Hospital Medicine

Hypertension management in stroke

Jump to Section

Management of Hypertension after Stroke

I. What every physician needs to know.

It is important to recognize that the risk of overaggressive lowering of blood pressure (BP) in the hyperacute period after ischemic stroke is an expansion of the area of infarction. The risk of hypertension-induced cerebral edema and hemorrhagic conversion must be balanced against the risk of decreasing cerebral blood flow to at-risk brain tissue (penumbra). BP is usually elevated after stroke and spontaneously falls by 10-15% in the first 24 hours.

The traditional concept is "permissive hypertension" for ischemic stroke not treated with thrombolysis with the American Heart Association/American Stroke Association (AHA/ASA) 2007 guidelines recommending no new antihypertensives unless BP is above 220/120 millimiters mercury (mmHg) in the first 24 hours. Some clinicians may feel uncomfortable with BPs in this range but it is important to recognize that the unique physiology of cerebral perfusion after stroke may create harm with reduction in BP.

The 2013 AHA/ASA Guidelines for the Early Management of Acute Ischemic Stroke concedes that while the ideal blood pressure range is still inconclusive, the initial recommendation for a blood pressure target of <220/120 mmHg within the first 24 hours after an acute ischemic stroke remains reasonable. Some patients with acute ischemic stroke may have co-existing conditions that may be worsened by acute arterial hypertension, such as myocardial ischemia, aortic dissection, or heart failure, amongst others. The approach to blood pressure management for these patients should be determined on a case-by-case basis, and using best clinical judgement. If it is deemed necessary by the physician to reduce the blood pressure, a 15% reduction in systolic pressure while monitoring for neurological deterioration is a reasonable goal.

Patients who receive thrombolysis have both increased risk of hemorrhagic conversion and once the thrombotic occlusion to the major vessel has lysed there is less need to drive cerebral perfusion through collateral vessels. Thus, in the setting of thrombolytic therapy, the goal BP will be lower than for ischemic stroke not-treated with thrombolysis. AHA/ASA guidelines recommend BP to be less than 185/110 mmHg prior to thrombolysis and less than 180/105 mmHg after lysis.

For a patient with a primary hemorrhagic stroke there is a great risk of expanding the hematoma from uncontrolled hypertension and little evidence for penumbra, and so BP should be even more tightly controlled as long as cerebral perfusion pressure (CPP) is maintained. The 2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage suggest that for intracranial hemorrhage (ICH) patients presenting with systolic blood pressures between 150 and 220 mmHg, not only is the acute lowering of systolic blood pressure to a goal of <140 mmHg safe, but may also improve functional outcomes. While the data for patients presenting with systolic BP > 220 mmHg is less clear, aggressive reduction with continuous intravenous (IV) anti-hypertensives is reasonable.

Long-term, elevated BP is clearly associated with secondary stroke events and reduction to a normotensive state is recommended once the acute stroke period has passed. Suggested BP targets by recent AHA/ASA guidelines for secondary stroke prevention are systolic BP < 130 mmHg and diastolic BP < 80 mmHg for patients after ICH, and systolic BP < 140 mmHg and diastolic BP < 90 mmHg for most patients with ischemic stroke.

II. Diagnostic Confirmation: Are you sure your patient has hypertension after stroke?

Elevation in BP after stroke is easily measured using sphygmomanometry or automated electronic oscillometric measurement. Direct invasive measurement using an arterial line pressure transducer may be required for patients requiring intravenous antihypertensive therapy. Avoid arterial punctures prior to, or during, thrombolytic infusion. Normal BP is 120/80mmHg but this is rarely observed in the acute period after stroke. Hypertension is defined as a BP greater than 140/90mmHg.

In the acute post-stroke setting, the cerebral blood flow becomes linearly associated with the mean arterial pressure, thus mean arterial pressure is likely a better measure of cerebral perfusion than either systolic or diastolic pressure.

A. History Part I: Pattern Recognition:

The symptoms of a patient with stroke and hypertension will be dominated by the neurologic deficits caused by the stroke. The impact of the BP on perfusion may not be apparent until the BP changes. In some cases, the severity of neurologic deficits will visibly wax as the BP drops and may improve as the BP rises.

Assess for symptoms of adverse impact of BP on other organ systems as this will alter decisions on goal BP. For instance, chest pain may be a clue to myocardial infarction (MI) or aortic dissection and shortness of breath can be a sign of decompensated heart failure. Target BP will be lower for stroke complicated by hypertensive emergency affecting another organ system.

B. History Part 2: Prevalence:

The majority of patients presenting with an ischemic stroke will have a BP over 160mmHg on presentation. Hemorrhagic strokes have even higher presenting BPs. Hypertension is a potent risk factor for stroke. Approximately one third of adults suffer from hypertension (74.5 million Americans) and it is even more prevalent in African Americans. Only about two thirds of patients with hypertension are being treated and most are not adequately controlled.

C. History Part 3: Competing diagnoses that can mimic hypertension after stroke.

In the differential diagnosis of hypertension following ischemic or hemorrhagic stroke, the most important consideration is hypertensive encephalopathy. Hypertensive encephalopathy usually occurs above the limits of autoregulation (MAP 150 mmHg) and will present with headache, nausea/vomiting, global decrease in consciousness, visual disturbances, and papilledema. Hypertensive encephalopathy symptoms develop over hours to days whereas symptoms of stroke generally have sudden onset and reach maximal intensity in minutes. Focal deficits are clues that the symptoms are due to stroke with secondary hypertension rather than hypertensive encephalopathy.

Imaging will be diagnostic with focal hemorrhage in hemorrhagic stroke seen on computed tomography/magnetic resonance imaging (CT/MRI) or ischemic infarct seen on CT (late finding) or MRI diffusion weighted images. In contrast, CT or MRI will show diffuse edema of the cortex and subcortical white matter in hypertensive encephalopathy. Symptoms should improve with reduction in BP in hypertensive encephalopathy whereas with stroke symptoms will be constant or even worsen with BP reduction.

D. Physical Examination Findings.

Physical exam findings of hypertension associated with stroke will be primarily manifest as the neurologic deficits caused by the primary stroke which will depend on the area of brain involved. Exam features of chronic hypertension can include cotton wool spots or retinal hemorrhages on fundiscopic exam but elevated BP after stroke can occur in patients without a prior diagnosis of hypertension due to the adrenergic response to the central nervous system event.

In large hemorrhagic stroke and as a later finding in very extensive ischemic strokes elevated intracranial pressure may induce hypertension as part of the Cushing’s reflex in which hypertension will be associated with bradycardia and decreased level of consciousness. Papilledema may be seen in cases with elevated intracranial pressure.

Examination of other organ systems for acute decompensation which would alter decisions on BP goals is merited. Unequal pulses in the upper extremities or aortic regurgitation murmur could be a sign of aortic dissection. Cardiac S3 gallop or rales of pulmonary edema may be clues to myocardial infarction or congestive heart failure. Decreased urine output may signal renal failure resulting from the elevated BP.

E. What diagnostic tests should be performed?

The most important testing is close monitoring of the BP itself. BP in the first few days after stroke is a dynamic target which is likely to fluctuate even without therapy. BP tends to fall 10-15% in the first 24 hours and up to 20% 10 days later. Patients who have received thrombolysis should have their BP checked every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours and then hourly for the next 16 hours.

Invasive arterial monitoring may be needed for patients requiring intravenous antihypertensive therapy although the author does not advise placing an arterial catheter during thrombolytic therapy due to bleeding risk and certainly not at a non-compressible site.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

No laboratory test is needed to establish the diagnosis of hypertension after stroke. Laboratory tests ordered as part of the routine stroke evaluation may offer insight as to the effect of chronic hypertension or impact of the acute BP elevation on other organ systems which could lead to reduced BP goals in the hyperacute period.

Creatinine

Chronic renal insufficiency can be a sign of longstanding hypertensive nephropathy.

Acute renal failure and active sediment with microscopic hematuria, proteinuria, and/or red blood cell casts on urinalysis microscopic evaluation can provide evidence of acute hypertensive nephropathy.

Electrocardiogram

Left ventricular hypertrophy can be an indication of long standing hypertensive cardiomyopathy. Acute ST elevation, depression, or T wave inversions suggests acute myocardial infarction.

Troponin

Elevation is seen in myocardial injury associated with stroke. Stroke may be a complication of myocardial infarction (1% of cases) or the stress of stroke may induce myocardial injury. Troponin elevation is seen in 1 out of 6 patients in the first week after stroke, although most of this represents demand ischemia rather than acute coronary thrombotic occlusion.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

No imaging test is needed to establish the diagnosis of hypertension after stroke. Imaging tests ordered as part of the routine stroke evaluation may offer insight into the effect of chronic hypertension or impact of the acute BP elevation on other organ systems, which could lead to reduced BP goals in the hyperacute period.

Chest radiography

Cardiomegaly can be a sign of compensatory hypertrophy in response to longstanding hypertension. Pulmonary edema can be seen with decompensated heart failure as a result of acute BP elevation. Widened mediastinum can be seen with aortic dissection.

Echocardiography

Left ventricular hypertrophy seen in response to longstanding uncontrolled hypertension. Focal wall motion abnormalities suggest infarction which, if new, symptomatic, or associated with elevated troponins suggests acute myocardial infarction which would alter BP goals.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Elevated BP is seen commonly after stroke with up to 80% of stroke patients presenting with a BP above 140/90 mmHg. Markedly elevated BP above 200 mmHg systolic are common in the first 24 hours, especially with large ischemic or hemorrhagic strokes.

As a consequence, performing a work-up for secondary hypertension in all patients with elevated BP on presentation with stroke is unlikely to be of high yield. Patients with persistently elevated BP despite 3 antihypertensives, severe hypertension at an early age, or new onset hypertension in advanced age are more appropriate targets for the secondary hypertension work-up.

III. Default Management.

1. Determine whether stroke is hemorrhagic or ischemic and whether patients with ischemic stroke are eligible for thrombolysis.

2. Measure the patient’s BP in both upper extremities.

3. Establish the presence or absence of hypertensive emergency affecting other organ systems (MI, acute decompensated congestive heart failure [CHF], aortic dissection, malignant hypertensive nephropathy, hypertensive encephalopathy). In the setting of a hypertensive emergency impacting another organ system, lower BP goals to preserve that organ’s function may be necessary on a case by case basis, using the physician’s best judgement. If so, a 15% reduction in systolic BP while monitoring for worsening neurological symptoms is reasonable.

4. Based on the above considerations, choose a guideline concordant BP goal for the patient during the hyperacute period:

  • Less than 220/120 mmHg for ischemic stroke not eligible for thrombolysis

  • Less than 185/110 mmHg for ischemic stroke prior to thrombolysis

  • Less than 180/105 mmHg for ischemic stroke following thrombolysis

  • Less than 140 mmHg systolic for hemorrhagic stroke patients who present with a systolic BP < 220 mmHg

5. If the patient is above goal, begin reduction with target of 10-15% lowering in the first 24 hours. Given the danger of worsening perfusion with over-correction, a preference is given for treatment with rapid onset and ability to be titrated in the hyperacute period. This can typically be best-achieved with intravenous agents. Little evidence-based data drives the decision for one agent over another and so choice is driven by provider preference informed by relevant co-morbidities. Labetalol and Nicardipine are two commonly used medications that can be given as a one-time bolus administration as well as a continuous IV infusion.

6. It is reasonable to discontinue home antihypertensive agents at the onset of acute stroke. You may want to simply reduce the dose for some medications that carry a risk of antihypertensive withdrawal syndrome, such as beta blockers or clonidine. After passing swallow evaluation, or when safe enteral access is obtained, starting long-term oral antihypertensive treatment may be considered. The optimal time for starting oral medications after an acute ischemic stroke has not been established, however, the AHA/ASA guidelines suggest that starting at 24 hours post-stroke is reasonable.

Hydrochlorothiazide may be prudent to hold until sodium levels are stable in significant strokes, given the potential for syndrome of inappropriate antidiuretic hormone (SIADH) as a complication of the stroke with hyponatremia, further exacerbated by diuretic induced renal salt wasting.

7. Once the hyperacute period has resolved (at least 24 hours) and perfusion via penumbra is no longer felt critical (likely depends on size and type of the stroke, with little evidence of penumbra in hemorrhagic or lacunar strokes, but penumbra being more relevant with large ischemic stroke or presence of stenosis of intra or extracranial blood vessels) then new oral antihypertensive agents may be initiated if needed.

The best evidence of benefit comes from data on diuretics or the combination of angiotensin-converting-enzyme (ACE) inhibitors and diuretics, but there is little direct comparison data to allow clear claims of superiority for any specific agent. Drug choice should be individualized based on considerations of the drug class best suited for the patient’s co-morbid illness.

8. New drug therapy to achieve normotensive goal should be started during hospitalization and not deferred to outpatient setting as evidence from the CHIPPS trial suggests mortality benefit can be seen in as little as 3 months.

A. Immediate management.

If the patient is above goal, begin reduction with target of 10-15% lowering in the first 24 hours. Given the danger of worsening perfusion with over-correction, a preference is given for agents with rapid onset and ability to be titrated in the hyperacute period. Little evidence-based data drives the decision for one agent over another and so choice is driven by provider preference informed by relevant co-morbidities. Labetalol and Nicardipine are two commonly used medications that can be given as a one-time bolus administration as well as a continuous IV infusion.

B. Physical Examination Tips to Guide Management.

Presence of hypertensive decompensation of another organ system would mandate a lower BP goal consistent with the appropriate guidelines for that disease state. In this setting, a balance will need to be achieved between the positive effect of elevated BP on the cerebral perfusion to the penumbra and the detrimental impact of ongoing hypertension on the other impaired organ. As an example, in a patient with aortic dissection complicated by stroke, the BP goal for the aortic dissection will take priority.

Monitor impact of changes in BP on the neurologic exam. Evidence of new or worsening neurologic deficit should prompt re-evaluation with non-contrast brain computed tomography for hypertensive hemorrhagic conversion as this would prompt a change to the lower BP goals of intracranial hemorrhage.

In some cases the patient’s stroke deficits may visibly wax as the BP falls and wane as it rises again. In cases such as this a more permissive approach to hypertension is indicated, including optimization of volume and cardiac output status. Induced hypertension is sometimes employed in cases such as this, although standard use of vasopressor induced hypertension after stroke has not been adequately proven to improve outcomes and is not routinely recommended.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Checking a basic metabolic panel to evaluate the impact of antihypertensive drugs and change in BP on electrolytes and creatinine after stroke is reasonable. This would be checked 1-2 days after significant BP shifts, and at least once in the week after initiation of an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker.

D. Long-term management.

Long-term reduction of BP to normotensive levels is critically important in secondary prevention of stroke. Therapy to reduce BP reduces risk of second strokes and appears to lack a threshold effect. As such, BP reduction to a target of < 140/90 mmHg is recommended for most patients after ischemic stroke as long as they can tolerate this reduction. For patients with ICH, a long-term BP goal of < 130/80 mmHg is reasonable.

This should start with lifestyle modification such as exercise, low salt diet, moderation of alcohol intake, and a healthy diet. No specific drug can be recommended for all stroke patients although diuretics alone or in combination with ACE inhibitors have fairly good evidence of benefit. Drug choice should be rationally targeted based on proven benefit for other co-morbid illness, cost, and ease of adherence.

E. Common Pitfalls and Side-Effects of Management

The most important pitfall in the management of BP after stroke is to be overaggressive in the treatment of initial elevation in the patient with ischemic stroke not eligible for thrombolysis and overshoot the planned 10-15% reduction. This is easy to do given that the average patient will have a spontaneous BP reduction of this size even without any therapy.

Case studies and experience with large trials of initiation of antihypertensive therapy in the hyperacute period clearly demonstrate the potential to dramatically worsen outcomes by over-correction of BP. Conversely, failure to achieve BP targets prior or following thrombolysis may increase risk of hemorrhagic conversion. Evidence suggests one third of patients receiving thrombolysis will require antihypertensive therapy in the first 24 hours.

Selected side effects of antihypertensive drugs used in the acute post-stroke period:

  • Nitroglycerin: Vasodilation can cause hemodynamic collapse in critical aortic stenosis and may increase intracranial or intraocular pressure.

  • Labetalol: May cause bradycardia or heart block, worsen inotropic function, or worsen bronchospasm.

  • Nicardipine: May induce tachycardia.

  • Nitroprusside: A poor choice in patients with renal failure, hepatic failure, or with prolonged use due to accumulation of cyanide and thiocyanate. Can increase ICP which may be a consideration for patients with very large ischemic strokes or hemorrhagic strokes. Draw thiocyanate level if using more than 48 hours. Do not use maximum dose longer than 10 minutes.

IV. Management with Co-Morbidities

The stroke patients’ co-morbid conditions influence choice of antihypertensive agent both in the acute and long-term setting. For most patients, the recommendations of the joint national committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure would apply.

A. Renal Insufficiency.

In acute renal failure during initial presentation felodipine may be chosen as a choice for antihypertensive therapy via intravenous infusion. While early initiation of ACE inhibitor or angiotensin-receptor blocker (ARB) therapy would not be appropriate in acute renal failure, a patient with chronic stable renal insufficiency is appropriate for these medications with close monitoring of potassium and creatinine.

B. Liver Insufficiency.

No significant change in recommendations.

C. Systolic and Diastolic Heart Failure

Patients with congestive heart failure are more appropriate for ACE inhibitors or ARBs. Beta-blockers may be avoided in favor of nitrates in acute decompensated heart failure but beta-blockers would be appropriate once the patient was compensated. Diuretics are usually a part of therapy both to maintain euvolemia and to reduce BP. Aldosterone antagonists are particularly appropriate in class III or IV heart failure, or in class II heart failure in patients with a history of cardiovascular hospitalization or elevated plasma natriuretic peptide levels. In African Americans, the combination of hydralazine and nitrates has been demonstrated effective.

D. Coronary Artery Disease or Peripheral Vascular Disease

Patients with coronary artery disease or myocardial injury are more appropriate for beta-blockers and nitroglycerin for BP control in stroke.

E. Diabetes or other Endocrine issues

Patients with diabetes are more appropriate for ACE inhibitors or ARBs for long-term BP control.

F. Malignancy

No change in recommendations.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in recommendations.

H. Primary Lung Disease (COPD, Asthma, ILD)

Avoid beta-blocking agents in reactive airway disease.

I. Gastrointestinal or Nutrition Issues

No change in recommendations.

J. Hematologic or Coagulation Issues

No change in recommendations.

K. Dementia or Psychiatric Illness/Treatment

No change in recommendations.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Clear communication as to the target BP based on the considerations above. The author favors using standardized protocols with prompts in the order set for both target BP and pharmacologic therapeutic intervention to initiate, if not at goal, rather than “call for BP greater than…” orders.

B. Anticipated Length of Stay.

Length of stay in stroke patients is driven by the evaluation and therapeutic needs of the stroke itself and rarely hinges on BP control as an isolated feature.

C. When is the Patient Ready for Discharge.

Blood pressure should be below acute goal for at least 24 hours without use of as needed medications prior to discharge. Discharge antihypertensive regimen should usually be started at least a day before discharge to assess response. Initiation of therapy in the hospital prior to discharge is likely to increase chance of appropriate treatment long-term.

D. Arranging for Clinic Follow-up

BP must be monitored on first post-stroke follow-up clinic appointment with active titration of blood pressure medications to achieve normotensive state. Discharge communication with both patient and primary care physician should emphasize the critical importance of this aspect of secondary stroke prevention.

1. When should clinic follow up be arranged and with whom.

As a general rule, the author favors a follow-up appointment one week after discharge from the hospital for stroke. This can occur in a dedicated stroke clinic, general neurology clinic, primary care clinic, or some combination of subspecialist and primary care with good communication between all sites of care. The National Stroke Association has suggested a “stroke report card” in which BP control to normotensive state would be one aspect of monitored post-discharge quality.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Discharge BP and last measured creatinine should be included in the communication between the hospital and the follow-up providers.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Electrolytes and creatinine for patients who have had new initiation of a diuretic, ACE inhibitor, ARB, or who experienced significant fluctuations in blood pressure.

E. Placement Considerations.

Placement considerations are driven by the deficits resulting from the stroke and not BP as an isolated entity. Communication is needed with accepting providers regarding BP goal to normotensive state, critical importance of further titration of antihypertensive therapy after hospital discharge to achieve this goal, last measured creatinine, and need for re-checking creatinine and electrolytes within a week based on degree of BP reduction and whether ACE inhibitors, ARBs, or diuretics are being prescribed.

F. Prognosis and Patient Counseling.

Approximately one quarter of the almost 800,000 strokes in the United States each year are recurrent events. Long-term blood pressure reduction is estimated to reduce risk of second stroke by approximately 1/4th and so initiation of antihypertensive therapy by the hospital providers, patient adherence, and titration to goal by outpatient providers has a significant impact on subsequent prognosis.

Patients should be counseled on their individualized target BP (usually the low end of the normotensive range), what medications are being used to achieve this goal, how to take them, and the importance of adherence. Patients should also be counseled about non-pharmacologic lifestyle interventions which can reduce BP, including exercise, moderation in alcohol use, low salt intake, weight loss, and a diet rich in fruits, vegetables, and low-fat dairy products.

Given full information about the impact of BP reduction on second strokes, the patient should be encouraged to take ownership in the process of achieving goal BP. The healthcare provider and patient together should agree on what steps to take immediately and when they hope to have achieved the target pressure. They should commit together to further actions if the blood pressure does not reach goal at that point.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.

BP is not currently one of the Joint Commission markers of quality for stroke care, but the evidence is strong that long-term BP reduction is a marker of quality care for patients who have suffered a stroke.

The Center for Medicare and Medicaid services now track and report 30-day readmissions for patients discharged after acute stroke as part of their ongoing Readmission Reductions Program. BP control and monitoring is part of the transition of care process to the outpatient setting for continued secondary prevention of stroke.

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

All prophylaxis measures relevant to stroke should be followed (see ischemic stroke section).

What's the evidence?

Hossmann, K. "Viability Thresholds and the Penumbra of Focal Ischemia". Annals of Neurology. vol. 36. 1994. pp. 557-565.

Wallace, J, Levy, L. "Blood pressure after stroke". JAMA. vol. 246. 1981. pp. 2177-2180.

Adams, HP, del Zoppo, G, Alberts, MJ. "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". Circulation. vol. 115. 2007. pp. e478-534.

Jauch, EC, Saver, JL, Adams, HP. "Guidelines for the early management of adults with ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association". Stroke. vol. 44. 2013. pp. 870-947.

Cumbler, E, Glasheen, J. "Management of Blood Pressure after Acute Ischemic Stroke: An Evidence-Based Guide for the Hospitalist". Journal of Hospital Medicine. vol. 2. 2007. pp. 261-267.

Hemphill, JC, Greenberg, SM, Anderson, CS. "Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association". Stroke. vol. 46. 2015. pp. 2032-60.

Roge, VL, Go, AS, Lloyd-Jones, DM, Benjamin, EJ, Berry, JD, Borden, WB, Bravata, DM, Dai, S, Ford, ES, Fox, CS, Fullerton, HJ, Gillespie, C, Hailpern, SM, Heit, JA, Howard, VJ, Kissela, BM, Kittner, SJ, Lackland, DT, Lichtman, JH, Lisabeth, LD, Makuc, DM, Marcus, GM, Marelli, A, Matchar, DB, Moy, CS, Mozaffarian, D, Mussolino, ME, Nichol, G, Paynter, NP, Soliman, EZ, Sorlie, PD, Sotoodehnia, N, Turan, TN, Virani, SS, Wong, ND, Woo, D, Turner, MB. "on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee AHA Statistical Update Heart Disease and Stroke Statistics—2012 Update- A Report From the American Heart Association". Circulation. vol. 125. 2012. pp. e2-e220.

"Tissue plasminogen activator for acute ischemic stroke". N Engl J Med. vol. 333. 1995. pp. 1581-1588.

Indredavik, B, Rohweder, G, Naalsund, E, Lydersen, S. "Medical Complications in a Comprehensive Stroke Unit and an Early Supported Discharge Service". Stroke. vol. 39. 2008. pp. 414-420.

Robinson, TG, Potter, JF, Ford, GA, Bulpitt, CJ, Chernova, J, Jagger, C, James, MA, Knight, J, Markus, HS, Mistri, AK, Poulter, NR. "Effects of Antihypertensive treatment after acute stroke in the Continue or Stop Post-Stroke Antihypertensives Collaborative Study". Lancet Neurol. vol. 9. 2010. pp. 767-75.

Potter, JF, Robinson, TG, Ford, GA, Mistri, A, James, M, Chernova, J, Jagger, C. "Controlling Hypertension and Hypotension Immediately Post-Stroke". Lancet Neurol. vol. 8. 2009. pp. 48-56.

Kaste, M, Fogelholm, R, Erila, T. "A randomized, doubleblind, placebo-controlled trial of nimodipine in acute ischemic hemispheric stroke". Stroke. vol. 25. 1994. pp. 1348-1353.

Brott, T, Lu, M, Kathari, R. "Hypertension and its treatment in the NINDS rt-PA Stroke Trial". Stroke. vol. 29. 1998. pp. 1504-1509.

Furie, KL, Kasner, SE, Adams, RJ. "Robert Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. vol. 42. 2011. pp. 227-276.

Kernan, WN, Obviagele, B, Black, HR. "Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association". 2014.

Chobanian, AV, Bakris, GL, Black, HR, Cushman, WC, Green, LA, Izzo, JL, Jones, DW, Materson, BJ, Oparil, S, Wright, JT, Roccella, EJ. "the National High Blood Pressure Education Program Coordinating Committee. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure". Hypertension. vol. 42. 2003. pp. 1206-1252.

Gorelick, PB, Testai, FD. "The National Stroke Association’s Preventing Recurrent Stroke: Targets for Managing Risk program".

Yancy, CW, Jessup, M, Bozkurt, B. "2013 ACCF / AHA guideline for management of heart failure: A report of the American College of Cardiology Foundation / American Heart Association Task Force on Practice Guidelines". Circulation. vol. 128. 2013. pp. e240-e327.

"Medicare.gov: the Official U.S. Government Site for Medicare. Readmissions and Deaths".

You must be a registered member of Psychiatry Advisor to post a comment.

Sign Up for Free e-newsletters