Conference

International Stroke Conference
January 24–26

Philip Chang, MD

This year’s International Stroke Conference revealed big advances and changes to the acute ischemic stroke guidelines. I had a great time at the Los Angeles Convention Center and learned a lot, as new exciting trials revolutionized the acute ischemic stroke treatment landscape, most notably tripling the reperfusion time windows. As with every conference, there were tons of different lectures and abstracts to go to, but I’ll highlight what I found the most interesting, and key take-home points from the conference.

International Stroke Conference
January 24–26

Danny R. Rose, Jr., MD

New advances in our understanding of intracerebral hemorrhage in recent years have led to new questions, as well as revisiting previously held notions about treatment and prevention.  The talks in this session covered coagulopathy reversal, anticoagulant usage in patients with a history of ICH, the relationship between statins and ICH and anti-edema therapy.

Dr. Thorsten Steiner, MD, PhD, began the session by discussing drug-induced coagulopathy reversal in ICH. The primary purpose of such therapies is to prevent hematoma expansion, which occurs in 30% of cases in the first 4 hours after ICH and is associated with increased morbidity and mortality. Anticoagulants increase this rate to upwards of 54% for vitamin K antagonists (VKAs) and 38% with direct-acting oral anticoagulants (DOACs). Timing is an important thing to consider in this scenario, given the half-life of VKAs are around 2 days, while DOACs are all around 14 hours, with peak effect somewhere between 3–4 hours. Specifically, many patients on DOACs may present in a time window when reversal would have little to no effect given the lack of active drug at the time. It is important to consider things that may cause variations in half-life for DOACs, including body size, inhibiting/inducing medications, and renal function (most important for dabigatran).

International Stroke Conference
January 24–26

Richa Sharma, MD, MPH

This was a very interesting presentation about a stroke etiology that we need to study further, namely symptomatic carotid plaque not resulting in severe stenosis. Currently, there is no compelling evidence for intervention more than medical management. However, the presenter, Vijay Sharma, argued that there are certain characteristics that make a plaque at risk for embolizing even if it does not meet NASCET criteria for severe stenosis. The researchers embarked on identifying imaging characteristics that are associated with a higher risk of embolization of these plaques. They utilized FDG-PET/CT and high-resolution, fat-suppressed MRI as modalities to help different plaque risk. A prospective study included patients with carotid plaque resulting in 50 to 70% stenosis, which was ipsilateral to a recent infarct which occurred within 30 days. These patients underwent FDG-PET to identify any regions of inflammation in the plaque since this may be an initiating event for plaque rupture. They also underwent MRI with high-resolution of the carotid, which yielded a ratio of the T1 hyperintensity of the plaque to the intensity of the ipsilateral sternocleidomastoid. The MRI presumably detects the lipid-rich necrotic core of the plaque and intraplaque hematoma. The endpoint of the study was whether the patients developed a recurrent stroke within a 90-day follow-up period. Interestingly, 11% of these patients suffered from a recurrent ischemic stroke (N=11), and these patients on average had higher T1 carotid-sternocleidomastoid ratios (p<0.0001) and higher SUV values by PET in the carotid plaque (p<0.0001). In multivariable modeling, a higher T1 carotid-sternocleidomastoid ratio and higher SUV values independently predicted recurrent ischemic stroke.

International Stroke Conference
January 24–26

Alexis N. Simpkins, MD, PhD

Session: Closing Main Event.
Date: Friday, January 26, 2018

Speaker: Patrick D. Lyden, MD, FAAN, FAHA, FANA, Carmen and Louis Warschaw Chair in Neurology, Cedars-Sinai Medical Center

At the closing remarks session, Dr. Patrick D. Lyden presented the first clinical trial use of a neuroprotectant post the new era of the embolectomy trials. The NeuroNEXT NN104 (RHAPSODY) Study was a phase II multi-center, double-blinded clinical trial in which a 3K3A-activated protein C (APC) was tested for safety. A secondary outcome measure included assessment of hemorrhagic transformation. The 3K3A-APC is both neuroprotective and vascular protective with preclinical evidence that suggests that it improves neurologic outcome and reduces risk of hemorrhagic transformation. In this study, patients received intravenous tPA and/or endovascular therapy, followed by 3K3A-APC within 2 hours of the acute intervention divided into 5 doses. Of the 110 patients enrolled, 45% of the patients received thrombolysis and endovascular therapy, and 54% were given tPA alone. There were 5 doses that were tested in the clinical trial using the continuous reassessment method, and the maximum dose was well tolerated. Hemorrhagic transformation was assessed on MRI 30 days post treatment.

International Stroke Conference
January 24–26

Alexis N. Simpkins, MD, PhD

Session: Acute Neuroimaging Oral Abstracts II.
Date: Thursday, January 25, 2018

Speaker: Steven Warach, MD, PhD, University of Texas Dell Medical School, University of Texas

Now that the time window for endovascular interventions in acute stroke patients has been extended up to 24 hours, it is important to evaluate the proportion of patients that would potentially be eligible during this window in the general population and determine factors that may predict whether a patient will have an acceptable imaging profile. Dr. Steven Warach presented data analyzed from the LESION database that provided some interesting findings on both fronts. After the presentation, I was able to ask Dr. Warach some follow-up questions about his findings.