Detection of Atrial Fibrillation on Stroke Units: Comparison of Manual versus Automatic Analysis of Continuous Telemetry.

BACKGROUND: Detection of atrial fibrillation (AF) is one of the primary diagnostic goals for patients on a stroke unit. Physician-based manual analysis of continuous ECG monitoring is regarded as the gold standard for AF detection but requires considerable resources. Recently, automated computer-based analysis of RR intervals was established to simplify AF detection. The present prospective study analyzes both methods head to head regarding AF detection specificity, sensitivity, and overall effectiveness. METHODS: Consecutive stroke patients without history of AF or proof of AF in the admission ECG were enrolled over the period of 7 months. All patients received continuous ECG telemetry during the complete stay on the stroke unit. All ECGs underwent automated analysis by a commercially available program. Blinded to these results, all ECG tracings were also assessed manually. Sensitivity, specificity, time consumption, costs per day, and cost-effectiveness were compared. RESULTS: 216 consecutive patients were enrolled (70.7 ± 14.1 years, 56% male) and 555 analysis days compared. AF was detected by manual ECG analysis on 37 days (6.7%) and automatically on 57 days (10.3%). Specificity of the automated algorithm was 94.6% and sensitivity 78.4% (28 [5.0%] false positive and 8 [1.4%] false negative). Patients with AF were older and had more often arterial hypertension, higher NIHSS at admission, more often left atrial dilatation, and a higher CHA2DS2-VASc score. Automation significantly reduced human resources but was more expensive compared to manual analysis alone. CONCLUSION: Automatic AF detection is highly specific, but sensitivity is relatively low. Results of this study suggest that automated computer-based AF detection should be rather complementary to manual ECG analysis than replacing it.

Cervical Artery Dissection Caused by Electrical Cupping Therapy with High-Negative Pressure - Case Report.

BACKGROUND: Cervical artery dissection is an important cause of stroke in the young. The etiology is still discussed controversial. The most obvious reason for a dissection of extracranial arteries is due to a trauma, eg. after car accidents or other high speed traumas such as high-velocity road traffic accidents. Besides these clear cases, chiropractic neck maneuvers represent potential reasons for vessel injuries. CASE PRESENTATION: We here report a rare case of secondary cervical artery dissection after so-called cupping therapy and a preventive treatment with a direct oral anticoagulant. CONCLUSIONS: Therapists using this technique should be aware of the potentially devastating side effects. The diagnosis of ICA dissection should be considered with any new onset of unknown neck pain or headache, specifically in combination with neurological deficits.

Discontinuous versus Continuous Weaning in Stroke Patients.

BACKGROUND: An increasing number of stroke patients have to be supported by mechanical ventilation in intensive care units (ICU), with a relevant proportion of them requiring gradual withdrawal from a respirator. To date, weaning studies have focused merely on mixed patient groups, COPD patients or patients after cardiac surgery. Therefore, the best weaning strategy for stroke patients remains to be determined. METHODS: Here, we designed a prospective randomized controlled study comparing adaptive support ventilation (ASV), a continuous weaning strategy, with biphasic positive airway pressure (BIPAP) in combination with spontaneous breathing trials, a discontinuous technique, in the treatment of stroke patients. The primary endpoint was the duration of the weaning process. RESULTS: Only the 40 (out of 54) patients failing in an initial spontaneous breathing trial (T-piece test) were included into the study; the failure proportion is considerably larger compared to previous studies. Eligible patients were pseudo-randomly assigned to one of the two weaning groups. Both groups did not differ regarding age, gender, and severity of stroke. The results showed that the median weaning duration was 10.7 days (±SD 7.0) in the discontinuous weaning group, and 8 days (±SD 4.5) in the continuous weaning group (p < 0.05). CONCLUSIONS: To the best of our knowledge, this is the first clinical study to show that continuous weaning is significantly more effective compared to discontinuous weaning in mechanically ventilated stroke patients. We suppose that the reason for the superiority of continuous weaning using ASV as well as the bad performance of our patients in the 2 h T-piece test is caused by the patients' compliance. Compared to patients on surgical and medical ICUs, neurological patients more often suffer from reduced vigilance, lack of adverse-effects reflexes, dysphagia, and cerebral dysfunction. Therefore, stroke patients may profit from a more gradual withdrawal of weaning.

Atrial fibrillation in stroke-free patients is associated with memory impairment and hippocampal atrophy.

AIMS: To determine whether atrial fibrillation (AF) in stroke-free patients is associated with impaired cognition and structural abnormalities of the brain. AF contributes to stroke and secondary cognitive decline. In the absence of manifest stroke, AF can activate coagulation and cause cerebral microembolism which could damage the brain. METHODS AND RESULTS: We cross-sectionally evaluated 122 stroke-free individuals with AF recruited locally within the German Competence Network on AF. As comparator, we recruited 563 individuals aged 37-84 years without AF from the same community. Subjects underwent 3 T magnetic resonance imaging to assess covert territorial brain infarction, white matter lesions, and brain volume measures. Subjects with evidence for stroke, dementia, or depression were excluded. Cognitive function was assessed by an extensive neuropsychological test battery covering the domains learning and memory, attention and executive functions, working memory, and visuospatial skills. Cognitive scores and radiographic measures were compared across individuals with and without AF by stepwise multiple regression models. Stroke-free individuals with AF performed significantly worse in tasks of learning and memory (ß = -0.115, P < 0.01) as well as attention and executive functions (ß = -0.105, P < 0.01) compared with subjects without AF. There was also a trend (P = 0.062) towards worse performance in learning and memory tasks in patients with chronic as compared with paroxysmal AF. Corresponding to the memory impairment, hippocampal volume was reduced in patients with AF. Other radiographic measures did not differ between groups. CONCLUSION: Even in the absence of manifest stroke, AF is a risk factor for cognitive impairment and hippocampal atrophy. Therefore, cognition and measures of structural brain integrity should be considered in the evaluation of novel treatments for AF.

Antithrombin III inhibits nuclear factor kappaB activation in human monocytes and vascular endothelial cells.

The serpin antithrombin III (AT III), the most important natural inhibitor of thrombin activity, has been shown to exert marked anti-inflammatory properties and proven to be efficacious in experimental models of sepsis, septic shock, and disseminated intravascular coagulation. Moreover, clinical observations suggest a possible therapeutic role for AT III in septic disorders. The molecular mechanism, however, by which AT III attenuates inflammatory events is not yet entirely understood. We show here that AT III potently blocks the activation of nuclear factor kappaB (NF-kappaB), a transcription factor involved in immediate early gene activation during inflammation. AT III inhibited agonist-induced DNA binding of NF-kappaB in cultured human monocytes and endothelial cells in a dose-dependent manner, suggesting that AT III interferes with signal transduction leading to NF-kappaB activation. This idea was supported by demonstrating that AT III prevents the phosphorylation and proteolytic degradation of the inhibitor protein IkappaBalpha. In parallel to reducing NF-kappaB activity, AT III inhibited the expression of interleukin-6, tumor necrosis factor-alpha, and tissue factor, genes known to be under the control of NF-kappaB. The observation that chemically modified AT III that lacks heparin-binding capacity had no effect on NF-kappaB activation supports the current understanding that the inhibitory potency of AT III depends on the interaction of AT III with heparinlike cell surface glycosaminoglycans. This hypothesis was underscored by the finding that the AT III beta-isoform, known to have higher affinity for glycosaminoglycans, is more effective in preventing NF-kappaB transactivation than alpha-AT III. These data indicate that AT III can alter inflammatory processes via inhibition of NF-kappaB activation.