The critical issues for pacing in vasovagal syncope (VVS) are timing of onset, mode of pacing, stimulation rate, duration of stimulation and identifying patients that will receive sufficient benefit to justify such invasive permanent therapy. Research to date has answered none of these questions.
Timing of Onset
VVS manifests vasodepression (probably better stated as low venous return and, thus, low cardiac output), which usually precedes cardioinhibition – vagally mediated. In this knowledge, waiting for bradycardia will trigger pacing too late in the evolution of VVS. Earlier delivery of pacing might be better and can be triggered by rising right ventricular impedance reflecting falling venous return, this function is available as the Closed Loop System (Biotronik). A welldesigned randomised controlled trial is now ongoing. If successful, this trial will beg the question of how does pacing work in VVS – just by avoiding bradycardia?
Mode of Pacing
Consensus favours dual-chamber pacing and there is evidence suggesting that both right atrial and right ventricular pacing alone are inadequate.
Stimulation Rate
The rate drop response (RDR) algorithm (Medtronic) introduced higher-rate (~100 BPM) hysteresis-type pacing for a programmable period (~60 sec) as used in the ISSUE-3 study (Pacemaker Therapy in Patients with Neurally-Mediated Syncope and Documented Asystole. Third International Study on Syncope of Uncertain Etiology (ISSUE-3): A Randomized Trial study). As this algorithm has had some success (ISSUE-3) despite its handicap of waiting for bradycardia, perhaps this aspect has some value?
Duration of Stimulation
In RDR, the duration of stimulation is programmable, typically ~60 seconds, and is terminated by rate step-down to ~70 BPM to meet the recovering sinus rhythm. This aspect of the algorithm has received little study.
Which Patients May Benefit Sufficiently to Balance the Aggression of the Therapy?
Emphasis to date has been on older patients, which is reasonable considering that their tolerance for trauma (induced by falls) is not good, epidemiologically their attacks increase in frequency and their therapy time is reduced, which limit long-term complications. We know that some young patients, even those who are highly symptomatic, have recovered fully to present no clinical need for pacing. Older patients (usually >60 years) must be symptomatic to be considered for pacing, involving more than two attacks in the previous 2 years and severe attacks, often without warning, prompting traumatic falls and frequently associated with incontinence of urine and abnormal movements during attacks. These latter features tend to reflect asystole in the attack. It would be useful to know how helpful these criteria are for selection of pacing in older patients and affecting outcomes when applied to younger patients. These decisions are currently clinical with little evidence base, especially in younger patients.
This brief commentary accompanies a very detailed review of VVS by Gopinathannair and Olshansky (page 95). The points raised here are referenced in that review.