Intensive heart rhythm monitoring to decrease ischemic stroke and systemic embolism-the Find-AF 2 study-rationale and design.

BACKGROUND: Atrial fibrillation (AF) is one of the most frequent causes of stroke. Several randomized trials have shown that prolonged monitoring increases the detection of AF, but the effect on reducing recurrent cardioembolism, ie, ischemic stroke and systemic embolism, remains unknown. We aim to evaluate whether a risk-adapted, intensified heart rhythm monitoring with consequent guideline conform treatment, which implies initiation of oral anticoagulation (OAC), leads to a reduction of recurrent cardioembolism. METHODS: Find-AF 2 is a randomized, controlled, open-label parallel multicenter trial with blinded endpoint assessment. 5,200 patients ≥ 60 years of age with symptomatic ischemic stroke within the last 30 days and without known AF will be included at 52 study centers with a specialized stroke unit in Germany. Patients without AF in an additional 24-hour Holter ECG after the qualifying event will be randomized in a 1:1 fashion to either enhanced, prolonged and intensified ECG-monitoring (intervention arm) or standard of care monitoring (control arm). In the intervention arm, patients with a high risk of underlying AF will receive continuous rhythm monitoring using an implantable cardiac monitor (ICM) whereas those without high risk of underlying AF will receive repeated 7-day Holter ECGs. The duration of rhythm monitoring within the control arm is up to the discretion of the participating centers and is allowed for up to 7 days. Patients will be followed for at least 24 months. The primary efficacy endpoint is the time until recurrent ischemic stroke or systemic embolism occur. CONCLUSIONS: The Find-AF 2 trial aims to demonstrate that enhanced, prolonged and intensified rhythm monitoring results in a more effective prevention of recurrent ischemic stroke and systemic embolism compared to usual care.

Event-related potentials in different subtypes of multiple sclerosis--a cross-sectional study.

Impairment of cognitive skills is found in up to 65% of patients suffering from multiple sclerosis (MS). Little is known concerning the natural history or characteristics of progression of these cognitive dysfunctions. Furthermore, it has not been investigated to date whether there are differences in the course of cognitive impairment with respect to different diagnostic subgroups of MS. Event-related potentials (ERP) are an objective tool to evaluate cognitive processing. We performed a cross-sectional study on 179 consecutive patients suffering from MS (107 relapsing-remitting MS; 17 primary progressive MS; 50 secondary progressive MS; 5 undetermined). ERP were measured by a visual oddball paradigm, latencies of P3 components were correlated with demographic and clinical data. We found pathologically increased P3 latencies in 56% of all patients. Patients with secondary progressive MS showed significantly increased P3 latencies as compared to the other subgroups. There was a significant correlation between expanded disability status scale (EDSS) score and P3 latency (r=0.48; p<0.001). We conclude that ERP are an appropriate method to follow up cognitive dysfunction in MS and that cognitive dysfunction as measured by ERP is progressively impaired in the course of MS, in particular in the secondary progressive subtype.

Therapy of Sneddon syndrome.

We report the case of a young woman with progressive cognitive decline and epilepsy. She showed ischemic cerebrovascular disease and proximal livedo racemosa. Antiphospholipid antibody (aPL) could not be detected and there were no microemboli on continuous transcranial Doppler ultrasonography monitoring. Histology of cerebral vessels showed intimal hyperplasia in small leptomeningeal venous vessels and micronecrosis of grey and white matter. We subsequently made the diagnosis of aPL-negative Sneddon Syndrome (SNS). Anticoagulation with warfarin could not be initiated because of a drug-resistant epilepsy with the risk of falls and subsequent bleeding; immunosuppression with steroids and azathioprine was ineffective, as was initial antiplatelet therapy with clopidogrel alone. However, when we intensified antiplatelet therapy by combining clopidogrel and ASS, a slowing of disease progression, as assessed by neuropsychological testing and magnetic resonance imaging, was noted on a follow-up after 6 months. Therapeutic options in SNS in both aPL-positive and aPL-negative patients with SNS are discussed.