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

Abstract

Ventricular pacing is performed during programmed electrical stimulation and during normal functioning of single chamber (VVI or VVIR) pacemakers. In many patients, retrograde ventriculo-atrial (V-A) conduction may occur and evoke hemodynamic and reflex neurohumoral responses, which are unique to this pacing mode. Accordingly, forearm blood flow, forearm vascular resistance, mean and phasic arterial pressure, cardiac output and plasma norepinephrine, epinephrine and dopamine were measured during atrial, ventricular and V-A pacing at a cycle length of 600 ms (100 beats/min) before and after regional a blockade with intraarterial phentolamine in 16 patients with a left ventricular ejection fraction >35% and little or no symptoms of congestive heart failure. During V-A pacing, cardiac output decreased by 10%, whereas forearm vascular resistance increased from 52 ± 7 to 70 ± 9 U (p < 0.001) and plasma norepinephrine increased from 183 ± 27 to 232 ± 27 pg/ml (p < 0.01). Phentolamine nearly abolished the increase in forearm vascular resistance in response to V-A pacing (18 ± 4.1 U before vs 5.8 ± 1.5 U after, p < 0.05). The change in forearm vascular resistance with V-A pacing correlated with systolic arterial pressure, but not with changes in mean arterial pressure, pulse pressure, cardiac output, mean or peak right atrial pressure, pulmonary artery or pulmonary capillary wedge pressure. These results suggest that forearm vascular resistance responses to V-A pacing are mediated mainly by α-adrenergic receptors, through the arterial baroreflexes. These sympathetic vasoconstrictor and humoral responses may be important in compensating for hemodynamk abnormalities during ventricular arrhythmias, and inadequate sympathetic responses may play a role in the genesis of pacemaker syndrome.