Amongst other anti arrhythmic medications disopyramide class

Amongst other anti-arrhythmic medications, disopyramide (class 1A AAM) has anticholinergic side effects such as dry mouth, urinary hesitancy, constipation and exacerbation of conditions like glaucoma and myasthenia gravis. Disopyramide acts by targeting the fast sodium mglur in the cardiac tissue. However, it also blocks potassium channels in pancreatic cells, which increases insulin secretion, leading to episodes of hypoglycemia, resulting in coma and neurological damage. This side effect is seen at normal therapeutic levels [34], therefore it should be avoided in patients taking potassium (ATP) channel inhibitor such as glimepiride [35]. Procainamide was widely used in the past; however, its use has been limited as its chronic administration leads to frequent side effects manifested mainly by lupus like syndrome in around 30% of patients [36]. On the other hand, bone marrow toxicity is a serious but less frequent side effect, manifested in less than 0.22% of the patients. It should be considered in any patient who develops pancytopenia once procainamide treatment is stopped [37]. Mexelitine is a well-tolerated class 1B antiarrhythmic drug. Its side effects are limited to gastrointestinal (GI) and neurological manifestation such as dizziness and numbness [38]. However more serious effects like thrombocytopenia are rare, and are based on case reports [39]. Propafenone is a Class 1C antiarrhythmic drug. It has been reported to be associated with suppressive sympathetic effects such as dizziness, nausea, visual disturbances [40]. A negative inotropic effect of propafenone significantly increases pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, and cardiac output especially in patients with low ejection fraction, leading to increase in non-cardiac mortality and morbidity [41]. Although GI side effects such as nausea and metallic taste are frequent and mild, propafenone has been implicated in acute cholestatic hepatitis as described in a case report [42].
Conclusion
Conflict of interest
Introduction Catheter ablation is an effective therapy for atrial fibrillation (AF). Pulmonary vein isolation (PVI) has become an accepted treatment for AF [1]. Atrial substrate modification is considered necessary in patients with non-paroxysmal AF (NPAF) rather than paroxysmal AF (PAF) [2,3]. The endpoint of the ablation procedure has been suggested to be the non-inducibility of PAF. For PAF, an additional ablation of non-PV AF triggers is considered necessary in addition to the PVI. However, prior reports showed AF recurrence rates of 19–33% in the non-induced group and 36–55% in the induced group [4–6]. The diagnostic accuracy of AF induction tests after ablation seems to be low for predicting AF recurrences. Therefore, the need for further ablation of the induced atrial arrhythmias after the PVI in PAF patients remains unclear. The efficacy of PVI is sometimes insufficient, and atrial substrate modification of target specific AF signals indicating the substrate responsible for AF perpetuation has been proposed [7,8]. Complex fractionated atrial electrograms (CFAEs), which are electrograms that show continuous fractionation and very short cycle lengths during AF, may represent the substrate of AF [7]. In addition, atrial sites that represent local electrograms with high dominant frequencies (DFs) may be associated with AF maintenance [8]. A recent study reported that high-DF sites and continuous CFAE sites as the atrial substrate following PVI were present even in paroxysmal AF [8]. Accordingly, the present study aimed to evaluate the need of such an atrial substrate modification for the induced atrial arrhythmias after circumferential PVI to guide the non-inducibility in PAF patients.
Materials and methods
Results
Discussion
Conclusions
Funding
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Acknowledgments