Abstract TP331: Right Insular Damage is Associated With New Onset Atrial Fibrillation in Patients With Acute Intracerebral Hemorrhage

Introduction: The frequency and risk factors for new-onset atrial fibrillation (nAF) after acute intracerebral hemorrhage (ICH) are uncertain. Hypothesis: By analogy with ischemic stroke, we hypothesized that insular cortex damage may be a risk factor for nAF. Methods: This is an observational study of consecutive patients with spontaneous ICH. All patients underwent continuous bedside cardiac monitoring for at least 24 hours. We excluded patients with previous history of AF, recent myocardial infarction and ischemic stroke. We prospectively collected the following variables: Demographic data (age and sex), traditional vascular risk factors, neurological severity (assessed with the Glasgow scale coma score), vital signs, laboratory and radiological data (localization and volume of the hematoma, concomitant intraventricular or subarachnoid hemorrhage), and detection of nAF. A blind evaluator using an interactive brain atlas assessed the insular cortex damage. Bivariate and multivariate regression analyses were performed to describe nAF risk factors. Results: We included 167 patients who fulfilled the inclusion/exclusion criteria. Mean age was 70.5±14.7 years and 56.8% were men. Cardiac monitoring was initiated after a median of 240 minutes (interquartile range 67-720) of the onset of ICH symptoms. We detected nAF in 9 patients (5.3%). Patients with nAF were older (75.6±13.1 vs 70.5±14.7 years, p=0.30) and most of them were men (8/9 vs 87/158, p=0.07) but these differences did not reach the statistical significance. We observed that right insular cortex damage (3/9 vs 9/158, p=0.019) and any insular cortex damage (5/9 vs 25/158, p=0.010) were more frequent in nAF patients. In the logistic regression analysis right insular cortex damage (OR 8.2; 95% CI 1.7-38.4, p=0.007) was associated with nAF. Conclusion: The frequency of nAF in patients with spontaneous ICH is 5.3%. Insular cortex lesions, probably due to the central autonomous nervous system dysregulation, are associated with nAF. This finding may have important implications in the hemodynamic and antithrombotic management.