Abstracts

Rationale: Cardiac arrhythmias and respiratory disturbances have been proposed as likely causes for sudden unexpected death in epilepsy. Oxygen desaturation occurs in one-third of patients with localization-related epilepsy (LRE) undergoing inpatient video-EEG telemetry (VET) as part of their pre-surgical workup.Both abnormal lengthening and shortening of the corrected QT interval (QTc) on the electrocardiogram (EKG) have been reported with seizures. QTc abnormalities are associated with increased risk of sudden cardiac death. We hypothesized that there may be an association between ictal hypoxemia and cardiac repolarization abnormalities. Methods: VET data from patients with refractory LRE were analyzed. Consecutive patients having at least one seizure with accompanying oxygen desaturation below 90% and artifact free EKG data were selected. EKG during the one minute prior to seizure onset (PRE) and during the ictal/postictal period with accompanying oxygen desaturation below 90% (DESAT) was analyzed. Consecutive QT and RR intervals were measured. In the same patients, DESAT seizures were compared with seizures without accompanying oxygen desaturation below 90% (NODESAT).Results: 37 DESAT seizures were analyzed in 17 patients with localization-related epilepsy. A total of 2448 QT and RR intervals were analyzed during PRE. During DESAT, 1554 QT and RR intervals were analyzed. 12 of the 17 patients had at least one NODESAT seizure. A total of 19 NODESAT seizures were analyzed, including 1558 QT and RR intervals during PRE and 3408 QT and RR intervals during NODESAT. The odds ratio for an abnormally prolonged (>457 msec) QTcH (Hodges correction method) during DESAT relative to PRE was 10.64 (p<0.0001). The odds ratio for an abnormally shortened (<372 msec) QTcH during DESAT relative to PRE was 1.65 (p<0.0001). Seizure-related shortening and prolongation of QTc during DESAT were also observed when Fridericia correction of the QT was applied. During DESAT seizures, the mean range of QT values (QTr) (61.14 msec) was significantly different from that during PRE (44.43 msec) (p=0.01). There was a significant association between DESAT QTr and oxygen saturation nadir (p=0.025) and between DESAT QTr and duration of oxygen desaturation (p < 0.0001). Both QTcH prolongation and shortening also occurred with NODESAT seizures. A seizure-associated prolonged QTcH was more likely during DESAT than NODESAT with an odds-ratio of 4.30 (p<0.0001). A seizure-associated shortened QTcH was more likely during DESAT than NODESAT with an odds-ratio of 2.13 (p<0.0001).Conclusions: The likelihood of abnormal QTcH prolongation is increased 4.3-fold with seizures that are associated with oxygen desaturation compared with seizures that are not. The likelihood of abnormally shortened QTcH increases with seizures that are accompanied by oxygen desaturation with an odds-ratio of 2.13 compared with seizures without desaturations. There is a significant association between the depth and duration of oxygen desaturation and QTr increase. These findings may be related to the pathophysiology of SUDEP.