Dynamic electrophysiological mechanism in patients with long-standing persistent atrial fibrillation.

Background: Improved understanding of the mechanisms that sustain persistent and long-standing persistent atrial fibrillation (LSpAF) is essential for providing better ablation solutions. The findings of traditional catheter-based electrophysiological studies can be impacted by the sedation required for these procedures. This is not required in non-invasive body-surface mapping (ECGI). ECGI allows for multiple mappings in the same patient at different times. This would expose potential electrophysiological changes over time, such as the location and stability of extra-pulmonary vein drivers and activation patterns in sustained AF. Materials and methods: In this electrophysiological study, 10 open-heart surgery candidates with LSpAF, without previous ablation procedures (6 male, median age 73 years), were mapped on two occasions with a median interval of 11 days (IQR: 8-19) between mappings. Bi-atrial epicardial activation sequences were acquired using ECGI (CardioInsight™, Minneapolis, MN, United States). Results: Bi-atrial electrophysiological abnormalities were documented in all 20 mappings. Interestingly, the anatomic location of focal and rotor activities changed between the mappings in all patients [100% showed changes, 95%CI (69.2-100%), p < 0.001]. Neither AF driver type nor their number varied significantly between the mappings in any patient (median total number of focal activities 8 (IQR: 1-16) versus 6 (IQR: 2-12), p = 0.68; median total number of rotor activities 48 (IQR: 44-67) versus 55 (IQR: 44-61), p = 0.30). However, individual zones showed a high number of quantitative changes (increase/decrease) of driver activity. Most changes of focal activity were found in the left atrial appendage, the region of the left lower pulmonary vein and the right atrial appendage. Most changes in rotor activity were found also at the left lower pulmonary vein region, the upper half of the right atrium and the right atrial appendage. Conclusion: This clinical study documented that driver location and activation patterns in patients with LSpAF changes constantly. Furthermore, bi-atrial pathophysiology was demonstrated, which underscores the importance of treating both atria in LSpAF and the significant role that arrhythmogenic drivers outside the pulmonary veins seem to have in maintaining this complex arrhythmia.

Endogenous arterial blood pressure increase after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Spontaneous blood pressure rise is a frequently observed phenomenon following aneurysmal subarachnoid hemorrhage (SAH). Facing the risk of aneurysmal rebleeding and the occurrence of delayed cerebral ischemia it is unclear how to react to these endogenous-driven blood pressure changes, as their predictive value for clinical course and functional outcome is still unknown. PATIENTS AND METHODS: Endogenous blood pressure characteristics within 21 days after SAH were retrospectively analyzed in 93 patients. Any use of vasopressors for active induction of hypertension marked the end of data collection. Mean arterial blood pressure (MAP) was related to the onset of cerebral vasospasm and patient characteristics (Hunt&Hess, age, pre-existing hypertension, antihypertensive therapy, sedation). Predictors for cerebral infarction and functional outcome were calculated using a logistic regression model. RESULTS: A significant MAP increase was observed in all patients from day 3 to day 7. Patients developing cerebral vasospasm had an overall steeper increase of MAP during this period (11.1 ± 11.4 mmHg vs. 6.5 ± 8.9 mmHg, p = 0.04). MAP rise started already 3 days before detection of vasospasm. Lower MAP values were recorded in patients with poor Hunt&Hess grade, under sedation and thus in patients with poor outcome. MAP had no impact on the development of cerebral infarction. In univariate analysis MAP on day 5 (OR 0.95, 95 %-CI: 0.89-0.99), MAP on day 6 (OR 0.95, 95 %-CI: 0.91-1.00), Hunt&Hess grade (OR 1.72, 95 %-CI: 1.14-2.60), sedation (OR 17.04, 95 %-CI: 2.08-139.51) and stroke (OR 5.82, 95 %-CI: 1.63-20.82) were predictors for poor outcome. In multivariable analysis, only sedation (OR 13.72, 95 %-CI: 1.62-115.94) and ischemic stroke (OR 4.48, 95 %-CI: 1.16-17.31) remained significant. CONCLUSION: Spontaneous MAP increase occured in all patients following SAH. It was highly influenced by clinical parameters, thereby limiting its prognostic value for functional outcome. However, a steep increase of MAP might be an early clinical marker to identify patients at risk for developing cerebral vasospasm.