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47/Analysis of predictive factors for propafenone proarrhythmia. Does exercise ECG play a role during long term propafenone treatment?

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Published Online: Oct 4th 2008 European Journal of Arrhythmia & Electrophysiology. 2019;5(Suppl. 1):abstr47
Authors: PJ Kalmar (Presenting Author) – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; K Medves-Vaczi – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; K Hodosi – University of Debrecen, Department of Internal Medicine, Debrecen, Hungary A Bodi – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; GT Szabo – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; Clemens – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; Z Csanadi – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary; E Nagy-Balo – University of Debrecen, Department of Cardiology and Cardiovascular Surgery, Debrecen, Hungary
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Background: Propafenone proarrhythmia (PPA) is a rare but potentially life-threatening complication of propafenone therapy (PT). PPA is defined as significant QRS widening on resting ECG during PT or wide QRS tachycardia during follow up. Limited data exist assessing the potential predictors for PPA in structurally normal heart patients and the benefit of exercise ECG (EECG) is also questionable. Therefore, we aimed to investigate the predictors for PPA and to study the role of EECG.

Methods and results: A total of 142 patients (age: 66 ± 10 years, 44% male) with structurally normal heart treated with propafenone between January 2010 and September 2018 were enrolled in this study if they were on ongoing PT or PT was stopped because of PPA. Patients on ongoing PT (n=114) underwent an EECG and we considered it to be positive if an increase of baseline QRS duration was ≥40 msec (n=10; 8%). When comparing patients with positive and negative EECG the duration of PT (97.1 versus 40.2 months; p=0.001) and the incidence of baseline ECG alterations (4% versus 13%; p=0.05) were significantly different. During a mean follow-up of 46 ± 50 months 1 PPA (10%) occurred in patients with positive EECG, while no PPA occurred in the negative EECG group. The following parameters were analysed as potential predictive factors: age, sex, comorbidities, history of recovered tachycardiomyopathy (TCMP), duration of PT, dose of propafenone, dose of beta blocker, ejection fraction, left atrial diameter and baseline ECG alterations. On a multivariate analysis only history of TCMP was predictive for PPA (HR: 7.995 CI: 2.456–26.028; p=0.001). Besides, a longer duration of PT was predictive for a positive EECG (HR: 1.016 CI: 1.006–1.028; p=0.002).

Conclusions: Previous TCMP is an independent predictor of PPA in patients with apparently normal heart. The impact of EECG in prediction of PPA is controversial as the result of EECG may be changed during treatment and positive EECG occurred only in a minority of patients.

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