Ventricular pacing: to pace or not to pace

Pacing from the right ventricular apex has been the clinical standard for decades but has recently come into question with a growing trend towards reducing ventricular pacing as much as possible. The earliest devices provided asynchronous ventricular pacing in patients whose indication for pacing was asystolic complete heart block. RV apical pacing was literally the difference between life and death. Over the decades, as technology has advanced allowing the medical community to more closely model normal cardiac physiology, we have seen the progressive introduction of demand function, single-chamber atrial pacing, dual-chamber pacing, dual-chamber rate-modulated pacing, and in the past decade, cardiac resynchronization pacing. During this evolution, it has been noted that pacing from the right ventricular apex, even in the presence of high-grade AV block, may contribute to ventricular dysfunction associated with the disordered ventricular activation sequence associated with the paced left bundle branch block pattern. ‘Pacemaker syndrome’ or the adverse haemodynamics associated with a technically normal pacing system was rarely recognized in the late 1960s when complete heart block was the indication for implantation. Its recognition blossomed in the 1980s with the introduction of dual-chamber pacing systems and an increase in the relative indications for permanent pacing including individuals who only needed pacing on an intermittent basis or whose primary indication for pacing was sinus node dysfunction. Pacemaker syndrome was usually associated with a loss of appropriate atrial transport (atrioventricular synchrony) and was able to be corrected by upgrading a patient with a single-chamber VVI pacing system to a DDD pacing system. 3 The standard location for the ventricular lead during the first four decades of cardiac pacing was the RV apex. The first generation of DDD pacemakers had limited AV delay programmability such that there was either full ventricular pacing or consistent ventricular fusion. On the basis of multiple studies, DDD pacing was clinically superior to VVI pacing, particularly when pacing was required for a large percentage of the time. The progressive symptoms of heart failure occurring over the ensuing decades were attributed to the progression of the patient’s underlying disease. It was not until the onset of cardiac resynchronization therapy that the clinical community began to appreciate the potentially adverse consequences of a disordered ventricular activation sequence, be it spontaneous as with an endogenous left bundle branch block or iatrogenic with RV apical ventricular pacing. On the basis of pacing studies demonstrating DDD pacing was superior to VVI pacing, the device manufacturers introduced dualchamber ICDs (VVED). The medical profession rapidly embraced dual-chamber ICDs, reasoning that both haemodynamics and supraventricular tachycardia discrimination with the addition of the atrial lead would be improved. No studies had been done. In the late 1990s, the DAVID trial was initiated in an effort to determine whether there was a benefit of DDD pacing over VVI pacing in a population of patients requiring ICD therapy. One of the entry criteria to participate in the DAVID trial was the requirement that the patient did not require pacing. The patients were then assigned to one of two groups, one with the pacing component of the ICD programmed to VVI at 40 bpm providing back-up heart rate support should delivery of high-voltage therapy be followed by a period of asystole. The second group was programmed to the DDD mode at a base rate of 70 bpm. Programming the AV delay was left to the discretion of the investigator at each participating medical centre. A majority of physicians left the paced and sensed AV delays at the shipped values of 170/150 ms, respectively. The primary endpoint for the DAVID study was a composite endpoint of death or worsening or new heart failure resulting in hospitalization. The data were monitored on a periodic basis by the