Just when the hell will we get researchers to work with this to deliver tPA directly to the blood clot, with a much smaller and less dangerous bolus? I'm guessing never since no one in the stroke medical world has two functioning neurons that can put 2+ 2 together to come up with this solution.
http://www.rdmag.com/news/2016/11/tiny-super-magnets-could-be-future-drug-delivery?et_cid=5675688&
Microscopic crystals could soon be zipping drugs around your body,
taking them to diseased organs. In the past, this was thought to be
impossible - the crystals, which have special magnetic properties, were
so small that scientists could not control their movement. But now a
team of Chinese researchers has found the solution, and their discovery
has opened new applications that could use these crystals to improve -
and perhaps even save - many lives.
Kezheng Chen and Ji Ma from Quingdou University of Science and
Technology, Quingdou, China have published a method of producing
superparamagnetic crystals that are much larger than any that have been
made before. They recently published their findings in Physics Letters A.
If some magnetic materials, such as iron oxides, are small enough -
perhaps a few millionths of a millimeter across, smaller than most
viruses - they have an unusual property: their magnetization randomly
flips as the temperature changes.
By applying a magnetic field to these crystals, scientists can make
them almost as strongly magnetic as ordinary fridge magnets. It might
seem odd, but this is the strongest type of magnetism known. This
phenomenon is called superparamagnetism.
In theory, superparamagnetic particles could be ideal for drug
delivery, as they can be directed to a tumor simply by using a magnetic
field. Their tiny size, however, has made them difficult to guide
precisely - until now.
"The largest superparamagnetic materials that we have been able to
make before now were clusters of nanocrystals that were together about a
thousand times smaller than these," commented Dr. Chen. "These larger
crystals are easier to control using external magnetic fields, and they
will not aggregate when those fields are removed, which will make them
much more useful in practical applications, including drug delivery."
Chen and Ma explained that the high temperature and pressure under
which the crystals form made tiny meteorite-like 'micro-particles' of
magnetite escape from their surface. This caused the unusual pock-marked
appearance of the crystal surfaces and induced a high degree of stress
and strain into the lattice of the growing crystals.
Crystals that grow under such high stresses and strains form with
irregularities and defects in their crystal lattice, and it is these
irregularities that are responsible for the unusual magnetic properties
of Chen's crystals.
Magnetite crystals of a similar size that are grown at a lower
temperature and under normal pressure are only very weakly magnetic.
This method of making larger superparamagnetic crystals paves the way
for the development of superparamagnetic bulk materials that can be
reliably controlled by moderate external magnetic forces,
revolutionizing drug delivery to tumors and other sites in the body that
need to be targeted precisely.
And this is just the beginning. Chen's crystals might, for example,
be useful in the many engineering projects that need "smart fluids" that
change their properties when a magnetic field is applied. These can
already be used to make vehicle suspension systems that automatically
adjust as road conditions change, increasing comfort and safety, and to
build more comfortable and realistic prosthetic limbs.
Now that superparamagnetism is no longer restricted to minute
particles that are difficult to handle, researchers can start exploring
in which ways this can contribute to improving our lives.
Showing posts with label bolus. Show all posts
Showing posts with label bolus. Show all posts
Monday, November 14, 2016
Thursday, April 21, 2016
High Burden of Brain Microbleed May Up tPA Bleeding Risk
I would think the solution to this is reduce the size of the bolus substantially and direct the tPA directly to the clot. I could see no solution that was presented to fix this problem. Don't just tell me there is a problem, suggest a solution. What a waste of research dollars otrherwise.
The risk of symptomatic brain bleeds after treatment was found to be higher in patients with evidence of cerebral microbleeds compared with patients without cerebral microbleeds (risk ratio 2.36, 95% CI 1.21-4.61, P=0.01), reported Georgios Tsivgoulis, MD, of the University of Athens School of Medicine in Greece, and colleagues
Nine studies were included in the analysis, which showed high cerebral microbleed (CMB) burden, identified through MRI, to be a significant independent risk factor for symptomatic brain bleeds in stroke patients treated with tPA, they wrote in JAMA Neurology.
The findings suggest that pre-treatment MRI assessment of cerebral microbleed burden can serve as an independent predictor of brain bleeding risk in ischemic stroke patients receiving tPA, the authors wrote.
They added that the reliance on CT scans, and not MRI, for patient assessment in the stroke emergency care setting remains a significant challenge to identifying cerebral microbleed burden.
While cerebral microbleeds are considered an independent predictor of higher cerebral bleeding risk, earlier studies assessing their clinical impact on brain bleed risk in stroke patients treated with tPA have been mixed and many have not assessed the impact of cerebral microbleed burden, the researchers noted.
"The potential association of CMB presence with the risk of symptomatic intracerebral hemorrhage in patients with acute ischemic stroke treated with intravenous thrombolysis remains controversial," they wrote.
In an effort to better understand the impact of a high cerebral microbleed burden detected by MRI scan prior to tPA treatment on symptomatic intracerebral hemorrhage risk in the ischemic stroke setting, the researchers analyzed studies reporting intracerebral bleeding rates in ischemic stroke patients with known pre-tPA cerebral microbleed burden.
The meta-analysis, which included a total of 2,479 patients, confirmed a higher risk for symptomatic brain bleeds following treatment with tPA in patients with a cerebral microbleed burden of more than 10, compared with patients with zero to 10 cerebral microbleeds or one to 10 cerebral microbleeds on pretreatment MRI.
The authors also reported a higher risk for symptomatic intracerebral hemorrhage after tPA treatment was detected in patients with high cerebral microbleed burden (>10) when compared with patients with zero to 10 cerebral microbleeds (RR 12.10, 95% CI 4.36-33.57, P<0.001) or one to 10 cerebral microbleeds (RR 7.01, 95% CI 3.20-15.38, P<0.001) on pretreatment MRI.
In an individual-patient data meta-analysis, high cerebral microbleed burden was associated with increased likelihood of symptomatic brain bleeding before (unadjusted odds ratio 31.06, 95% CI 7.12-135.44, P<0.001) and after (adjusted OR 18.17, 95% CI 2.39-138.22, P=0.005) adjusting for potential confounders.
A study limitation was the lack of data on brain bleed risk by cerebral microbleed count stratification in four of the nine studies included in the meta-analysis and lack of information on key baseline characteristics in three of the nine studies. There was also incomplete information on antithrombotic medications taken before hospital admission for stroke treatment.
Despite these limitations, the researchers concluded that cerebral microbleed burden should be considered in the stroke, pre-tPA risk stratification setting.
"The challenge remains in identifying CMB burden without MRI in the setting of acute ischemic stroke management where only a noncontrast computed tomography is standard of care," they stated.
In an accompanying editorial, Mark Fisher, MD, of the University of California Irvine School of Medicine, noted that cerebral microbleeds have been shown to be present in more than 20% of older people, while they are rare in younger populations.
"Cerebral microbleeds have received enormous attention in the literature," he wrote. "Nevertheless, the nature of the underlying lesion of cerebral microbleeds has proved elusive."
Fisher noted that despite the meta-analysis findings, the critical factor relevant to tPA treatment "appears to be not the microbleeds themselves, but the arteriolar injury contributing to micro hemorrhage development."
"The principal challenge for the clinician addressing microbleeds in acute ischemic stroke will be to distinguish primary from secondary microbleeds," he wrote. "It is the disseminated processes of primary microbleeds that create the substrate of the brain vulnerable to arteriolar ischemic necrosis and development of intracerebral hemorrhage. The more restricted process or prior ischemic injury producing secondary microbleeds will be of far less concern in this context. Ultimately, the number of cerebral microbleeds present will be less important than the nature of the process driving microbleed development."
Magnetic nanoparticles could stop blood clot-caused strokes
High Burden of Brain Microbleed May Up tPA Bleeding Risk
Stroke patients with cerebral microbleeds had a twofold greater risk for intracerebral hemorrhage following intravenous thrombolysis (tPA), and bleeding risk increased by as much as 12-fold among patients with the highest (>10) microbleed burden, according to a meta-analysis.The risk of symptomatic brain bleeds after treatment was found to be higher in patients with evidence of cerebral microbleeds compared with patients without cerebral microbleeds (risk ratio 2.36, 95% CI 1.21-4.61, P=0.01), reported Georgios Tsivgoulis, MD, of the University of Athens School of Medicine in Greece, and colleagues
Nine studies were included in the analysis, which showed high cerebral microbleed (CMB) burden, identified through MRI, to be a significant independent risk factor for symptomatic brain bleeds in stroke patients treated with tPA, they wrote in JAMA Neurology.
The findings suggest that pre-treatment MRI assessment of cerebral microbleed burden can serve as an independent predictor of brain bleeding risk in ischemic stroke patients receiving tPA, the authors wrote.
They added that the reliance on CT scans, and not MRI, for patient assessment in the stroke emergency care setting remains a significant challenge to identifying cerebral microbleed burden.
While cerebral microbleeds are considered an independent predictor of higher cerebral bleeding risk, earlier studies assessing their clinical impact on brain bleed risk in stroke patients treated with tPA have been mixed and many have not assessed the impact of cerebral microbleed burden, the researchers noted.
"The potential association of CMB presence with the risk of symptomatic intracerebral hemorrhage in patients with acute ischemic stroke treated with intravenous thrombolysis remains controversial," they wrote.
In an effort to better understand the impact of a high cerebral microbleed burden detected by MRI scan prior to tPA treatment on symptomatic intracerebral hemorrhage risk in the ischemic stroke setting, the researchers analyzed studies reporting intracerebral bleeding rates in ischemic stroke patients with known pre-tPA cerebral microbleed burden.
The meta-analysis, which included a total of 2,479 patients, confirmed a higher risk for symptomatic brain bleeds following treatment with tPA in patients with a cerebral microbleed burden of more than 10, compared with patients with zero to 10 cerebral microbleeds or one to 10 cerebral microbleeds on pretreatment MRI.
The authors also reported a higher risk for symptomatic intracerebral hemorrhage after tPA treatment was detected in patients with high cerebral microbleed burden (>10) when compared with patients with zero to 10 cerebral microbleeds (RR 12.10, 95% CI 4.36-33.57, P<0.001) or one to 10 cerebral microbleeds (RR 7.01, 95% CI 3.20-15.38, P<0.001) on pretreatment MRI.
In an individual-patient data meta-analysis, high cerebral microbleed burden was associated with increased likelihood of symptomatic brain bleeding before (unadjusted odds ratio 31.06, 95% CI 7.12-135.44, P<0.001) and after (adjusted OR 18.17, 95% CI 2.39-138.22, P=0.005) adjusting for potential confounders.
A study limitation was the lack of data on brain bleed risk by cerebral microbleed count stratification in four of the nine studies included in the meta-analysis and lack of information on key baseline characteristics in three of the nine studies. There was also incomplete information on antithrombotic medications taken before hospital admission for stroke treatment.
Despite these limitations, the researchers concluded that cerebral microbleed burden should be considered in the stroke, pre-tPA risk stratification setting.
"The challenge remains in identifying CMB burden without MRI in the setting of acute ischemic stroke management where only a noncontrast computed tomography is standard of care," they stated.
In an accompanying editorial, Mark Fisher, MD, of the University of California Irvine School of Medicine, noted that cerebral microbleeds have been shown to be present in more than 20% of older people, while they are rare in younger populations.
"Cerebral microbleeds have received enormous attention in the literature," he wrote. "Nevertheless, the nature of the underlying lesion of cerebral microbleeds has proved elusive."
Fisher noted that despite the meta-analysis findings, the critical factor relevant to tPA treatment "appears to be not the microbleeds themselves, but the arteriolar injury contributing to micro hemorrhage development."
"The principal challenge for the clinician addressing microbleeds in acute ischemic stroke will be to distinguish primary from secondary microbleeds," he wrote. "It is the disseminated processes of primary microbleeds that create the substrate of the brain vulnerable to arteriolar ischemic necrosis and development of intracerebral hemorrhage. The more restricted process or prior ischemic injury producing secondary microbleeds will be of far less concern in this context. Ultimately, the number of cerebral microbleeds present will be less important than the nature of the process driving microbleed development."
Primary Source
JAMA Neurology
Source Reference: Tslvgoulis G, et al "Risk of symptomatic intracerebral hemorrhage after intravenous thrombolysis in patients with acute ischemic stroke and high cerebral microbleed burden: a meta-analysis" JAMA Neurol 2016; DOI: 10.1001/jamaneurol.2016.0292.Secondary Source
JAMA Neurology
Source Reference: Fisher M "Cerebral microbleeds and thrombolysis: Clinical consequences and mechanistic implications" JAMA Neurol 2016; DOI: 10.1001/jamaneurol.2016.0576.
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