Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, November 15, 2011

Lipitor, Crestor Both Turn Back Plaque

So who is going to test these against watermelon juice?
http://oc1dean.blogspot.com/2011/11/watermelon-juice-reverses-hardening-of.html

http://www.medpagetoday.com/Cardiology/Atherosclerosis/29684?utm_source=breaking-news&utm_medium=email&utm_campaign=breaking-news
Action Points
  • Explain that aggressive treatment with potent statins appears to reverse the build-up of plaque in arteries, and the benefit was the same whether the statin used was rosuvastatin (Crestor) or atorvastatin (Lipitor).


  • Note that patients treated with rosuvastatin achieved significantly greater increases in HDL and decreases in LDL than patients treated with atorvastatin.

ORLANDO -- Aggressive treatment with potent statins appears to reverse the build-up of plaque in arteries, and the benefit is the same whether the statin used was rosuvastatin (Crestor) or atorvastatin (Lipitor), researchers said here.

Using intravascular ultrasound (IVUS) to assess atheroma, Stephen J. Nicholls, MBBS, PhD, of the Cleveland Clinic, and colleagues found that the percent atheroma volume (PAV) decreased by 0.99% among patients treated with 80 mg of atorvastatin daily versus an average regression of 1.22% in patients taking 40 mg of rosuvastatin -- a statistical dead heat (P=0.10).

A secondary efficacy endpoint, normalized total atheroma volume, favored rosuvastatin with a reduction of 6.4 cubic mm versus 4.4 cubic mm in the atorvastatin arm (P=0.01).

The finding, reported today at the American Heart Association meeting here and published online by The New England Journal of Medicine, is likely to have implications for clinical practice since atorvastatin will be available as a generic this month, while rosuvastatin is available only as the brand drug Crestor.

"Both groups did amazingly well, with more regression than we have ever seen with IVUS," said Steven E. Nissen, MD, director of cardiovascular medicine at the Cleveland Clinic and a co-investigator of the Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin versus Atorvastatin (SATURN) trial.

For that reason, Nissen said, it was not possible to say if the findings made a case for the use of either of the drugs.

"Neither Dr. Nicholls nor I tell doctors what drug to prescribe," Nissen told MedPage Today. Asked about his own practice, he said that he always "tries in using statins to customize the treatment for each patient, which is why I have plenty of patients on 40 mg simvastatin, which is safe and is a generic, and will have some patients on generic atorvastatin when it becomes available. But for people in whom it is difficult to get LDL down, I use and will use rosuvastatin."

Nissen added that atorvastatin "is just a very good drug -- there is a reason that it is the only [drug] to reach $10 billion in sales."

Rosuvastatin, by contrast, is known to be the most potent of the statins, and lipid numbers in SATURN confirm that reputation: After 104 weeks of treatment, patients taking rosuvastatin achieved mean LDL cholesterol levels of 62.6±1.0 mg/dL versus 70.2 mg/dL in the atorvastatin arm (P<0.001), and HDL increase was likewise greater with rosuvastatin, for a mean of 50 mg/dL versus 49 mg/dL (P=0.02).

"These values resulted in a lower ratio of LDL cholesterol to HDL cholesterol during treatment with rosuvastatin (1.30±0.02 versus 1.50±0.02 with atorvastatin; P<0.001), a greater proportion of rosuvastatin-treated patients in whom LDL cholesterol levels below 70 mg/dL (1.81 mmol per liter) were achieved (72.1% versus 56.1% with atorvastatin; P<0.001), and a smaller proportion of rosuvastatin-treated patients whose LDL cholesterol levels remained higher than the current treatment goal of 100 mg/dL (2.6 mmol per liter) (4.6% versus 7.7% with atorvastatin; P=0.04)," the researchers wrote.

The trial recruited 1,385 patients and reported on 519 from the atorvastatin group and 520 from the rosuvastatin arm. The average age of patients was 57, more than 70% were men, and roughly 95% were white.

In a statement Nicholls said, "Doctors have been reluctant to use high doses of statins, but in this study the drugs were safe, well tolerated, and had a profound impact on lipid levels, the amount of plaque in vessel walls, and the number of cardiovascular events."

Safety was, in fact, better than expected with "not a single case of rhabdomyolysis," Nissen noted. There was a handful of atorvastatin patients -- 17 -- who had measurable increases in liver enzymes, and five patients -- four in the atorvastatin arm -- had creatine kinase levels more than 10 times the upper limit of normal, but those were isolated readings.

Among the limitations of the study was the lack of a placebo group to measure plaque progression.

Moreover, because all patients were undergoing clinically-indicated angiography, it "remains uncertain whether our findings apply to primary prevention in asymptomatic patients."

Also, 25% of patients did not undergo the final IVUS assessment, and those patients may have had different rates of progression.

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