The development of advanced atrioventricular block (AVB) in patients on bradycardic and/or antiarrhythmic therapy (drug-related AVB) represents a clinical challenge, raising the question of whether the AVB is directly caused by these agents (drug-induced AVB) or if the offending drugs exacerbate an underlying conduction system disease. Traditionally, β-blockers, non-dihydropyridine calcium channel blockers, class Ic/III antiarrhythmics, and digoxin have been considered reversible causes of advanced AVB. However, recent evidence shows a weak cause-and-effect relationship between these drugs and AVB in the elderly, along with high recurrence rates of AVB despite initial resolution after drug discontinuation. This may also apply to patients on high doses of these medications, drug combinations, or with additional reversible factors such as hyperkalemia. Despite these considerations, the European Guidelines do not suggest permanent pacing for AVB due to transient causes that are correctable, including bradycardic/antiarrhythmic drug therapy. On the other hand, the American Guidelines recommend permanent pacing for selected patients with symptomatic second- or third-degree AVB on stable, necessary antiarrhythmic or β-blocker treatment, without waiting for drug washout or reversibility. Notably, an accumulating body of evidence indicates that true drug-induced AVB is rare, while recurrence rates are high. Therefore, early permanent pacing should be recommended, especially for frail elderly patients. Moreover, in patients with drug-related AVB and atrial tachyarrhythmias, adopting an early permanent pacing approach seems prudent when bradycardic and/or antiarrhythmic treatment is necessary. Finally, delays in permanent pacing are not justified when temporary pacing is needed, given the increased associated risks in such cases.

Michael Efremidis

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Introduction. Data regarding the left atrial (LA) electroanatomical substrate in patients with hypertrophic cardiomyopathy (HCM) and atrial fibrillation (AF) are missing. In this electroanatomical mapping (EAM) study, we evaluated the extent of LA fibrosis and its impact on catheter ablation outcomes in patients with HCM and AF. Methods. High-density LA EAM was performed during AF in 28 consecutive patients with obstructive HCM and AF (42.9% displayed paroxysmal AF and 57.1% persistent AF). After propensity matching (PS), 28 non-HCM patients with AF were selected, and served as controls. Two different cut-off values of bipolar signal amplitude were investigated for fibrosis characterization (≤0.25 mV and ≤0.4 mV). HCM patients underwent pulmonary vein antral isolation (PVAI) and roof line, while non-HCM patients PVAI only. Results. After the 3-month blanking period, 10 HCM patients (35.7%) displayed atrial arrhythmia recurrence. Univariate analysis revealed that the extent of LA fibrosis was the only predictor of AF recurrence. HCM patients with arrhythmia recurrence showed significantly greater low voltage areas defined as either bipolar voltage ≤0.25 mV (22.5±10% vs. 5.5±6.4%, p=0.001) or ≤0.4 mV (32±13.9% vs. 5.9±5.1%, p<0.001). The presence of low voltage areas ≤0.4 mV greater than 14.1% of the total LA area also predicted arrhythmia recurrence with excellent sensitivity (100%) and specificity (100%). After PS matching with non-HCM patients, patients with HCM exhibited wider fibrotic regions ≤0.25 mV compared to non-HCM patients (p=0.016). Conclusions. High-density EAM reveals extensive LA fibrotic disease in patients with HCM, an event with certain implications in catheter ablation outcomes.