9.8% versus 18.7%) were lower in the candesartan-treated group; however, the primary outcome of disability measured by Barthel index at 3 months was not different between the 2 treatment groups.
A post hoc analysis of hypertensive patients in the National Institutes of Neurological Disorders and Stroke (NINDS) recombinant tissue plasminogen (rtPA) trial42 who received antihypertensive therapy (intravenous labetalol and/or nitroprusside in selected patients) but no rtPA therapy within 24 hours of randomization showed no difference in rates of deterioration or death at 24 hours or in rates of favorable outcome at 3 months compared with hypertensive patients who received neither antihypertensive medication nor rtPA. The results from various studies suggest somewhat contradictory consequences of antihypertensive treatment in acute ischemic stroke: INWEST showed a detrimental effect; ACCESS, a favorable effect; and post hoc analysis of NINDS rtPA study showed no effect. The mean systolic BP in the ACCESS trial was higher than in INWEST (196 versus 162 mm Hg), and the mean value during the first 2 days was also higher (>150 versus <145 mm Hg). The average maximum MAP in the NINDS placebo group (those not given rtPA) who received antihypertensive medication (133 mm Hg) and the average lowest value during the first 24 hours (>110 mm Hg) also appear higher than those observed in INWEST. The difference in aggressiveness of BP reduction between the studies was also evident from the 60% incidence of diastolic BP values of 60 mm Hg during nimodipine treatment in INWEST. These differences stress the importance of BP thresholds and treatment targets in determining tolerability of antihypertensive treatment in acute ischemic stroke.
Another aspect that requires further consideration is the potential for differential benefit or harm between classes of antihypertensive medication. The differences in results between trials such as the BEST, INWEST, ACCESS, and NINDS rtPA studies may be related to the properties of the antihypertensive medication used. A systematic review64 of 7 randomized, controlled trials involving patients with prior stroke or transient ischemic attack demonstrated heterogeneity in outcomes that were related in part to the class of antihypertensive drugs used. Angiotensin-converting enzyme inhibitors and diuretics, separately and in combination, but not β-blockers, reduced vascular events. Another estimate of stroke reduction with different antihypertensive medications (angiotensin-converting enzyme inhibitors, calcium antagonists, angiotensin receptor blockers, and diuretics or β-blockers) using data from 29 randomized trials65 directed toward primary prevention suggested that the greatest reduction was observed with angiotensin receptor blockers, with small (borderline significance) differences between the other different classes of antihypertensive medication. Conclusive evidence for differential effects of different antihypertensive medications in the acute period is not available.
The management of high BP in acute ischemic stroke is highly controversial because of a lack of reliable evidence from randomized, controlled trials. The current recommendations regarding BP management in acute ischemic stroke46 are based on 2 observations. BP reduction is associated with an increased risk of neurological deterioration and worse outcome in patients with ischemic stroke in some studies,59,66 although a causal relationship has not been demonstrated conclusively. The benefit of acute BP lowering (unlike chronic treatment) in patients with ischemic stroke remains unclear.46 There may be a reduction of cardiovascular events with early institution of angiotensin receptor antagonists; however, the benefit is not conclusively related to BP reduction.47 Therefore, in the absence of definitive benefit, both the ASA and the European Stroke Initiative are consistent in not recommending routine lowering of BP unless it is repeatedly exceeds 200 to 220 mm Hg systolic or 120 mm Hg diastolic in the acute period.46,67,68 However, with the anticipated completion of several large clinical trials42,47,55–60 in the next 5 years (Table 1), these recommendations may be modified.
|
Patients With Acute Ischemic Stroke Receiving Thrombolysis |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
The acute hypertensive response among patients with ischemic stroke receiving thrombolysis is frequently transient69 and resolves after recanalization70; however, elevated BP before receipt of thrombolysis has been associated with an increased risk of ICH. In the Australian Streptokinase Trial,71 baseline systolic BP >165 mm Hg resulted in a 25% increased risk of major ICHs among patients with ischemic stroke treated with streptokinase. In a multicenter retrospective and prospective investigation72 of individual data from 1205 patients treated in routine clinical practice with intravenous rtPA within 3 hours of stroke symptom onset, elevated pretreatment MAP was associated with an increased rate of ICH. In a large audit of practices and outcomes in 29 hospitals in the Cleveland, Ohio, area,73 BP parameters recommended by the NINDS rtPA trial were not followed in 52% of the 70 patients treated with intravenous thrombolysis. The result was a 16% rate of symptomatic ICHs. A quality-improvement program in 9 of these hospitals74 decreased the rate of noncompliance to BP recommendations to 6% in 47 patients subsequently treated with rtPA. The rate of symptomatic ICH dropped to 6%, which indirectly supports the beneficial value of BP control in reducing rtPA-related ICHs.
Both the ASA and European Stroke Initiative guidelines recommend the reduction of BP according to the eligibility thresholds for inclusion in the NINDS rtPA efficacy trial42 (Figure7,42–47) before thrombolytics are administered.46,67,68 In the NINDS rtPA efficacy trial,42 patients were not eligible if they required aggressive antihypertensive therapy, defined as use of intravenous nitroprusside or repeated intravenous infusions of other medications. A post hoc analysis reported the frequency, course, and treatment of hypertension (>185/110 mm Hg before randomization or >180/105 mm Hg within the first 24 hours after randomization).42 Antihypertensive treatment before and after treatment with rtPA was used in 9% and 24%, respectively, of the patients treated with rtPA. Prethrombolysis use of antihypertensive treatment did not adversely affect the rate of favorable outcomes at 3 months. Postthrombolysis hypertension and use of antihypertensive treatment correlated with a lower rate of favorable outcome at 3 months. It remains unclear whether this adverse effect was related to more severe ischemic injury, persistent vascular occlusion, or pronounced reduction in BP. Patients treated with thrombolytics and antihypertensive therapy were more likely to have an abrupt decline in BP than those who were not treated. The higher susceptibility to hypotension associated with antihypertensive treatment after thrombolytic use (not seen in the placebo group) may be related to recanalization or reperfusion; however, the rate of ICH among patients with acute hypertension with appropriate control was similar to that observed in nonhypertensive patients. Another study75 reported that postthrombolytic acute hypertension occurred predominantly within 6 hours of receipt of thrombolysis, and if treated adequately, is not associated with an increased risk of ICH. Therefore, early BP reduction with rapidly acting antihypertensive treatment appears paramount for safe and beneficial thrombolysis among patients with acute ischemic stroke. Frequent BP monitoring and titration with short-acting intravenous agents are preferable to avoid uncontrolled decline in BP. The data about treating the acute hypertensive response after thrombolytic use are limited, because most studies excluded patients with difficult-to-control BP and did not use some of the newer antihypertensive agents. With the increasing use of thrombolytics and other endovascular treatment in acute ischemic stroke, new studies are required to address these issues.
|
Patients With ICH |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
One third of subjects presenting with ICH continue to demonstrate hematoma expansion (with subsequent deterioration and death) in the first few hours after onset.76 An initial systolic BP
200 mm Hg is associated with hematoma expansion77 and increased mortality78 among patients with ICH. Persistently higher systolic BP is also associated with perihematoma brain edema formation.79 Reducing BP may reduce the rate of hematoma expansion, although conclusive evidence of this is not available.29 Recent studies suggest that reduction of BP may be tolerated because of reduced metabolism (hibernation)80 and preserved autoregulation in the perihematoma region.81 A multicenter prospective observational study82 reported the use of intravenous labetalol, hydralazine, and/or nitroprusside for maintaining BP <160/90 mm Hg within 24 hours of symptom onset among patients with ICH. Low rates of neurological deterioration and hematoma expansion were observed in treated patients. Patients treated within 6 hours of symptom onset were more likely to be functionally independent at 1 month than patients who were treated between 6 and 24 hours. Another study83 evaluated the tolerability and safety of intravenous nicardipine infusion within 24 hours of symptom onset to reduce and maintain MAP <130 mm Hg, consistent with previous ASA guidelines. The primary outcome of tolerability was achieved in 86% of the patients. Low rates of neurological deterioration and hematoma expansion were observed among treated patients. Indirect comparisons suggest that intermittent intravenous bolus regimens of antihypertensive agents have greater variability in BP control than continous infusion regimens.83
The current ASA44 and European Stroke Initiative45 guidelines recommend lowering BP in patients with an ICH to maintain systolic BP below 180 mm Hg. Both guidelines acknowledge that there may be a subset of patients who can tolerate more aggressive BP reduction, such as those with good neurological status or those without chronic hypertension. A recent observational study suggested that more aggressive BP reduction may have greater benefit in reducing the rate of hematoma expansion. One study assessed the results of lowering systolic BP below targets of 140, 150, or 160 mm Hg.84 The rate of hematoma expansion was 9% in patients with systolic BP <150 mm Hg and 30% among patients treated to maintain systolic BP <160 mm Hg or a higher threshold. Several ongoing trials (Table 1) are prospectively evaluating whether more aggressive BP lowering is safe and reduces the rate of hematoma expansion. The NINDS-funded Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH)60 trial is presently determining the exact threshold of BP lowering (systolic BP <140 mm Hg, <170 mm Hg, or <200 mm Hg) for patients with ICH within 6 hours of symptom onset. Another pilot randomized study, Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage (INTERACT), is comparing clinical outcomes in patients treated with intensive BP lowering (systolic BP <140 mm Hg) versus those treated according to ASA guidelines within 6 hours of symptom onset. Both trials recently reported preliminary results that suggested that aggressive BP reduction to a target of <140 mm Hg probably decreases the rate of substantial hematoma enlargement84a without increasing adverse events.84b
A new consideration is the combination of intravenous hemostatic treatment and aggressive BP control. In an exploratory analysis from a study of recombinant activated factor VII85 in ICH, initial systolic BP <170 mm Hg was associated with a trend toward lower hematoma expansion rates. In another study,86 a total of 188 patients admitted within 24 hours of symptom onset were treated with a combination of rapidly administered antifibrinolytic agents and systolic BP maintained <150 mm Hg. Hematoma enlargement was observed in only 4.3% of patients, which supports further evaluation of this approach.
|
Antihypertensive Agents and Regimens |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
The agents that are recommended by the ASA for acute hypertensive response are either intravenous or transdermal agents with rapid onset and short duration of action to allow precise titration (Table 242,53,58,81–83,87–96). BP can be monitored adequately with an inflatable cuff in most patients with acute hypertensive response, whereas intra-arterial monitoring should be considered in patients who require frequent titration with intravenous antihypertensive agents and in patients whose neurological status is deteriorating. ICP monitoring may be necessary in patients with a suspected increased ICP, to measure and preserve cerebral perfusion pressure during systemic BP lowering. Patients with a poor level of consciousness, midline shift, or compression of basal cisterns on computed tomographic scan may be considered for ICP monitoring when being treated with antihypertensive agents. Of note, cerebral perfusion pressure may overestimate regional perfusion because of its inability to measure regional pressure and autoregulatory disturbances.
|
|
Management of Chronic Hypertension in the Immediate Poststroke Period |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Approximately 50% of patients are admitted with stroke while taking regular antihypertensive therapy.8 The abrupt discontinuation of antihypertensive medication may lead to enhanced sympathetic activity, rebound hypertension, and a consequent increase in cardiovascular events97,98 in patients with coronary artery disease using β-adrenergic blockers or those using high doses of centrally acting antiadrenergic drugs. In studies conducted in nonstroke patients, a slow increase in systemic BP99 and a low rate of cardiovascular events100 follows discontinuation of antihypertensive treatment. A small randomized trial101 was unable to demonstrate any difference in the rate of death or disability after discontinuation of antihypertensive treatment in patients with ischemic stroke within 72 hours of symptom onset. New multicenter trials are addressing this question (Table 1
). In the interim, the decision to continue or discontinue antihypertensive agents must be made on a case-by-case basis with the intent to avoid hypotension, excessive hypertension, and myocardial ischemia. Reduction of the dose of the current agent or a change to a short-acting intravenous antihypertensive agent may be considered. Another issue is the timing of initiation or aggressive titration of oral antihypertensive treatment in patients with stroke who have chronic hypertension or undetected hypertension. In the California Acute Stroke Prototype Registry,102 great variability in practices between hospitals and considerable room for improvement was noted among two thirds of patients with acute ischemic cerebrovascular events discharged from the hospital who were given 1 or more antihypertensive medications. The heterogeneity in practice despite the definitive benefit demonstrated in clinical trials103–105 is concerning. Theoretically, oral hypertensive agents can be initiated at 24 to 48 hours after symptom onset, because most of the acute processes, such as ischemic penumbra and hematoma expansion, are uncommon after the first 24 hours. In the ACCESS trial47 (discussed above), treatment was started with daily candesartan or placebo on day 1. On day 2, the dosage was increased 2- or 4-fold if BP was >160/100 mm Hg. If patients in the candesartan group showed a hypertensive profile on day 7 (mean daytime BP >135/85 mm Hg), candesartan was increased or an additional antihypertensive drug was added. The results support early initiation of antihypertensive treatment with gradual titration to more aggressive BP treatment targets.
The JNC 7 report7 recommends that BP be maintained at intermediate levels (around 160/100 mm Hg) until neurological stability is achieved. Special circumstances such as elevated ICP, progressive cerebral edema, ongoing cerebral ischemia due to occlusive vessel disease or symptomatic cerebral vasospasm, and postoperative cerebral changes require individualized management. After the first week, or when neurological stability is achieved, a more aggressive treatment can be initiated for secondary prevention of recurrent stroke.7,106 The ASA107 recommends that antihypertensive therapy be considered for all patients with ischemic stroke or transient ischemic attack, because benefit is seen in persons with and without a history of hypertension. Special consideration may be necessary for patients with bilateral severe carotid stenoses,108 who may bear a high risk of stroke with aggressive BP lowering until carotid revascularization is performed.
|
Conclusions |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
Different strategies are required to manage the acute hypertensive response in different subtypes of stroke. Therefore, early diagnosis and differentiation are critically important for timely institution of the appropriate strategy. The management of high BP in acute ischemic stroke is highly controversial because of a lack of reliable evidence from randomized, controlled trials. Aggressive BP reduction is currently not recommended in patients with ischemic stroke in the acute phase because of potentially deleterious effects observed in some observational studies and absence of a documented benefit of acute BP lowering. A reduction in BP before administration of thrombolytics in patients with ischemic stroke is important to reduce the risk of secondary ICHs. Reduction of BP in patients with ICH requires further evaluation for efficacy given recent studies that have documented clinical tolerability due to reduced metabolism (hibernation) with preserved autoregulation in the perihematoma region.
Further studies are required to demonstrate the clinical benefits of treating the acute hypertensive response in patients with stroke and to determine whether these benefits are agent specific. Imaging modalities need to be developed that allow bedside measurement of regional cerebral blood flow and metabolism so that titration of antihypertensive treatment can be based on critical variables. Most recommendations are based on expert opinions and general principles defined by observational studies and small clinical trials. With the anticipated completion of several large clinical trials in the next 5 years, these recommendations can be established on the basis of superior levels of scientific evidence.
|
Acknowledgments |
|---|
The author wishes to thank Donald Quick, PhD, for his careful review of the manuscript and helpful comments.
Sources of Funding
Dr Qureshi was supported in part by the National Institute of Neurological Diseases and Stroke, National Institutes of Health, as Principal Investigator of the Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH; R01-NS44976-01A2), medication for which was provided by Protein Design Labs. Dr Qureshi is also the recipient of an Established Investigator Award from the American Heart Association as principal investigator of Innovative Strategies for Treating Cerebral Hemorrhage (American Heart Association grant No. 0840053N).
Disclosures
Dr Qureshi was the recipient of an honorarium from the Emergency Medicine Cardiac Research Education Group.
|
References |
|---|
|
TopIntroductionDefinition of Acute Hypertensive...Prevalence of Acute Hypertensive...Characteristics of Acute...Underlying Causes of Acute...Cerebrovascular Physiology and...Management of Acute Hypertensive...Patients With Acute Ischemic...Patients With Acute Ischemic...Patients With ICHAntihypertensive Agents and...Management of Chronic...ConclusionsReferences |
|---|
1. Qureshi AI, Ezzeddine MA, Nasar A, Suri MF, Kirmani JF, Hussein HM, Divani AA, Reddi AS. Prevalence of elevated blood pressure in 563704 adult patients with stroke presenting to the ED in the United States. Am J Emerg Med. 2007; 25: 32–38.[CrossRef][Medline] [Order article via Infotrieve]
2. Qureshi AI, Suri MFK, Nasar A, Kirmani JF, Ezzeddine MA, Divani AA, Giles WH. Changes in cost and outcome among US patients with stroke hospitalized in 1990 to 1991 and those hospitalized in 2000 to 2001. Stroke. 2007; 38: 2180–2184.
3. International cardiovascular disease statistics (2007 update). Available at: www.americanheart.org/downloadable/heart/1140811583642InternationalCVD.pdf. Accessed November 21, 2007.
4. Lindenauer PK, Mathew MC, Ntuli TS, Pekow PS, Fitzgerald J, Benjamin EM. Use of antihypertensive agents in the management of patients with acute ischemic stroke. Neurology. 2004; 63: 318–323.
5. Lakshminarayan K, Anderson DC, Borbas C, Duval S, Luepker RV. Blood pressure management in acute ischemic stroke. J Clin Hypertens (Greenwich). 2007; 9: 444–453.[CrossRef][Medline] [Order article via Infotrieve]
6. Whitworth JA. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens. 2003; 21: 1983–1992.[CrossRef][Medline] [Order article via Infotrieve]
7. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003; 289: 2560–2572.
8. Bath P, Chalmers J, Powers W, Beilin L, Davis S, Lenfant C, Mancia G, Neal B, Whitworth J, Zanchetti A; International Society of Hypertension Writing Group. International Society of Hypertension (ISH): statement on the management of blood pressure in acute stroke. J Hypertens. 2003; 21: 665–672.[CrossRef][Medline] [Order article via Infotrieve]
9. Willmot M, Leonardi-Bee J, Bath PM. High blood pressure in acute stroke and subsequent outcome: a systematic review. Hypertension. 2004; 43: 18–24.
10. Leonardi-Bee J, Bath PM, Phillips SJ, Sandercock PA. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke. 2002; 33: 1315–1320.
11. Qureshi AI, Suri MF, Kirmani JF, Divani AA. Prevalence and trends of prehypertension and hypertension in United States: National Health and Nutrition Examination Surveys 1976 to 2000. Med Sci Monit. 2005; 11: CR403–CR409.[Medline] [Order article via Infotrieve]
12. Rodriguez-Yanez M, Castellanos M, Blanco M, Garcia MM, Nombela F, Serena J, Leira R, Lizasoain I, Davalos A, Castillo J. New-onset hypertension and inflammatory response/poor outcome in acute ischemic stroke. Neurology. 2006; 67: 1973–1978.
13. Wallace JD, Levy LL. Blood pressure after stroke. JAMA. 1981; 246: 2177–2180.
14. Aslanyan S, Fazekas F, Weir CJ, Horner S, Lees KR. Effect of blood pressure during the acute period of ischemic stroke on stroke outcome: a tertiary analysis of the GAIN International Trial. Stroke. 2003; 34: 2420–2425.
15. Arboix A, Roig H, Rossich R, Martinez EM, Garcia-Eroles L. Differences between hypertensive and non-hypertensive ischemic stroke. Eur J Neurol. 2004; 11: 687–692.[CrossRef][Medline] [Order article via Infotrieve]
16. Mattle HP, Kappeler L, Arnold M, Fischer U, Nedeltchev K, Remonda L, Jakob SM, Schroth G. Blood pressure and vessel recanalization in the first hours after ischemic stroke. Stroke. 2005; 36: 264–268.
17. Resstel LB, Correa FM. Involvement of the medial prefrontal cortex in central cardiovascular modulation in the rat. Auton Neurosci. 2006; 126–127:130–138.
18. Hilz MJ, Devinsky O, Szczepanska H, Borod JC, Marthol H, Tutaj M. Right ventromedial prefrontal lesions result in paradoxical cardiovascular activation with emotional stimuli. Brain. 2006; 129: 3343–3355.
19. Meyer S, Strittmatter M, Fischer C, Georg T, Schmitz B. Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex. Neuroreport. 2004; 15: 357–361.[CrossRef][Medline] [Order article via Infotrieve]
20. Nason MW Jr, Mason P. Modulation of sympathetic and somatomotor function by the ventromedial medulla. J Neurophysiol. 2004; 92: 510–522.
21. Barron SA, Rogovski Z, Hemli J. Autonomic consequences of cerebral hemisphere infarction. Stroke. 1994; 25: 113–116.[Abstract]
22. Robinson TG, James M, Youde J, Panerai R, Potter J. Cardiac baroreceptor sensitivity is impaired after acute stroke. Stroke. 1997; 28: 1671–1676.
23. Oppenheimer S. The anatomy and physiology of cortical mechanisms of cardiac control. Stroke. 1993; 24: I3–I5.[Medline] [Order article via Infotrieve]
24. Ichiyama RM, Waldrop TG, Iwamoto GA. Neurons in and near insular cortex are responsive to muscular contraction and have sympathetic and/or cardiac-related discharge. Brain Res. 2004; 1008: 273–277.[CrossRef][Medline] [Order article via Infotrieve]
25. Resstel LBM, Correa FMA. Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex. Eur J Neurosci. 2006; 23: 481–488.[CrossRef][Medline] [Order article via Infotrieve]
26. Murros K, Fogelholm R, Kettunen S, Vuorela AL. Serum cortisol and outcome of ischemic brain infarction. J Neurol Sci. 1993; 116: 12–17.[CrossRef][Medline] [Order article via Infotrieve]
27. Chamorro A, Amaro S, Vargas M, Obach V, Cervera A, Gomez-Choco M, Torres F, Planas AM. Catecholamines, infection, and death in acute ischemic stroke. J Neurol Sci. 2007; 252: 29–35.[CrossRef][Medline] [Order article via Infotrieve]
28. Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke. 1999; 30: 2086–2093.
29. Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF. Spontaneous intracerebral hemorrhage. N Engl J Med. 2001; 344: 1450–1460.
30. Qureshi AI, Geocadin RG, Suarez JI, Ulatowski JA. Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions. Crit Care Med. 2000; 28: 1556–1564.[CrossRef][Medline] [Order article via Infotrieve]
31. Qureshi AI, Wilson DA, Traystman RJ. Treatment of transtentorial herniation unresponsive to hyperventilation using hypertonic saline in dogs: effect on cerebral blood flow and metabolism. J Neurosurg Anesthesiol. 2002; 14: 22–30.[CrossRef][Medline] [Order article via Infotrieve]
32. Qureshi AI, Suri MFK, Ringer AJ, Guterman LR, Hopkins LN. Regional intraparenchymal pressure differences in experimental intracerebral hemorrhage: effect of hypertonic saline. Crit Care Med. 2002; 30: 435–441.[CrossRef][Medline] [Order article via Infotrieve]
33. Qureshi AI, Wilson DA, Traystman RJ. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: comparison between mannitol and hypertonic saline. Neurosurgery. 1999; 44: 1055–1063.[CrossRef][Medline] [Order article via Infotrieve]
34. Paulson OB, Strandgaard S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev. 1990; 2: 161–192.[Medline] [Order article via Infotrieve]
35. Aaslid R, Lindegaard KF, Sorteberg W, Nornes H. Cerebral autoregulation dynamics in humans. Stroke. 1989; 20: 45–52.
36. Symon L, Held K, Dorsch NW. A study of regional autoregulation in the cerebral circulation to increased perfusion pressure in normocapnia and hypercapnia. Stroke. 1973; 4: 139–147.
37. Strandgaard S. Autoregulation of cerebral blood flow in hypertensive patients: the modifying influence of prolonged antihypertensive treatment on the tolerance to acute, drug-induced hypotension. Circulation. 1976; 53: 720–727.
38. Olsen TS, Larsen B, Herning M, Skriver EB, Lassen NA. Blood flow and vascular reactivity in collaterally perfused brain tissue: evidence of an ischemic penumbra in patients with acute stroke. Stroke. 1983; 14: 332–341.
39. Dawson SL, Panerai RB, Potter JF. Serial changes in static and dynamic cerebral autoregulation after acute ischaemic stroke. Cerebrovasc Dis. 2003; 16: 69–75.[CrossRef][Medline] [Order article via Infotrieve]
40. Yamamoto S, Nishizawa S, Tsukada H, Kakiuchi T, Yokoyama T, Ryu H, Uemura K. Cerebral blood flow autoregulation following subarachnoid hemorrhage in rats: chronic vasospasm shifts the upper and lower limits of the autoregulatory range toward higher blood pressures. Brain Research. 1998; 782: 194–201.[CrossRef][Medline] [Order article via Infotrieve]
41. The Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrauma and Critical Care. Guidelines for cerebral perfusion pressure. J Neurotrauma. 2000; 17: 507–511.[Medline] [Order article via Infotrieve]
42. Brott T, Lu M, Kothari R, Fagan SC, Frankel M, Grotta JC, Broderick J, Kwiatkowski T, Lewandowski C, Haley EC, Marler JR, Tilley BC. Hypertension and its treatment in the NINDS rt-PA stroke trial. Stroke. 1998; 29: 1504–1509.
43. Moon JS, Janjua N, Ahmed S, Kirmani JF, Harris-Lane P, Jacob M, Ezzeddine MA, Qureshi AI. Prehospital neurologic deterioration in patients with intraparenchymal hemorrhage. Crit Care Med. 2008; 36: 172–175.[CrossRef][Medline] [Order article via Infotrieve]
44. Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, Mayberg M, Morgenstern L, Ogilvy CS, Vespa P, Zuccarello M. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke. 2007; 38: 2001–2023.
45. Steiner T, Kaste M, Forsting M, Mendelow D, Kwiecinski H, Szikora I, Juvela S, Marchel A, Chapot R, Cognard C, Unterberg A, Hacke W. Recommendations for the management of intracranial haemorrhage, part I: spontaneous intracerebral haemorrhage: the European Stroke Initiative Writing Committee and the Writing Committee for the EUSI Executive Committee [published correction appears in Cerebrovasc Dis. 2006;22:461]. Cerebrovasc Dis. 2006; 22: 294–316.[Medline] [Order article via Infotrieve]
46. Adams HP Jr, Del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan AJ, Grubb RL, Higashida RT, Jauch EC, Kidwell C, Lyden P, Morgenstern L, Qureshi AI, Rosenwasser RH, Scott P, Wijdicks EF. Guidelines for the early management of patients with ischemic stroke. Circulation. 2007; 115: e478–534.
47. Schrader J, Luders S, Kulschewski A, Berger J, Zidek W, Treib J, Einhaupl K, Diener HC, Dominiak P. The ACCESS Study: evaluation of acute candesartan cilexetil therapy in stroke survivors. Stroke. 2003; 34: 1699–1703.
48. McGee S, Abernethy WB III, Simel DL. The rational clinical examination: is this patient hypovolemic? JAMA. 1999; 281: 1022–1029.
49. Jivraj S, Mazer CD, Baker AJ, Choi M, Hare GMT. Case report: profound hypotension associated with labetalol therapy in a patient with cerebral aneurysms and subarachnoid hemorrhage. Can J Anaesth. 2006; 53: 678–683.[Medline] [Order article via Infotrieve]
50. McLaren GD, Danta G. Cerebral infarction due to presumed haemodynamic factors in ambulant hypertensive patients. Clin Exp Neurol. 1987; 23: 55–66.[Medline] [Order article via Infotrieve]
51. Janardhan V, Qureshi AI. Mechanisms of ischemic brain injury. Curr Cardiol Rep. 2004; 6: 117–123.[Medline] [Order article via Infotrieve]
52. Astrup J, Symon L, Branston NM, Lassen NA. Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. Stroke. 1977; 8: 51–57.
53. Elewa HF, Kozak A, Johnson MH, Ergul A, Fagan SC. Blood pressure lowering after experimental cerebral ischemia provides neurovascular protection. J Hypertens. 2007; 25: 855–859.[Medline] [Order article via Infotrieve]
54. Stead LG, Gilmore RM, Vedula KC, Weaver AL, Decker WW, Brown RD Jr. Impact of acute blood pressure variability on ischemic stroke outcome. Neurology. 2006; 66: 1878–1881.
55. Barer DH, Cruickshank JM, Ebrahim SB, Mitchell JR. Low dose beta blockade in acute stroke ("Best" Trial): an evaluation. BMJ. 1988; 296: 737–741.
56. Blood pressure in Acute Stroke Collaboration (BASC). Interventions for deliberately altering blood pressure in acute stroke. Cochrane Database Syst Rev. 2001: CD000039.
57. Bath PM, Willmot M, Leonardi-Bee J, Bath FJ. Nitric oxide donors (nitrates), L-arginine, or nitric oxide synthase inhibitors for acute stroke. Cochrane Database Syst Rev. 2002; (4): CD000398.
58. Horn J, Limburg M. Calcium antagonists for acute ischemic stroke. Cochrane Database Syst Rev. 2000; (2): CD001928.
59. Oliveira-Filho J, Silva SCS, Trabuco CC, Pedreira BB, Sousa EU, Bacellar A. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset. Neurology. 2003; 61: 1047–1051.
60. Qureshi AI. Antihypertensive treatment of acute cerebral hemorrhage (ATACH): rationale and design. Neurocrit Care. 2007; 6: 56–66.[CrossRef][Medline] [Order article via Infotrieve]
61. Ahmed N, Nasman P, Wahlgren NG. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke. 2000; 31: 1250–1255.
62. Lisk DR, Grotta JC, Lamki LM, Tran HD, Taylor JW, Molony DA, Barron BJ. Should hypertension be treated after acute stroke? A randomized controlled trial using single photon emission computed tomography. Arch Neurol. 1993; 50: 855–862.
63. Ahmed N, Wahlgren NG. Effects of blood pressure lowering in the acute phase of total anterior circulation infarcts and other stroke subtypes. Cerebrovasc Dis. 2003; 15: 235–243.[CrossRef][Medline] [Order article via Infotrieve]
64. Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review. Stroke. 2003; 34: 2741–2748.
65. Turnbull F; Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of different blood-pressure-lowering regimens on major cardiovascular events: results of prospectively-designed overviews of randomised trials. Lancet. 2003; 362: 1527–1535.[CrossRef][Medline] [Order article via Infotrieve]
66. Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Davalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004; 35: 520–526.
67. Hacke W, Kaste M, Skyhoj Olsen T, Bogousslavsky J, Orgogozo JM. Acute treatment of ischemic stroke: European Stroke Initiative (EUSI). Cerebrovasc Dis. 2000; 10 (suppl 3): 22–33.[CrossRef][Medline] [Order article via Infotrieve]
68. Klijn CJM, Hankey GJ; American Stroke Association and European Stroke Initiative. Management of acute ischaemic stroke: new guidelines from the American Stroke Association and European Stroke Initiative. Lancet Neurol. 2003; 2: 698–701.[CrossRef][Medline] [Order article via Infotrieve]
69. Broderick J, Brott T, Barsan W, Haley EC, Levy D, Marler J, Sheppard G, Blum C. Blood pressure during the first minutes of focal cerebral ischemia. Ann Emerg Med. 1993; 22: 1438–1443.[CrossRef][Medline] [Order article via Infotrieve]
70. Mattle HP, Kappeler L, Arnold M, Fischer U, Nedeltchev K, Remonda L, Jakob SM, Schroth G. Blood pressure and vessel recanalization in the first hours after ischemic stroke. Stroke. 2005; 36: 264–268.
71. Gilligan AK, Markus R, Read S, Srikanth V, Hirano T, Fitt G, Arends M, Chambers BR, Davis SM, Donnan GA. Baseline blood pressure but not early computed tomography changes predicts major hemorrhage after streptokinase in acute ischemic stroke. Stroke. 2002; 33: 2236–2242.
72. Tanne D, Kasner SE, Demchuk AM, Koren-Morag N, Hanson S, Grond M, Levine SR. Markers of increased risk of intracerebral hemorrhage after intravenous recombinant tissue plasminogen activator therapy for acute ischemic stroke in clinical practice: the multicenter rt-PA stroke survey. Circulation. 2002; 105: 1679–1685.
73. Katzan IL, Furlan AJ, Lloyd LE, Frank JI, Harper DL, Hinchey JA, Hammel JP, Qu A, Sila CA. Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience. JAMA. 2000; 283: 1151–1158.
74. Katzan IL, Hammer MD, Furlan AJ, Hixson ED, Nadzam DM; Cleveland Clinic Health System Stroke Quality Improvement Team. Quality improvement and tissue-type plasminogen activator for acute ischemic stroke: a Cleveland update. Stroke. 2003; 34: 799–800.
75. Aiyagari V, Gujjar A, Zazulia AR, Diringer MN. Hourly blood pressure monitoring after intravenous tissue plasminogen activator for ischemic stroke: does everyone need it? Stroke. 2004; 35: 2326–2330.
76. Davis SM, Broderick J, Hennerici M, Brun NC, Diringer MN, Mayer SA, Begtrup K, Steiner T. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology. 2006; 66: 1175–1181.
77. Kazui S, Minematsu K, Yamamoto H, Sawada T, Yamaguchi T. Predisposing factors to enlargement of spontaneous intracerebral hematoma. Stroke. 1997; 28: 2370–2375.
78. Dandapani BK, Suzuki S, Kelley RE, Reyes-Iglesias Y, Duncan RC. Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke. 1995; 26: 21–24.
79. Vemmos KN, Tsivgoulis G, Spengos K, Zakopoulos N, Synetos A, Kotsis V, Vassilopoulos D, Mavrikakis M. Association between 24-h blood pressure monitoring variables and brain oedema in patients with hyperacute stroke. J Hypertens. 2003; 21: 2167–2173.[CrossRef][Medline] [Order article via Infotrieve]
80. Kim-Han JS, Kopp SJ, Dugan LL, Diringer MN. Perihematomal mitochondrial dysfunction after intracerebral hemorrhage. Stroke. 2006; 37: 2457–2462.
81. Powers WJ, Zazulia AR, Videen TO, Adams RE, Yundt KD, Aiyagari V, Grubb RL Jr, Diringer MN. Autoregulation of cerebral blood flow surrounding acute (6 to 22 hours) intracerebral hemorrhage. Neurology. 2001; 57: 18–24.
82. Qureshi AI, Mohammad YM, Yahia AM, Suarez JI, Siddiqui AM, Kirmani JF, Suri MF, Kolb J, Zaidat OO. A prospective multicenter study to evaluate the feasibility and safety of aggressive antihypertensive treatment in patients with acute intracerebral hemorrhage. J Intensive Care Med. 2005; 20: 34–42.
83. Qureshi AI, Harris-Lane P, Kirmani JF, Ahmed S, Jacob M, Zada Y, Divani AA. Treatment of acute hypertension in patients with intracerebral hemorrhage using American Heart Association guidelines. Crit Care Med. 2006; 34: 1975–1980.[CrossRef][Medline] [Order article via Infotrieve]
84. Ohwaki K, Yano E, Nagashima H, Hirata M, Nakagomi T, Tamura A. Blood pressure management in acute intracerebral hemorrhage: relationship between elevated blood pressure and hematoma enlargement. Stroke. 2004; 35: 1364–1367.
84. Anderson C, Huang Y, Wang J, Jin R, Arima H, Neal B, Peng B, Heeley E, Skulina C, Parsons M, Kim JS, Heritier S, Morgenstern L, Chalmers J. The Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage (INTERACT) trial: results of the vanguard phase. Paper presented at: International Stroke Conference 2008; February 20–22, 2008; New Orleans, La.
84. Qureshi AI. Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) trial. Paper presented at: International Stroke Conference 2008; February 20–22, 2008; New Orleans, La.
85. Broderick JP, Diringer MN, Hill MD, Brun NC, Mayer SA, Steiner T, Skolnick BE, Davis SM. Determinants of intracerebral hemorrhage growth: an exploratory analysis. Stroke. 2007; 38: 1072–1075.
86. Sorimachi T, Fujii Y, Morita K, Tanaka R. Predictors of hematoma enlargement in patients with intracerebral hemorrhage treated with rapid administration of antifibrinolytic agents and strict blood pressure control. J Neurosurg. 2007; 106: 250–254.[CrossRef][Medline] [Order article via Infotrieve]
87. Fagan SC, Bowes MP, Lyden PD, Zivin JA. Acute hypertension promotes hemorrhagic transformation in a rabbit embolic stroke model: effect of labetalol. Exp Neurol. 1998; 150: 153–158.[CrossRef][Medline] [Order article via Infotrieve]
88. Patel RV, Kertland HR, Jahns BE, Zarowitz BJ, Mlynarek ME, Fagan SC. Labetalol: response and safety in critically ill hemorrhagic stroke patients. Ann Pharmacother. 1993; 27: 180–181.[Abstract]
89. Qureshi AI, Wilson DA, Hanley DF, Traystman RJ. Pharmacologic reduction of mean arterial pressure does not adversely affect regional cerebral blood flow and intracranial pressure in experimental intracerebral hemorrhage. Crit Care Med. 1999; 27: 965–971.[CrossRef][Medline] [Order article via Infotrieve]
90. Zhang F, Iadecola C. Nitroprusside improves blood flow and reduces brain damage after focal ischemia. Neuroreport. 1993; 4: 559–562.[Medline] [Order article via Infotrieve]
91. Kuroda K, Kuwata N, Sato N, Funayama M, Yabuta A, Taguchi S, Suzuki M, Takahashi A, Ogawa A. Changes in cerebral blood flow accompanied with reduction of blood pressure treatment in patients with hypertensive intracerebral hemorrhages. Neurol Res. 1997; 19: 169–173.[Medline] [Order article via Infotrieve]
92. Willmot M, Ghadami A, Whysall B, Clarke W, Wardlaw J, Bath PMW. Transdermal glyceryl trinitrate lowers blood pressure and maintains cerebral blood flow in recent stroke. Hypertension. 2006; 47: 1209–1215.
93. Waldemar G, Vorstrup S, Andersen AR, Pedersen H, Paulson OB. Angiotensin-converting enzyme inhibition and regional cerebral blood flow in acute stroke. J Cardiovasc Pharmacol. 1989; 14: 722–729.[Medline] [Order article via Infotrieve]
94. Smeda J, Vasdev S, King SR. Effect of poststroke captopril treatment on mortality associated with hemorrhagic stroke in stroke-prone rats. J Pharmacol Exp Ther. 1999; 291: 569–575.
95. Dziedzic T, Slowik A, Pera J, Szczudlik A. Beta-blockers reduce the risk of early death in ischemic stroke. J Neurol Sci. 2007; 252: 53–56.[CrossRef][Medline] [Order article via Infotrieve]
96. Rehman F, Mansoor GA, White WB. "Inappropriate" physician habits in prescribing oral nifedipine capsules in hospitalized patients. Am J Hypertens. 1996; 9: 1035–1039.[CrossRef][Medline] [Order article via Infotrieve]
97. Houston MC. Abrupt discontinuation of antihypertensive therapy. South Med J. 1981; 74: 1112–1123.[Medline] [Order article via Infotrieve]
98. Houston MC. Abrupt cessation of treatment in hypertension: consideration of clinical features, mechanisms, prevention and management of the discontinuation syndrome. Am Heart J. 1981; 102: 415–430.[CrossRef][Medline] [Order article via Infotrieve]
99. Sieg-Dobrescu D, Burnier M, Hayoz D, Brunner HR, Waeber B. The return of increased blood pressure after discontinuation of antihypertensive treatment is associated with an impaired post-ischemic skin blood flow response. J Hypertens. 2001; 19: 1387–1392.[CrossRef][Medline] [Order article via Infotrieve]
100. Kostis JB, Espeland MA, Appel L, Johnson KC, Pierce J, Wofford JL. Does withdrawal of antihypertensive medication increase the risk of cardiovascular events? Trial of Nonpharmacologic Interventions in the Elderly (TONE) Cooperative Research Group. Am J Cardiol. 1998; 82: 1501–1508.[CrossRef][Medline] [Order article via Infotrieve]
101. Popa G, Voiculescu V, Popa C, Stnescu A, Nistorescu A, Jipescu I. Stroke and hypertension: antihypertensive therapy withdrawal. Rom J Neurol Psychiatry. 1995; 33: 29–35.[Medline] [Order article via Infotrieve]
102. Ovbiagele B, Hills NK, Saver JL, Johnston SC. Antihypertensive medications prescribed at discharge after an acute ischemic cerebrovascular event. Stroke. 2005; 36: 1944–1947.
103. Gueyffier F, Boissel JP, Boutitie F, Pocock S, Coope J, Cutler J, Ekbom T, Fagard R, Friedman L, Kerlikowske K, Perry M, Prineas R, Schron E. Effect of antihypertensive treatment in patients having already suffered from stroke: gathering the evidence: the INDANA (Individual Data Analysis of Antihypertensive Intervention Trials) Project Collaborators. Stroke. 1997; 28: 2557–2562.
104. Rezaiefar P, Pottie K. Blood pressure and secondary prevention of strokes: how low should we go? Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Can Fam Physician. 2002; 48: 1625–1629.
105. Arima H, Chalmers J, Woodward M, Anderson C, Rodgers A, Davis S, Macmahon S, Neal B, Group PC. Lower target blood pressures are safe and effective for the prevention of recurrent stroke: the PROGRESS trial. J Hypertens. 2006; 24: 1201–1208.[Medline] [Order article via Infotrieve]
106. Chalmers J, Todd A, Chapman N, Beilin L, Davis S, Donnan G, Frommer M, Huxley R, Lenfant C, MacMahon S, Mancia G, Mendis S, Whitworth J, Zanchetti A; International Society of Hypertension Writing Group. International Society of Hypertension (ISH): statement on blood pressure lowering and stroke prevention. J Hypertens. 2003; 21: 651–663.[CrossRef][Medline] [Order article via Infotrieve]
107. Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, Goldstein LB, Gorelick P, Halperin J, Harbaugh R, Johnston SC, Katzan I, Kelly-Hayes M, Kenton EJ, Marks M, Schwamm LH, Tomsick T; American Heart Association/American Stroke Association Council on Stroke, Council on Cardiovascular Radiology and Intervention, American Academy of Neurology. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Circulation. 2006; 113: e409–e449.
108. Rothwell PM, Howard SC, Spence JD; Carotid Endarterectomy Trialists’ Collaboration. Relationship between blood pressure and stroke risk in patients with symptomatic carotid occlusive disease. Stroke. 2003; 34: 2583–2590.
This article has been cited by other articles:
 |
|
 |
|
  M. Doumas, V. Papademetriou, J. Fichet, C. Bressolle, R. O. Fournier, J.-M. Achard, A. Fournier, S. Yusuf, H.-C. Diener, and R. L. Sacco Telmisartan for prevention of cardiovascular events. N. Engl. J. Med., January 15, 2009; 360(3): 302 - 303. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||