Yet I can see no strategy to these trials. Absolutely nothing on the neuronal cascade of death. Don't expect anything better in the next 50 years until we actually get a stroke leader and strategy.
http://www.medscape.com/viewarticle/861294?src=sttwit
I am Christoph Diener, neurologist from the University of Essen,
Germany. I would like to summarize the most important studies that were
presented at the American Heart Association International Stroke
Conference in Los Angeles, California, in February 2016.
The Findaf study[1]
randomized patients who had ischemic stroke in two groups. One group
received extended ECG recording over 6 months and the other group had
prolonged Holter monitoring directly after the stroke and after 3 and 6
months, with the endpoint being the detection of atrial fibrillation
(AF). The detection rate with prolonged Holter monitoring was 13.5% vs
4.5% in the control group. This indicates that it is worthwhile to
monitor not only patients with cryptogenic stroke, but also patients
with other stroke mechanisms, because they can have large-vessel disease
and AF.
The ACT I study[2,3]
included 1453 patients with a high degree of asymptomatic stenosis of
the internal carotid artery. These patients were randomized to either
endarterectomy or stenting. No differences in complication rates or
long-term outcomes were reported, with event rates being extremely low.
The ARUBA study,[4]
reporting 5-year follow-up data, was a randomized trial in 226 patients
with arterial venous malformations (AVMs). These patients were
randomized to optimum medical therapy or interventional therapy
(neurosurgical removal of the vascular malformation with embolization or
radiation). Stroke or death occurred in 15 of 110 patients in the
medical group and in 41 of 116 patients in the interventional group. The
resulting number-needed-to-harm is 5, and this would indicate that in
many patients with AVM, a wait-and-see approach is justified. However,
there will be patients with high bleeding risk who will require therapy,
which should be discussed with neurosurgeons, neurologists, and
radiologists.
One of the positive trials was from the HERMES collaboration,[5,6]
a single case meta-analysis of five thrombectomy trials, which reported
that tPA plus thrombectomy is superior to tPA alone. The odds ratio for
a good outcome in these 1287 patients was a positive 2.49, whereas the
number-needed-to-treat was an incredible 2.6. The real challenge over
the next 5 years will be to implement thrombectomy in patients with
occlusions of the distal internal carotid artery and the proximal middle
cerebral artery on a countrywide level.
A few small trials in acute stroke were presented. One was ARTSS-2,[7]
which compared argatroban plus tPA vs tPA alone. Argatroban, a thrombin
inhibitor, showed no difference in major bleeding complications.
In the ICTuS-2 trial[8]
thrombolysis plus hypothermia was compared with thrombolysis alone in
120 patients. There was no difference reported in outcomes, but there
was an increased mortality with hypothermia. When we have thrombectomy
available, there is no justification for using thrombin antagonists or
hypothermia.
In the MultiStem® trial,[9] active group patients received 1.2 billion progenitor cells vs placebo. As expected, there was no difference in outcome.
The ACTION trial[10]
looked at natalizumab, a drug with anti-inflammatory properties used to
treat multiple sclerosis. No differences were reported in 129 stroke
patients.
More important, the CLEAR III trial[11]
studied patients with intraventricular hemorrhage. The local
application of tPA vs placebo was investigated in 500 patients. The
overall results showed no benefit, but patients who had a large
intraventricular hemorrhage showed improvement.
The INCH study[12]
looked at patients who had vitamin K antagonist–induced cerebral
bleeds, and compared prothrombin complex concentrate (PCC) with fresh
frozen plasma. The surrogate endpoint for this small study was the
normalization of the international normalized ratio (INR), which was
achieved in 77% of patients who received PCC vs 9% of those who received
fresh frozen plasma. This is a strong argument for initiating PCC
therapy in patients with anticoagulation-induced bleeding.
In
future, more patients will be switched over to non–vitamin K antagonist
novel oral anticoagulants (NOACs). We have one antidote already approved
(idarucizumab), and andexanet alfa (a reversal agent for the
anti-factor Xa agents) is expected to be approved shortly. If we want to
prevent intracerebral hemorrhage, it would be a good idea to treat
patients with AF with NOACs and not with vitamin K antagonists.
At
this year's conference, more neutral or negative trials were presented
than positive trials, but we need to continue research for the treatment
of acute stroke and stroke prevention.
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