Ask your doctor to resolve these differences, preferably before you have your next stroke. You don't want her/him researching on the internet just as you get out of the ER. This is what protocols are for; so our doctors don't have to think up individualized responses.
Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke
Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons
Acute statin therapy improves survival after ischemic stroke
And the latest research here:
Mixed Results for Low-Dose Statin in Second Stroke - Pravastatin didn't reduce incidence of recurrent stroke, but did offer other benefits
Treating stroke
patients with low-dose pravastatin (Pravachol) did not appear to
prevent the occurrence of a second stroke, Japanese researchers reported
here.
In patients with noncardioembolic ischemic stroke, the risk of stroke
was 2.55% a year among patients taking 10-mg daily pravastatin compared
with 2.65% a year for patients taking other medications at the
discretion of their physician after a median follow-up of nearly 5
years, said Masayasu Matsumoto, MD, PhD, of the University of Hiroshima, and colleagues.
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However, there appeared to be a decline in
atherosclerotic-type strokes among the patients treated with low-dose,
Matsumoto noted in a press conference at the International Stroke Conference.There were no statistically significant differences at baseline in total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, cause of the index stroke, or in the use of antiplatelet agents, Matsumoto stated.
But after 4.9 years of follow-up, patients taking pravastatin achieved about a 10% reduction in total cholesterol (P<0.001) and significant reductions in LDL cholesterol (P<0.001) and triglycerides, (P=0.006) along with an increase in HDL cholesterol (P=0.004).
Nevertheless, treatment with pravastatin was not potent enough to significantly impact overall stroke occurrence, which was the primary endpoint of the so-called J-STARS trial, Matsumoto said.
"In Japan, it is still unclear if hyperlipidemia is a risk factor of recurrent stroke in the ischemic stroke patients without coronary heart disease," Matsumoto explained. He noted that in other trials, the use of statins decreased the incidence of cardiovascular diseases, including coronary heart disease and ischemic stroke, in this patient population.
Matsumoto's group hypothesized that the cholesterol-lowering effects could be expected to attenuate cerebrovascular inflammation and atherosclerosis.
They planned to recruit 3,000 patients for J-STARTS trial, but after 7 years enrollment was truncated at 1,578 patients. They assigned 793 patients to pravastatin and 785 patients to control. Matsumoto pointed out that follow-up was achieved despite earthquakes and a tsunami in the area where many of the patients and researchers lived.
Looking at secondary endpoints, the research team noted that, almost from the start of the follow-up period, the incidence curves separated when atherothrombotic strokes were observed. For patients on pravastatin, the risk of this type of stroke was 0.21% per year compared with a rate of 0.65% a year for controls (hazard ratio 0.33, 95% CI 0.15-0.74). This was a statistically significant finding even after adjustment for the index subtype of stroke, elevated blood pressure, and diabetes status, they reported.
In commenting on the trial, press conference moderator Bruce Obviagele, MD, cautioned that the trial results may not apply to many U.S. patients.
Obviagele, who is professor and chair of neurology at the Medical University of the South Carolina in Charleston, said he was intrigued by the difference in the atherothrombotic-caused strokes. "It makes sense that treatment with a cholesterol-lowering agent might make a difference in these strokes caused by atheromas which are more similar to heart disease," he said. "I think there is something there; something to investigate."
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