At presentation, the patient is in sinus rhythm. At the programmed sensing configuration, each QRS complex is sensed appropriately. Thus, changing the sensing vector empirically to another configuration would not be indicated.
The stored electrogram demonstrates clear evidence of a change in QRS morphology associated with T-wave oversensing in the initial portion of the tracing. The electrogram by the end of the tracing is sensed appropriately and resembles the electrogram obtained at the patient’s device interrogation on presentation. Since the device detected the rhythm as a ventricular arrhythmia, simply ignoring the observation would not be suggested. On the other hand, it is premature to consider repositioning the ICD lead. T wave oversensing is by FAR the most common cause of oversensing in the subcutaneous ICD and this is typically evaluated by ETT and changing the sensing vector.
The most likely explanation is that the patient develops a rate-related bundle branch block during which the current programmed sensing configuration cannot adequately distinguish between QRS complexes and T waves. Thus, an exercise stress test will be useful to optimize the sensing configuration using a template acquired during exercise when the rate related QRS morphology can be replicated.

The ECG shows a markedly prolonged QT interval (about 580 ms corrected). Combined with a history of sudden syncope while exercising and family history of sudden cardiac death, long QT Syndrome Type 1 (LQT1) is the most likely diagnosis. Beta blocker therapy is a Class 1 recommendation in LQT1 patients with syncope. ICD therapy is reserved for patients who have recurrent symptoms on beta blockers or have survived cardiac arrest.

An apical RV lead would be expected to be situated in a lower position than the one shown in PA view. The lateral chest X-ray shows the ventricular lead to be posterior, whereas an RV lead would be anteriorly located in a patient implanted with an apical RV lead. An endocardial left ventricular lead does not course at the border of the cardiac silhouette, contrary to a CS lead which is epicardial.

The decision to inactivate the shock function of a defibrillator needs to take into account patient preferences and overall prognosis, especially when heart failure symptoms have progressed despite optimal medical therapy. ACC/AHA guidelines suggest that a reasonable prognosis for survival of at least 1 year applies to de novo implants; the same applies to generator changes. Similarly, there are no randomized clinical trials that support CRT upgrades with this degree of heart failure, though case series have been published. There is no role for atrial pacing at this juncture; the patient clearly has diffuse conduction disease and the natural history will not be impacted. There are no data to support the use of any beta-blocker with intrinsic sympathomimetic activity for any stage of heart failure.

Sudden death secondary to torsades de pointes or ventricular fibrillation has been reported after AV junction ablation. This outcome is possibly related to increased dispersion of ventricular refractoriness produced by sudden heart rate slowing and ventricular pacing. After ablation, the ventricular pacing rate is usually set between 90 bpm and 100 bpm and then gradually tapered over several months.