Clinical Electrophysiology -> SCA Risk Assessment: -> Signal Processing Techniques (SAECG/TWA, HRV, QT interval) D-PO04 - Poster Session IV (ID 15) Poster

D-PO04-228 - Qt Interval Is Prolonged Post Cardiac Arrest Regardless Of Hypothermia Induction And Medications (ID 506)


Background: Prolongation of the QT interval is a common finding immediately following sudden cardiac arrest (SCA). Although considered to be multifactorial, the prolongation in QT may be exacerbated by hypothermia induction and exposure to antiarrhythmic medications.
Objective: We aimed to evaluate the temporal dynamics in the corrected QT interval (QTc) in the first 10 days following SCA with respect to the etiology, hypothermia induction and administration of QT prolonging medications.
Methods: We enrolled 73 consecutive adult survivors of SCA from any etiology in whom daily ECG was available for at least 3 days following SCA. We retrospectively followed their QTc (Bazett) and QRS intervals for the first 10 days of hospitalization. We stratified patients by 4 groups: (1) coronary artery disease (CAD) etiology (2) treatment with hypothermia protocol, (3) delivery of electrical cardioversion and (4) treatment with QTc prolonging medications. Genetic information obtained during hospitalization was analyzed.
Results: Median age of survivors was 43±13 years. Maximal QTc prolongation was observed in day 2 (QTc=503±60). Overall, there were no differences in daily QTc and QRS intervals between patients with or without hypothermia induction, nor between patients who received QTc prolonging medications or not. QTc interval was prolonged (>460 ms) in all subgroups. Patients with CAD etiology of SCA exhibited faster normalization of the QTc and had significantly shorter maximal QTc interval as compared to patients with non-CAD etiology (day 5 vs. day 7 and 484±61 vs. 515±58 ms, p=0.05), despite similar exposure to hypothermia (59% vs. 67%, p=0.32) and QT prolonging medications (70% vs. 74%, p=0.25). Even amongst patients with extremely long QTc greater than 600 ms on presentation, a QT prolonging mutation was not found and QTc prolongation was normalized by day 10.
Conclusion: QTc interval is significantly prolonged post SCA, regardless of known QT prolonging interventions. Normalization of the QTc post cardiac arrest should be expected only after day 6 of hospitalization, regardless of hypothermia induction, QTc prolonging medications or etiology of the arrest. Even in patients with extremely long QTc post SCA, the incidence of a QT prolonging mutation is low.