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Stroke Ė Acute Management and Prevention

There are approximately half a million new strokes per year which is an underestimated number. The approximate number is probably 700,000. There are 150,000 stroke deaths per year. Itís less than a minute for one stroke in the United States and approximately every three minutes somebody dies from a stroke in the United States. This is the leading cause of adult disability because it doesnít kill you right away but it leaves a permanent damage and it is still the third leading cause of death. So itís a fairly frequent cause of death.

There are several causes of stroke. The classification of ischemic stroke which accounts for 85% of all strokes, and 15% for hemorrhagic strokes. The ischemic stroke could be divided into cerebral vascular atherosclerosis which is a synonym to the large vessel artery stenosis. 20% of 85% or so represent penetrating artery disease or what we call small vessel disease. 15% represents cardiogenic embolism. The embolism most commonly related to atrial fibrillation and 5% other meaning, it could be a dissection, coagulopathies, this type of 

I am going to concentrate on the treatment of ischemic stroke as this is probably the major public health impact because it accounts for 85% of all strokes. I will leave 15% to the surgeons to take care of. We are usually dealing with ischemic strokes

The main message from this presentation for the acute management of stroke is that any of these sub-titled strokes should be considered for thrombolytic therapy. Thrombolytic therapy is currently the standard of treatment and the tissue plasminogen activator is the only type of thrombolytic that is currently approved by the FDA. Streptokinase trials were prematurely terminated because of excessive risk of hemorrhagic transformation. So we only deal with the tissue plasminogen

Briefly, it was a double blind randomized 624 patients enrolled in two studies. The TPA dose was .9 milligrams per kilogram which is a lower dose than in an MI. I think an MI is 1.1 milligram per kilogram. It should not exceed 90 milligram even though a patientís weight maybe over 100 kilos and this should be infused over

The key elements for this treatment is that it has to be started less than 3 hours from the stroke onset. This is very difficult to accomplish nowadays, particularly the patients do not come in right away. And because you have to do a CAT scan of the brain in the hospital before the treatment is started. You have to exclude

The hemorrhagic transformations occurred more frequently than in placebo but on this graph may also be a benefit in favor of TPA because the overall risk as you can see is lower in terms of the death rate than in the placebo. So you may say, well there are fewer patients dying with TPA than without it. It did not reach the

So how do we approach nowadays patients with acute ischemic stroke or maybe a TIA? We donít know exactly whether it is an evolving stroke or a TIA at the time of the treatment, sometimes at least. In emergency room we follow the step l which is complete blood count, platelet, PT and glucose. Sometimes a low

Anybody who had a stroke in the previous 3 months is not eligible for TPA. You donít know how severe a stroke was and we donít know what the deficit was at that time. So this was an exclusion. Anybody who had a hemorrhage in the past at any time was excluded from that study. So you have to follow what they have done to reach the similar benefit or risk ratio. Any GI, urinary bleeding in previous three weeks is an exclusion. Somebody who wakes up from the surgery

Other laboratory data is that patients who have INR above 1.7. So somebody who is on Coumadin who is fully anti-coagulated is not eligible for a TPA. Somebody who is on Heparin and the PTT is above 37. 37 is upper normal limit at our institution ,so you have to go by what your institution has for an upper

So nowadays, every hospital is trying to set up an emergency response system which includes a stroke team, or radiology team, CT scan availability, 24 hours, 7 days a week, and patients have to be screened by the triage nurse in emergency room for those with onset of less than 6 hours because there are a number of

Letís now turn our attention to stroke prevention and the major four categories of stroke. 85% are ischemic strokes and out of that 60% is cerebral atherosclerosis which relates to the stenosis, ulcerated plaque, any flow-limiting or stenosis in large arteries. So this is basically a large artery disease. Large arteries include ascending aorta, where sometimes we see a plaque of trans-esophageal echocardiogram which is now considered an independent risk factor of stroke if the diameter is more than 4 mm. You may have large artery stenosis at the aortic arch which is not accessible by any modality, except the angiogram nowadays and MRA is very difficult to interpret because of motion artifact in this area. Any origins of large vessels are subject to atherosclerotic changes. But the

For the basal artery, this is a basal artery posterior cerebral on one side , posterior cerebral on the other side and anterior posterior view and there is a high grade stenosis at the junction with the other vertebral, which is not visualized well. It could be a dissection, it could be atherosclerotic change, but the non-invasive way, meaning this is an angiogram, invasive modality to diagnose this condition. Non-invasive way is through the trans-cranial Doppler which is a Doppler probe

For carotids though, carotid ultrasound is the mainstay modality of choice for diagnosing any degree of carotid stenosis and this is a B-mode, actually duplex because it combines the color coded B-mode and in this area where sampling is. Then we get a Doppler signal and based upon Doppler signal we evaluate the

Surgery is relatively simple. A longitudinal incision, removal of the plaque that is very focally sighted, and sutured back. The problem is that patients may develop

Now, what you see here are two types of conditions: One is a severe carotid stenosis that has symptoms, that produce symptoms, and divide into medical treatment and surgical treatment. On your right side, you have similar condition in patients who have no symptoms. Symptoms meaning vision loss in one eye,

So in asymptomatic carotid stenosis even though there is a benefit of surgery, you also have to think about risk factors, hypertension, smoking, use of lipid lowering drugs, educate patient about TIA symptoms which may signal shift to high risk symptomatic stenosis. You have to identify and treat coronary artery disease if present in those patients, use anti-platelet therapy, and follow the carotid stenosis every 12 months. Some patients, if you tell them that there is a slight benefit of surgery but it is not an overwhelming benefit in the long term, they prefer not to have anything done. Also you have to know the surgeonís skill. The surgeon who you are referring this patient to.

The second type of stroke is a small vessel disease which is a penetrating artery disease or you may call lacuna syndrome which is sometimes reported on CT scan or MRI scan . And itís a cavity type of lesion and related to the small penetrating artery that comes off from the little cerebral artery. These are end vessels

Iím not going to talk much about smoking. It has been well documented in the Framingham study that in both males and females, that more cigarettes you smoke

What about the aspirin? It is the first line agent for stroke prevention. It reduces the risk of subsequent stroke by about 25%. It reduces a risk of a minor stroke threatened patients. It is all well documented but the dose is unknown. The optimal dose ranges somewhere from between 75 mg. and 1,300 mg. In fact, the FDA still recommends this

dose for stroke prevention based upon 1978 study from Canada. Many experts recommend the once a day but I tend to use twice a day. If you look at Canadians, they use 4 times a day. Europeans tend to use baby aspirin. So you have to choose which dose you would prefer to avoid GI toxicity. Somebody

Ticlopidine. This is a ticlopidine versus aspirin study, a so-called TAS study, that compared over several years the stroke incidence during the observation period between high dose of aspirin. This was a comparison between 1,300 mg. of aspirin versus ticlopidine, the standard dose of 250 mg. twice a day. And ticlopidine

We will be talking about atrial fibrillation in a moment: 15% of all ischemic strokes are embolic from the heart which is a significant number, and the most common cause of cardiogenic embolism is atrial fibrillation: 50% of all strokes related to the heart, are from an a-fib and it has been shown in 1,2,3,4,5 clinical trials from

There is also some sub-analyses performed in the Stroke Prevention Atrial Fibrillation Study and also in meta-analysis, pooled analysis, and there were high risk variables identified and if you look at those high risk variables, patients who have history of hypertension, prior TIA, or stroke, diabetes, or recent heart failure. If you have any of these, that puts you into high risk category which is approximately more than 7% per year risk of stroke recurrence if you 

Low subcutaneous heparin reduces DVT not stroke. What about intravenous heparin? This is a controversial issue. There are no clinical trials that show unequivocal benefit in favor of heparin. Sometimes people advocate for progressing ischemic stroke, especially vertebral basilar territory but the hard evidence is lacking. So people have used a low molecular heparin, low molecular weight heparin. The first drug evaluated in a large study from Hong Kong was flaxsoperin and it showed the benefit if used within 48 hours of acute ischemic stroke but next studies really could not find that benefit. That study was kind of strange

Well, what about aspirin? A similar trial from Britain used a couple of groups of patients that were taking aspirin versus none, and that was compared. There was