New insights into pacemaker syndrome gained from hemodynamic, humoral and vascular responses during ventriculo-atrial pacing

New Developments in Cardiac Pacemakers

“…AV synchrony has an important role in the regulation of cardiac output, mainly at rest and during low levels of exercise, and is especially useful in those patients who depend on optimized ventricular filling such as those with diastolic dysfunction. 45,46 Many small trials in the past [47][48][49] have shown that dualchamber pacing is superior to single-chamber pacing, improving exercise capacity and symptoms and avoiding pacemaker syndrome. Furthermore, the patient preference in most studies is DDD pacing.…”

Complications of Pacemaker Implantation

“…The reduction in cardiac output associated with non physiologic pacing and loss of atrioventricular synchrony triggers changes in vascular tone. The autonomic nervous system enhances sympathetic activity modulated by arterial baroceptors which are triggered by low blood pressure (Alicandri et al, 1978;Ellenbogen et al, 1990;Pehrsson et al, 1988). The increase in left atrial, pulmonary and left ventricular filling pressures result in inhibitory reflexes mediated by vagal nerve and in increased production of atrial natriuretic peptide, a potent arterial and venous vasodilator (Theodorakis et al, 1992).…”

“…In presence of atrio-ventricular block a rapid atrial pacing (AAI or AAIR) prevents the regular atrial filling and reduce cardiac output. Many patients cannot tolerate the rapid pacing associated with activity mode (Ellenbogen et al, 1997;Ellenbogen et al, 2007). An inappropriate mode switching of DDDR pacing in response to interference noise or dying battery, then rhythm change, can also cause PM syndrome.…”

Evidence Base for Pacemaker Mode Selection

“…However, every pacemaker clinician has experienced the patient who develops profound hypotension with ventricular pacing, and it is in these patients that the role of the autonomic nervous system becomes most relevant. [53][54][55] Hypotension during ventricular pacing is now thought to be due to individual variation in compensatory sympathetic outflow, the effects of vasodilator drugs or vascular disease, and the activation of cardioinhibitory reflexes that are brought into play by atrial distension, and that counteract the reflex increases in adrenergic tone.…”