Identifying occult paroxysmal atrial fibrillation as the etiology of cryptogenic stroke has been a top research priority in the past decade. This is because prompt initiation of anticoagulation has significantly decreased subsequent stroke risk. Available evidence suggests that prolonged cardiac monitoring after stroke increases the likelihood of detecting atrial fibrillation. However, further research is required to fill in the gaps in regard to the optimal period of monitoring, candidates for monitoring, etc. Here, we review the current evidence supporting the use of prolonged monitoring for cryptogenic stroke patients and discuss the directions of future research.

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This case describes some of the commonly overlooked device-related issues in patients who have reportedly failed to respond to cardiac resynchronization therapy (CRT). The case demonstrates voltage-dependent right ventricular capture instead of right atrial capture by a subtly malpositioned right atrial lead. CRT therapy failed to improve symptoms of heart failure and the diagnosis of "CRT nonresponder" was made. With a detailed fact-finding approach, the mechanism behind this nonresponse was identified, and the outcome of CRT was significantly improved with rectification of the problems. C ardiac resynchronization therapy (CRT) is a well-established device therapy for heart failure (HF) that is based on simultaneous pacing of both ventricles in order to mimic normal cardiac electromechanical contraction. Unfortunately, about one-third of CRT-implanted patients do not respond to this therapy, and most causes remain a conundrum. Nevertheless, suboptimal lead placement is commonly overlooked in clinical practice. Here, we describe a detailed evaluation with successful rectifi cation of the mechanisms in a case of a CRT nonresponder. CASE DESCRIPTIONAn 80-year-old woman with paroxysmal atrial fi brillation, left bundle branch block (QRS of 154 ms), and severe nonischemic cardiomyopathy (ejection fraction of 30%) underwent implantation of a CRT with a defi brillator for management of severe HF symptoms despite optimal medical therapy. Th ree months later, she continued to have HF class III-IV symptoms. Device interrogation showed 74% biventricular pacing and 74% right atrial (RA) pacing with stable lead impedances since implant. Pacing thresholds of the right ventricular (RV) and left ventricular (LV) lead were 0.9 V at 0.5 ms and 0.75 V at 0.5 ms, respectively. During a detailed and step-by-step RA lead capture threshold testing with continuous 12-lead electrocardiogram monitoring, RV capture instead of RA capture starting at 5 V at 0.8 ms down to 1.75 V at 0.8 ms was discovered. Interestingly, at or lower than 1.5 V at 0.8 ms, RV capture by pacing through RA lead was switched to RA capture only, with an RA capture threshold of 0.75 V at 0.8 ms (Figures 1 and 2). Malposition of the RA lead was suspected.After chest radiography was found to be inconclusive, a computed tomography scan demonstrated that the RA lead tip was near the atrioventricular groove abutting the base of the RV outfl ow tract (Figure 3). As such, the RA lead pacing at pulse amplitude ≥1.75 V was indeed capturing the RV, and true biventricular pacing using the RV and LV lead was not happening, as the RV had already been inappropriately captured by RA lead pacing. In other words, DDD pacing (atrial-paced biventricular paced rhythm) with RA pacing amplitude at or above 1.75 V was resulting in right ventricular VVI pacing only, as there was no RA capture (loss of atrial kick), RV and LV were in the refractory period, and pacing through the RV and LV leads was not capturing (eff ectively 0% biventricular pacing). Pacing outputs were therefore reprogr...