Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, May 6, 2017

ATACH Analysis Hints at Benefit of Blood Pressure Control - post Hemorrhage

Or is this better?

Intravenous glyburide treatment may reduce dangerous brain swelling after stroke

Or this?

Nanoparticles show early promise in reducing inflammation after brain bleed

Or this?

Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling

But this to think about:

Don't go too low with blood pressure in hypertensive CAD patients

 

 

 


http://www.medpagetoday.com/meetingcoverage/aan/64910

Reducing blood pressure to below 140 mm Hg shows trends for reduced hematoma

  • by
    Contributing Writer, MedPage Today
BOSTON – A post hoc analysis of the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2) trial showed hints of benefit to lowering blood pressure in patients presenting with brain hematoma, but even the new secondary analysis did not produce significant findings, researchers said here at the annual meeting of the American Academy of Neurology.
About 18% of patients assigned to intensive blood pressure treatment -- keeping systolic blood pressure between 110 and 139 mm Hg -- had increases in hematoma volume compared with 24.4% of the patients who were in the standard therapy group and whose blood pressure was maintained between 140 and 179 mm Hg, said Adnan Qureshi, MD, professor of neurology at the University of Minnesota, Minneapolis.
"That certainly looks like it is going in the right direction," Qureshi said in presenting the secondary analysis of the trial that was halted for futility. Qureshi and colleagues were attempting to find out why the trial failed to produce evidence that intensively lowering blood pressure would benefit patients by reducing the size of expanding hematomas, and therefore producing less disability.
The deep dive into the data found some trends to benefits: fewer patients with intensive blood pressure control had more than a 33% increase in the size of the hematomas; more of the intensively treated patients had better control of larger hematomas; there appeared to be a numerical benefit in disability measures. But overall, Qureshi said, none of those secondary analyzes reached statistical significance.
He said there were at least two main explanations for the failure of the trial.
One, there were many very small hematomas which might have made showing a difference difficult. Overall, 450 patients were assigned to intensive blood pressure control and 426 patients were assigned to standard treatment. But just 221 of the intensively treated patients presented with hematomas of 10 cm or greater and 217 of the standard treated patients had these large hematomas. There was a trend to better control of these hematomas in the intensively treated patient group.
Two, Qureshi said that in practice most of the standard-treatment patients had blood pressure controlled at below 160 mm Hg, and they represented what could be considered a "pseudo crossover" patient. "Virtually all patients in this trial had blood pressures reduced to less than 160 mm Hg in both arms so once you get a person below 160 mm Hg, there isn't going to be much benefit to be gained. It is possible that any real benefit would have been achieved by keeping blood pressure below 160 mm Hg in any event," he said.
The original trial was proposed to enroll 1280 patients, but it was halted for futility after 100 patients were enrolled. Qureshi analyzed those patients for whom complete data were available. The mean systolic pressure at enrollment was 200.6 mm Hg. Their mean age was 61.9 years; 56.2% of the cohort were Asian. In the primary outcome 38.7% of the intensive-treatment patients died or were disabled compared with 37.7% of the standard-treatment patients. The rate of renal adverse events within 7 days after randomization was significantly higher in the intensive-treatment group than in the standard-treatment group (9.0% versus 4.0%, P=0.002).
The goal of treatment was to reduce and maintain the hourly minimum systolic blood pressure in the range of 140 to 179 mm Hg in the standard-treatment group and in the range of 110 to 139 mm Hg in the intensive-treatment group throughout the period of 24 hours after randomization. No effort was made to conceal the treatment assignment from the participants or treating physicians.
Qureshi noted, "We have a change that appears to be affecting our biomarker – expansion of the hematoma. And a biomarker that is linked to disability. So why didn't we get the result we wanted? It may be that we need to lower blood pressure further. We must need a bigger change in expansion to have an impact on outcomes."
There are no plans at the moment to continue this line of investigation, he said.
"We have learned from the ATACH studies that these are hard things to do," commented Natalia Rost, MD, director of the Acute Stroke Service at Massachusetts General Hospital, Boston. "Stroke is complicated and we keep missing the targets on both the cutoffs and on the use of markers. We use intermediate markers such as what we see on an image. But we don't have evidence that these markers are perfect. But I think we may be making some progress.
In the ATACH trial, Rost told MedPage Today, "I think there probably was a cutoff that wasn't tested – the 160 mm Hg, but there is a good indication that might be a good cutoff for effectiveness. I think this is one reason we keep missing the target – we aim either too high or too low. So 160 mm Hg sounds reasonable, but we do not have class 1 evidence.
"We usually try to lower the blood pressure in patients who present with hematomas and often we try to get blood pressure under 140 mm Hg, but I don't think doctors should get too flustered if the patients is around 160. If they are over 180 mm Hg I would be very worried and I would want to treat them to lower blood pressure," she said.
Qureshi disclosed no relevant relationships with industry.
Rost disclosed relevant relationships with Boston Biomedical Associates, Merck and Broadview Ventures.

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