By Dr Rajiv Advani

Diagnosis / Investigation of Stroke Etiology and Pathophysiology

Chairs: Mirjam Rachel Heldner and Amit Kishore

Heart rate turbulence in acute ischemic stroke: an analysis of Holter ECG data from the HEBRAS study – Helena Stengl

Heart rate turbulence (HRT) as a marker of stroke aetiology. HRT, a turbulence in rhythm, with its compensatory acceleration and deceleration on ECG have been seen in heart failure and severe arrhythmia. Investigating it’s potential implications in stroke aetiology was the goal of the HEBRAS study. Echocardiography, HOLTER, cardiac MRI to detect myocardial fibrosis in addition to ECG was performed. Using this the patients were stratified into low, medium or high-risk groups, category 0, 1 and 2. The 3 categories were aimed at identifying risk with endpoints such as predictor of AF and clinical outcome (mRS). Higher stratification scores, especially category 2, was associated with worse clinical outcome. HRT can potentially be used as a marker to identify patients in need of further cardiac follow up as well as potentially identifying those at risk of poor prognosis.

Cardiac Findings Following Acute Ischemic Stroke Are Different in Men and Women – Anton Schmick

The Brain Heart axis. It is well known that the heart can led to strokes especially due to AF, but can the brain effect the heart. A retrospective cohort study, with its potential selection biases, was performed and aimed at trying to answer this question. Did patients post stroke patients (acute non cardioembolic) develop cardiac abnormalities in a cohort of previously cardiac-healthy patients. Patients screened with ECG, Echocardiography, coronary MRI SPECT in a follow-up lasting one year post stroke. The cardiac comorbidities were significantly more common in males, AV blocks, polymorphic VES, SVT, left ventricular hypokinesia amongst others. Polymorphic VES and SVT can indicate serious underlying cardiac pathology – risk of sudden cardiac death. However no such correlations were seen in the female cohort.

Long term outcome of acute stroke patients undergoing cardiac CT as part of the initial stroke imaging protocol – Leon Rinkel

Acute cardiac CT has a higher yield in terms of detection of cardioembolic source of stroke. What are the long-term implications of this acute cardiac CT? A prospective study including a 2 year follow up was performed in the Netherlands. High risk sources of embolism were identified and included cardiac thrombi, endocarditis, myxoma, aortic dissection amongst others. Long term outcomes were MACE, mortality, mRS and recurrent ischemic stroke. This cohort was not adjusted for stroke severity/LVO. 450 patients were included, with 55 of them having a high-risk source of embolism. Those with a high-risk source of embolism had ssignificantly worse prognosis at 2 years with worse functional outcomes (mRS). Even when this  was adjusted for stroke severity the same poor prognosis was seen. In the group with only cardiac thrombi the same trend was seen.

The Contribution of Competing Mechanisms in Stroke Despite Anticoagulation in Patients with Atrial Fibrillation– Rahul Herlekar

The contribution of competing mechanisms in the presence of atrial fibrillation in patients with a new stroke who are already anticoagulated. 33% of strokes in this cohort occur in patients on anticoagulant therapy. The cohort was dichotomised into OAC naive vs OAC treated patients. Investigations were performed to determine small vessel disease, large vessel atherosclerosis, other cardioembolic source as a competing stroke mechanism. Finding of a high-risk competing mechanism based on the TOAST classification. 600 patients, OAC treated patients were older, with more history of stroke. Almost 20% of these had large vessel disease and 9% had small vessel disease. Twice the incidence as compared to the OAC naive group. The latter finding (small vessel disease) was non-significant but showed a strong trend. New prevention strategies are needed in these patients in terms of total antithrombotic therapy and duration of such therapies.

PFO Closure to avert recurrent stroke: The PASCAL stratification system distinguishes patient groups with net benefit and net harm – Jeffrey Saver

PFO causes 40% of strokes in young adults. PFO closure decreases risk of stroke but increases the risk of AF. PASCAL score was applied to evaluate PFO as the probable, possible or unlikely source of stroke aetiology. Harm was defined as > 45 day AF occurrence in addition to recurrent stroke and other outcomes. This was a metanalysis of 6 RCTs where almost 2000 patients who underwent closure were identified. The group where PFO was identified as the probable cause had a significant risk reduction in terms of recurrent stroke post closure, but the group with unlikely stratification showed harm, with more incidence of recurrent stroke. In the unlikely cause of stroke group, 5 more strokes were caused and 36 more patients had a late onset AF per 1000 patients. Closure for patients in probable and possible etiological source groups had benefit of closure but harm was seen in the unlikely group.

Microthrombi formed following ischemic stroke open the blood brain barrier – Igor Khalin

Microthrombi lead to the damage of the blood brain barrier and this leads to the accumulation of nanoparticles in the brain tissue. This has been seen on electron microscopy in animals. The microthrombi persist after stroke and are still persistent after recanalization. This has implications for clinical course after an acute occlusion and mediates increased infarct volume and SAH. The microthrombi are very varying in composition and can contain leukocyte, fibrin, hemosiderin, etc. Pharmacological and clinical implications of this are interesting future perspectives.


Assessing the Sensitivity of the Boston Criteria Version 2.0 in Dutch-type Hereditary Cerebral Amyloid Angiopathy – Reinier van der Zwet

Validation of the Boston 2.0 criteria in hereditary CAA. Dutch hereditary type CAA occurs due to a specific APP gene mutation; a population with a definitive diagnosis. 3T MRI was used to look for the MRI criteria in the Boston criteria version 2.0. 64 patients were included and split into symptomatic and pre symptomatic groups. The sensitivity of Boston 1.5 vs 2.0 was the same in both pre symptomatic and symptomatic groups for Dutch type CAA; around 31%. However, using possible and probable CAA based on Boston criteria 2.0 the sensitivity increased from 31% to 74% in Dutch hereditary type CAA. These finding reaffirm the findings of the original study.