STROKE MANAGEMENT
Three experts discuss dos and don'ts
By Wednesday Sevilla, MD
Correspondent
The pathological entity that is stroke cannot be defined by a single clinical form, but is more aptly described as a syndrome because of its various manifestations. Also called a brain attack to describe the mechanism of the disease, it is caused by a number of identifiable conditions that compromise cerebral perfusion. Thus, management itself is compounded by a lot of variables.
These variables--what to do and what not to do--were the subject of a symposium during the 2005 joint annual convention of the Philippine Society of Hypertension and the Philippine Lipid Society.
Neurologists Abdias Aquino, consultant at the Capitol Medical Center; Cristina San Jose of St. Luke's Medical Center (SLMC); and Gerardo Legaspi, chair of the neurosurgery section at the University of the Philippines-Philippine General Hospital, took turns giving pointers on stroke management.
Circulation defects
Primarily caused by defects in the circulatory system of the brain, a brain attack may be more specifically induced by intracranial atherosclerosis, penetrating-artery disease, carotid-artery stenosis, arteriogenic emboli from the carotid artery and aortic-arch plaques, and cardioembolic emboli from known valvular disease and myocardial dysfunction.
Stroke may be hemorrhagic, which causes cerebral hypoperfusion from a ruptured vessel (usually from an aneurysm) or ischemic, in which circulation is cut off by a block (arterial plaque or a cardiogenic embolus) in the brain vessels. Other less common causes are increased coagulation states, arteritis, aortic dissection, and drug abuse. Ischemic stroke accounts for 85 percent of
cases.
NVAF and cardioembolic stroke
An embolus forms within the chambers of the heart when there is a known anatomic defect, whether in the valves or the muscular walls. The modification in the cardiac function in turn alters the flow of blood, causing pathologic turbulence that will be the focus of blood aggregation forming the solid embolus. When these emboli dislodge and migrate to the brain circulation, a stroke happens. Conditions that alter the circulation mechanics within the heart--atrial fibrillation, mitral stenosis, rheumatic heart disease, prosthetic valves, dilated cardiomyopathy, and myocardial infarction, to name a few--predispose an individual to the formation of cardiogenic emboli.
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According to Aquino, the basic clinical features that lead to the detection of a cardioembolic stroke are seen in a patient who exhibits a hemispheric neurological deficit (for example, left-sided body weakness) with or without loss of consciousness. But the event that differentiates it from the other mechanisms of stroke is the evident resolution of the neurologic deficit. The abrupt occlusion causes the deficit, but the lysis and eventual recanalization of the block produces the apparent shrinking deficit.
Although there are many known risk factors for a cardioembolic stroke, it is caused by a nonvalvular atrial fibrillation in 70 percent of CASes. Patients may be classified into high risk (eight to 12 percent chance of developing a stroke per year), moderate (four percent), or low (<1 percent).
Aquino stressed that in the management of NVAF, the basic tenets of primary and secondary prevention apply.
A metaanalysis of trials for medical treatment of NVAF showed that oral anticoagulation significantly reduced the risk of developing ischemic stroke, with warfarin faring better than aspirin in both primary- and secondary-prevention treatment strategies. However, there was no benefit of combination treatment. Applying the results to a risk-stratified patient, it was pointed out that risk reduction was significant in both high- and moderate-risk patients, with warfarin reducing risk more significantly. But in low-risk patients, both drugs did not show significant reduction.
Aquino also cited a study by Prof. Hylek (New England Journal of Medicine, 2003), which said that "among patients with nonvalvular atrial fibrillation, anticoagulation that results in an INR (international normalized ratio) of 2.0 or greater reduces not only the frequency of ischemic stroke but also its severity and the risk of death from stroke." He noted that lower INR target levels in patients with atrial fibrillation have shown no known benefit.
An issue has risen regarding anticoagulation in tertiary prevention, i.e. patients who have had an acute embolic stroke. Aquino warned that the decision to treat is often difficult since a physician will have to balance between the risks of a hemorrhagic conversion and the benefit of decreasing early stroke recurrence. Unfortunately, no guidelines have been set so treatment has to be done on a CASe-to-CASe basis. A study did show that in cardioembolic-stroke patients, acute anticoagulation may be given safely but no clear benefit was seen for all stroke patients.
Carotid-artery stenosis: CEA or stenting?
In Western populations, carotid-artery stenosis (CAS) accounts for 20 percent of stroke CASes. But local data suggest a much lower seven percent, according to San Jose, citing data from the SLMC stroke databank. But it remains a risk for Asians since intracranial and extracranial disease may occur simultaneously. San Jose pointed out that the risk of a stroke from CAS is related to the degree of stenosis and the history of a previous neurologic event. It has been known that the greater the degree of stenosis, the greater the risk. Other factors contribute to this risk--the character of the plaque, hypertension, and the rate of stenosis progression.
In asymptomatic patients with CAS of greater than 60 percent of the lumen, the risk is low at two percent per year. But when symptoms appear, this risk increases to 13 to 15 percent.
"The first important point in the treatment of patients with CAS is to apply the best medical management, the main goal[s] of which [are] stabilizing and halting the progression of the carotid plaque," San Jose explained. This is done through the administration of antiplatelets or antithrombotics.
An equally essential arm in management is the modification of risk factors present in the patient-diabetes mellitus, hypertension, dyslipidemia, alcohol intake, and lifestyle. Studies have shown that the risk for developing a stroke in asymptomatic CAS patients, although low at two percent per year, is still significant; thus best medical management cannot be undermined.
On the extreme end of the management scale is surgical intervention through carotid endarterectomy (CEA). San Jose cited three important trials that have contributed greatly to the choice of CEA as an option: the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the European Carotid Surgery Trial (ECST), and the Veterans Affairs Cooperative Symptomatic Carotid Surgery Trial.
In a pooled analysis of these studies, researchers concluded that :
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there is a benefit to the performance of CEA within two years upon diagnosis of CAS, after which the benefit progressively declines;
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in severe CAS of 70 to 90 percent, the risk reduction is significant up to five years after CEA;
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risk reduction is only moderate and almost nil in 50 to 69 percent and 30 to 49 percent stenosis; and
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CEA is harmful in 30 percent stenosis.
Applying this to practice, it is thus important to accurately assess the degree of stenosis through a reliable angiogram and using the NASCET formula in evaluating the stenosis.
In asymptomatic patients with CAS, it has been noted in two studies (the Asymptomatic Carotid Stenosis Study and the Asymptomatic Carotid Stenosis Trial) that results were roughly similar to those in symptomatic patients. However, the data are yet to be viewed differently since the number of patients needed to be treated to prevent one stroke was high (67). Thus, it is important for the physician to assess the baseline stroke risk of patients as well as their perioperative risk.
San Jose also described a subgroup of patients that need special consideration--those who are asymptomatic but with severe stenosis and symptomatic with only moderate stenosis. Individual risk stratification will have to be done through further imaging with perfusion and hemodynamic studies to better visualize cerebral perfusion.
Developments in techniques of inter-ventional treatment have allowed the use of carotid stenting. Its proponents emphasize the fact that the procedure is minimally invasive, causing fewer cranial-nerve palsies and hemorrhage. Of the 5,210 procedures done since 2000, technical success was computed at 98 percent and perioperative stoke events a mere five percent. Although studies have described low restenosis rates at six and 12 months after procedures, these rates were obtained only from a CASe series.
Two trials have described the effecicay of carotid stenting: the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) and the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial. Both trials showed that stenting may be done in patients with a high surgical risk because of comorbid conditions. The procedure is also preferred for patients in whom surgery is technically difficult, there is restenosis after a previous CEA, and the lesion is surgically inaccessible.
Unruptured cerebral aneurysm
One major cause of hemorrhagic stroke is unruptured cerebral aneurysm (CA) with an annual frequency of 5,000.
Legaspi related that a survey of Filipino neurosurgeons showed that they encounter on the average six to eight CASes of unruptured CA per year. Increasing pick-up rate has been noted, promising to decrease the rate of occurrence of hemorrhagic strokes in general.
Legaspi noted that the management of unruptured CA remains controversial since most CASes are detected incidentally during angiography following detection of a suspected lesion by computed tomography or magnetic resonance imaging. Usually, unruptured CA is diagnosed in a patient with nonspecific symptoms, prompting the physician to ask for imaging.
"The gold standard for diagnosis is still angiography (the procedure itself carrying a one- to two- percent risk of stroke)," Legaspi said. The development of three-dimensional angiography has significantly improved the diagnosis through better visualization. Computed tomography angiography, on the other hand, is best used for follow-up studies of small CAS not treated surgically. It is also used for screening in familial CA.
The question commonly asked is, "Do we routinely screen for unruptured CAS?" The answer is "no," said Legaspi, noting that the American Heart Association gave no recommendation on screening for the general population or even for patients with polycystic kidney disease or familial CA. It is, however, recommended for patients who have more than one first-degree family member diagnosed with a CA and among whom the prevalence is eight-percent.
In 2003, a study was made to describe the natural history and clinical outcomes of unruptured CAS and the risks of surgical and endovascular treatment. It identified the different predictors of CA rupture--hypertension (>35 percent risk), coronary-artery disease, alcohol use, smoking, and oral-contraceptive use. The morphology of the aneurysm played the biggest role in outcome. This emphasizes the importance of risk modification through medical management and behavioral changes.
While sizes of <7 mm posed a very minimal risk, the risk increased as the CA got larger. Another factor is the anatomic position of the aneurysm, with CAS in the posterior aneurysm posing lesser risk than those found in the anterior. Regarding surgical treatment of aneurysms, the poor outcome of untreated ruptured CAS was pegged at 65 percent, while those unruptured and treated with surgery had a low rates at 12.6 percent maximum. This translates to an increased survival for those who underwent treatment once the CA was diagnosed. The study also showed that patients less than 50 years old benefited from surgical treatment. Although age does not directly relate to rupture rate, it does so on the postoperative outcome as seen by lower rate of morbidity in younger patients undergoing surgical treatment. It pointed out, however, that even though endovascular surgery through vascular coils posed less immediate risk, long-term effects and morbidity are not yet completely known.
Risk stratification for nonvalvular atrial fibrillation
and practical guidelines for antithrombotic therapy
High risk (8- to 12-percent annual risk)
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All patients with previous transient ischemic attack or cerebrovascular accident.
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All patients 75 years and older with diabetes or hypertension.
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All patients with clinical evidence of valve disease, heart failure, thyroid disease, and impaired left ventricular function on echocardiography.*
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Treatment. Give warfarin (target INR 2-3) if possible in clinical practice and there are no contraindications.
Moderate risk (four-percent annual risk)
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All patients less than 65 with clinical risk factors: diabetes, hypertension, peripheral vascular disease, ischemic heart disease.
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All patients more than 65 not in high-risk group.
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Treatment. Either warfarin (INR 2-3) or aspirin 75 to 300 mg daily. In view of insufficient clear-cut evidence, treatment may be decided on individual CASes. Referral and echocardiography may help.
Low risk (one-percent annual risk)
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All patients aged less than 65 with no history of embolism, hypertension, diabetes, or other clinical risk factors.
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Treatment. Give aspirin 75 to 300 mg daily.
Assess risks and reassess regularly.
Dos and Don'ts
The symposium stressed several practical points in the management of stroke, with the condition and wellness of the patient as the final end point.
DO
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stratify patients according to the risk factors present with continuous monitoring and reassessment.
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apply trial data as may be appropriate, using the given guidelines.
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consider the risks and benefits in any treatment before utilizing it, keeping in mind the individual characteristic of a patient.
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give warfarin to patients with non-valvular atrial fibrillation.
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best medical management in patients with carotid artery stenosis.
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consider carotid endarterectomy in patients with symptomatic severe vcarotid artery stenosis.
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consider carotid stenting in patients in whom carotid endarterectomy in contraindicated or technically not feasible.
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use noninvasive screening tests such as Doppler studies to screen patients with known complicating factors such as post-CABG (coronary-artery bypass graft) peripheral-artery disease or a prior stroke.
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accurately define the degree of stenosis through angiography utilizing the NASCET criteria prior to doing a carotid endarterectomy.
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know the facts that influence the clinical behavior or unruptured cerebral aneurysms as this will allow the provision of proper patient advice.
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opt for computed-tomography angiography over magnetic-resonance angio-graphy; it offers better visualization.
DON'T
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use stenting indiscriminately.
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perform mass screening as it is not cost-effective.
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do routine screening of cerebral aneurysm in the general population.
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unscrupulously label a patient with a cerebral aneurysm as a "time bomb" as this will adversely affect his well-being and decision-making.
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