American Heart Association

Author Interview: Alexandros Rentzos, MD, and Pia Löwhagen Hendén, MD, PhD

Alexandros Rentzos, MD, and Pia Löwhagen Hendén, MD, PhD

Alexandros Rentzos, MD, and Pia Löwhagen Hendén, MD, PhD

A conversation with Alexandros Rentzos, MD, Diagnostic and Interventional Neuroradiology, Sahlgrenska University Hospital, and Pia Löwhagen Hendén, MD, PhD, Anesthesiology and Intensive Care department, Sahlgrenska University Hospital, about the role of anesthesia and conscious sedation for patients undergoing embolectomy for stroke.

Interviewed by José G. Merino, MD, Associate Professor of Neurology, University of Maryland School of Medicine.

They will be discussing the paper, “General Anesthesia Versus Conscious Sedation for Endovascular Treatment of Acute Ischemic Stroke: The AnStroke Trial (Anesthesia During Stroke),” published in the June 2017 issue of Stroke.

Dr. Merino: Could you please summarize the key findings of your study and put them in context of what was known on the topic?

Drs. Rentzos and Löwhagen: Since a number of retrospective studies showed that general anesthesia during endovascular stroke treatment was associated with poor neurological outcome, conscious sedation became the main method in most neurointerventional centers after 2010. However, the retrospective studies were limited by important selection bias, such as inclusion of posterior strokes (in some of the series) and, importantly, more severe stroke in patients treated under GA. Furthermore, most retrospective studies on anesthesia technique did not describe the anesthesia technique, nor the anesthetic management!

At our institute, we have used mainly general anesthesia since 1991 when we started with endovascular stroke treatment, and, in our experience, patients treated with GA did not have worse neurological outcome. That is why we started the randomized trial AnStroke in 2013. The results were presented in ESOC 2017 in Prague on May 18. In our trial, general anesthesia did not lead to worse neurological outcome compared to conscious sedation.

Author Interview: Santosh Murthy, MD, MPH

Santosh Murthy

Santosh Murthy

A conversation with Santosh Murthy, MD, MPH, Assistant Professor of Neurology and Neuroscience, Weill Cornell Medicine, about the decision on when to restart anticoagulation after intracranial hemorrhage.

Interviewed by José G. Merino, MD, Associate Professor of Neurology, University of Maryland School of Medicine.

They will be discussing the paper “Restarting Anticoagulant Therapy After Intracranial Hemorrhage: A Systematic Review and Meta-Analysis,” published in the June 2017 issue of Stroke.

Dr. Merino: Can you please summarize the key findings of your study and place them in context of what was already known on the topic?

Dr. Murthy: There is a lack of standardized recommendations regarding the use of anticoagulant therapy after intracerebral hemorrhage (ICH). Our meta-analysis of observational studies suggests that compared with withholding anticoagulation, resumption of anticoagulant therapy after ICH significantly lowers the risk of ischemic stroke and myocardial infarction (MI) with no discernable elevation in the risk of ICH recurrence. While our results help summarize the existing literature and may serve as a guide to clinicians in making informed decisions, randomized clinical trials are needed to determine the true risk-benefit profile of anticoagulation resumption after ICH.

Calorie-free, But Perhaps Not Risk-free: Artificial Sweeteners and the Risk of Stroke and Dementia

Neal S. Parikh, MD
@NealSParikhMD

Pase MP, Himali JJ, Beiser AS, Aparicio HJ, Satizabal CL, Vasan RS, et al. Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia: A Prospective Cohort Study. Stroke.

In this entry, I discuss a recent publication by Matthew Pase and colleagues regarding the risks of stroke and dementia associated with the consumption of sugar-sweetened and artificially sweetened beverages.

Citing conflicting data, the authors sought to examine the association of sugar- or artificially sweetened soft drink intake with incident stroke and dementia in the Framingham Heart study.

Author Interview: Colin Derdeyn, MD

Colin Derdeyn

Colin Derdeyn

A conversation with Colin Derdeyn, MD, Chair and Departmental Executive Officer of the Department of Radiology, University of Iowa Carver College of Medicine, about the late complications of stenting for intracranial atherosclerotic disease and the challenges posed by new stroke treatments.

Interviewed by José G. Merino, MD, Associate Professor of Neurology, University of Maryland School of Medicine.

They will be discussing the paper, “Nonprocedural Symptomatic Infarction and In-Stent Restenosis After Intracranial Angioplasty and Stenting in the SAMMPRIS Trial (Stenting and Aggressive Medical Management for the Prevention of Recurrent Stroke in Intracranial Stenosis),” published in the June 2017 issue of Stroke.

Dr. Merino: Good afternoon. Can you tell us what prompted this secondary analysis of the SAMMPRIS data?
Dr. Derdeyn: From SAMMPRIS, we learned that there’s potentially great value for dual antiplatelets and statins, along with aggressive risk factor management for patients with intracranial atherosclerotic disease (ICAD).  We also learned that in this setting, there is a much higher complication rate from stenting than we thought, mainly due to a lot of perforator strokes, particularly in the basilar territory, and that the procedure is associated with a risk of intracranial hemorrhage, perhaps due to reperfusion. These short-term complications limit the value of stenting for ICAD.

Some Interesting Late-breaking Abstracts

European Stroke Organisation Conference (ESOC)
May 16–18, 2017

May 18, 2017
Should you restart anticoagulation after a cerebral haemorrhage? And other questions.

There are few things as devastating as a large ischaemic stroke in a patient who you had previously advised not to take anticoagulation.

As a stroke physician, I’ve been asked questions about whether I should give anticoagulation to a patient who has had an intracerebral haemorrhage (ICH). Many people who have had an ICH are at high risk of having an ischeamic stroke. At the late-breaking trials session of ESOC, there was some useful evidence that will help me sleep after these consults.

What Causes Lacunar Stroke, and How Should You Treat It?

European Stroke Organisation Conference (ESOC)
May 16–18, 2017

May 17, 2017
What if I told you that nearly 1/4 of ischaemic strokes weren’t caused by emboli at all? With the focus on retrieving clots with clever devices, and preventing them from forming with anticoagulants, it’s easy to forget that some ischeamic strokes have quite a different cause.  Lacunar strokes are caused by small vessel disease: an intrinsic disease of the small deep perforating arteries. Small vessel disease also causes vascular dementia, and is likely to  play a role in gait disturbance and falls.

At ESOC, there was an excellent session on SVD, which gave plenty of practical advice and food for thought.

Untangling Post-stroke Dementia

European Stroke Organisation Conference (ESOC)
May 16–18, 2017

May 16, 2017
It was refreshing to see a full hall at the ESOC session about the impact of stroke and cognition. In stroke research, it is easy to get distracted by exciting and dramatic things (such as thombectomy working for people who wake up with stroke) and forget some of the other things that are just as important to our patients. Fortunately, the relationship between stroke and cognitive impairment is now firmly on the research agenda.

We know that stroke increases the risk of dementia, but it’s difficult to say just HOW much. The existing data is quite confusing; if you look at patients who have had a large stroke, many will have cognitive impairment, but again many will be unable to take part in cognitive tests. The picture is quite different if we only look at patients with a mild stroke or TIA, as far fewer will have cognitive impairment. The problem is that many studies are only able to recruit patients with milder stroke. To make the problem worse, patients with severe stroke will not survive, so if you are not careful, it can seem that patients with milder stroke are more likely to have dementia at one year.

A Session for the Ages

European Stroke Organisation Conference (ESOC)
May 16–18, 2017

May 16, 2017
The 3rd European Stroke Organization Conference (ESOC) session titled “Official Welcome and Large Clinical Trials” kicked off what was to be a spectacular conference with one of the most impactful 90 minutes I have ever witnessed. The session in the Grand Hall of the Prague Conference Center was standing room only and, after a warm introduction, incorporated 8 presentations from large clinical trials each lasting 8 minutes. The conference itself drew over 4,200 participants, challenging the International Stroke Conference in impact and attendance. This is a remarkable achievement for a conference in its third year of existence.

Higher Admission Heart Rate Associated with Death and Poor Functional Outcome in ICH

Alexander E. Merkler, MD

Qiu M, Sato S, Zheng D, Wang X, Carcel C, Hirakawa Y, et al. Admission Heart Rate Predicts Poor Outcomes in Acute Intracerebral Hemorrhage: The Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial Studies. Stroke. 2016

Intracerebral hemorrhage is a devastating disease with a one-month mortality of 40%. Larger ICH volume, older age, and hematoma expansion are some of the factors associated with both poor functional outcome and death. Admission heart rate (HR) has previously been shown to predict higher mortality in coronary artery disease and ischemic stroke, but its impact on patients with ICH is unknown. 


In this study, Drs. Qiu et al perform a post-hoc analysis on data from the INTERACT trials to evaluate the effect of admission heart rate on outcome in ICH. Clinical outcomes included mortality and functional outcome (mRS) at 90 days. Imaging outcome was hematoma growth on 24 hour CT. HR was divided into quartiles (<65, 65-74, 75-84, ≥85) and Cox logistic regression was used to account for possible confounders in the relationship between admission HR and the outcomes of interest.

Of 3185 patients with ICH, patients with higher admission HR had higher BP, more frequent intraventricular extension of hematoma, and were less likely enrolled in China; patients with lower admission HR were more likely older, more often were taking a beta-blocker or antithrombotic, and had larger hematomas that were less likely to be in a lobar location.  Overall, higher admission HR was associated with higher mortality (adjusted hazard ratio for HR ≥85 vs. <65: 1.5; CI, 1.07-2.11). In addition, higher admission HR was associated with worse functional outcome at 90 days (adjusted odds ratio 1.33; CI 1.08-1.63). There was no significant association between admission HR and hematoma expansion on 24 hour CT.

Similar to coronary artery disease and ischemic stroke, admission HR appears to be associated with increased mortality and poor functional outcomes in patients with ICH. As the authors suggest, perhaps higher admission HR is a marker of poor general health, dehydration, anemia, or a marker of cardiac disease, all of which are predictors of poor outcome after stroke. One major limitation is the lack of adjustment for heart rate variability, which has also been shown to be associated with poor outcomes after stroke.  

In conclusion, admission HR is associated with increased mortality and poor functional outcome in patients with ICH. 

Elevated Blood Pressure Significantly Associated with Risk of Vascular Dementia

Danny R. Rose, Jr., MD


Vascular dementia is the second most common cause of dementia, but many aspects of the disease are poorly understood. In particular, there is conflicting evidence regarding the relationship between blood pressure and vascular dementia. Elevated blood pressure in midlife has been found to have a positive association with future development of dementia, but several other studies have found low blood pressure in old age to be associated with an increased risk of dementia. One possible explanation of these findings is that it represents “reverse causality,” meaning vascular dementia is responsible for low blood pressure by decreasing sympathetic drive. Blood pressure medication may also play a confounding role in this association. Emdin et al. sought to further clarify this association by conducting an analysis of 4.28 million individuals without vascular disease or dementia, supplemented with an analysis of a prospective population-based cohort of patients with TIA and stroke.

The study included patients from age 30 to 90 and excluded patients with pre-existing cardiovascular disease to minimize the potential of reverse causality related to advanced age and cardiovascular disease causing reduced blood pressure, respectively. The endpoint of the primary analysis was an inclusive definition of vascular dementia based on ICD 10 coding and was inclusive of patients with co-existing Alzheimer’s disease. Secondary analysis excluded these patients and excluded patients treated with medications commonly used to treat AD. The first four years of follow-up were excluded in the primary analysis to mitigate the effect of patients with undiagnosed dementia. Cox models, stratified by practice, were used to determine hazard ratios for the association for clustering of patients by practice. The primary analysis was adjusted for age, sex, body mass index and smoking status. The Oxford Vascular Study cohort was used to confirm findings independently.

Out of a cohort of 4.28 million individuals free of vascular disease and dementia, 14,934 cases were reported to have vascular dementia. After excluding for presentations during the first four years of follow-up, 11,114 cases were included. The association between usual SBP and risk of vascular dementia followed a linear progression within the age groups of 30-50 and 51-70. The age group of 71-90 did not show a significant association. The strength of association decreased with increasing age category. Overall for individuals aged 70 years or less at baseline, 20 mm Hg higher usual SBP was associated with a 26% higher risk of vascular dementia (HR 1.26 CI 1.17, 1.34). Significant negative associations with systolic and diastolic blood pressures were observed for the age group 71-90, but after excluding for the first eight years of follow-up, no significant association was observed. Adjusting for patients in the primary care cohort that had TIA and stroke events reduced the HR to 1.18, indicating that 30% of the excess risk of vascular dementia per 20mm Hg higher SBP is mediated through risk of future stroke and TIA. The OXVASC cohort did not show a relationship between the most recent SBP or DBP in patients relative to their diagnosis of new dementia, but did show significant positive associations with DBP and SBP in 5-9 years prior to the TIA/stroke and particularly 10-20 years prior.

This study supports prior positive associations between blood pressure in mid-life and vascular dementia and also suggests that elevated blood pressure attributes a significant risk for the development of vascular dementia at least until the age of 70. The authors’ rationale for excluding confounders in the cohort appears to be sound and had the intended effect of strengthening the associations studied. The study refutes previous reports of a negative association with blood pressure and vascular dementia in the elderly, likely in part due to the aforementioned adjustments, strengthening the authors’ hypothesis of reverse causality. This study represents by far the largest analysis of the association between blood pressure and risk of vascular dementia and although it is susceptible to limitations related to the diagnosis of dementia in a primary care setting, it represents a significant advancement in our understanding of the complex pathophysiology of vascular dementia.