Current literature reveals three types of paroxysmal atrioventricular block (AVB) that can cause syncope:Intrinsic paroxysmal atrioventricular block is due to an intrinsic disease of the AV conduction system; this type of “cardiac syncope” is also called Stokes-Adams attack;Extrinsic vagal paroxysmal atrioventricular block is linked to the effect of the parasympathetic nervous system on cardiac conduction and is one of the mechanisms involved in “reflex syncope.”Extrinsic idiopathic paroxysmal atrioventricular block is associated with low levels of endogenous adenosine and is supposed to be one of the mechanisms involved in “low-adenosine syncope.”These three types of paroxysmal AVB present different clinical and electrocardiographic features. Additionally, the efficacy of cardiac pacing and theophylline therapy to prevent syncopal recurrences is also different for these three types of AVB.

We have shown that syncope recurs not infrequently in patients with BF-B who received pacing for syncope. Nearly one in four patients who had empiric pacing suffered syncope recurrence compared to no recurrences in patients who received a PM following a positive EPS or documentation of transient AVB.

Cardiac pacing is highly effective in preventing syncopal recurrences when AVB is documented. Syncope may recur in a non-negligible minority of paced patients when AVB is suspected but not documented and in patients without SHD.

Introduction Dyssynchrony persists in many patients despite cardiac resynchronization therapy (CRT). Aim of this proof‐of‐concept study was to achieve better CRT, with a QRS approximating the normal width and axis, by using His bundle pacing (HBP) and nonconventional pacing configurations. Methods and Results In 20 patients with CRT indications, we performed an acute intrapatient comparison between conventional biventricular (CONV) and three nonconventional pacing modalities: HBP alone, His bundle, and coronary sinus pacing (HBP + CS), and HBP + CS plus right ventricular pacing (TRIPLE). Electrical dyssynchrony was assessed by means of QRS width and axis; “quasi‐normal” axis meant an R/S ratio ≥ 1 in leads I and V6 and ≤1 in V1. Mechanical dyssynchrony was assessed by speckle tracking echocardiography. QRS width was 153 ± 18 ms on CONV, shortened to 137 ± 16  ms on HBP + CS (P = .001) and to 130 ± 14 ms on TRIPLE (P = .001), while it remained unchanged on HBP (159 ± 32 ms; P = .17). The rate of patients with “quasi‐normal” axis was 5% on CONV, and increased to 90% on HBP (P = .0001), to 63% on HBP + CS (P = .001), and to 44% on TRIPLE (P = .02). On radial strain analysis, the time‐to‐peak difference between anteroseptal and posterolateral segments was 143 ± 116 ms on CONV, shortened to 121 ± 127 ms on HBP (P = .79), to 67 ± 70 ms on HBP + CS (P = .02), and to 76 ± 55 ms on TRIPLE (P = .05). On discharge, HBP was chosen in 15% of patients, HBP + CS in 55%, and TRIPLE in 30%; CONV was never chosen. Conclusion Nonconventional modalities of CRT provide acute additional electrical and mechanical resynchronization. An interpatient variability exists.

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