Older adults are particularly vulnerable to pacemaker syndrome due to age-related ventricular stiffening and increased reliance on the atrial contribution to cardiac output.
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May prompt closer monitoring for pacemaker syndrome in older adults; leaves open optimal age-specific pacing strategies pending prospective data.
Pacemaker syndrome arises from adverse electrophysiological and haemodynamic consequences of pacing— in particular ventricular pacing—despite normal pacemaker function [1, 2]. The symptoms are diverse, ranging from breathlessness, syncope, palpitations, neck pressure, dizziness and flushing to more vague symptoms of lethargy and impaired exercise tolerance. Clinical signs include cannon ‘a’ waves in the jugular venous pressure waveform, intermittent or sustained hypotension and congestive cardiac failure [3]. In the normal cardiac cycle there is a sequential electrical depolarization from atria to ventricles. Loss of this co-ordinated sequence has profound consequences on cardiac output [4]. When ventricular function is normal, the atrial contribution to cardiac output can be up to 25% [5]. With advancing years the ventricles thicken and become stiffer, and consequently the atrial contribution to cardiac output becomes even more important [6]. Thus, older adults are more vulnerable to the consequences of loss of atrioventricular synchrony. Loss of atrioventricular synchrony occurs with single chamber ventricular pacing.
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Robert S. Ross (2000) studied this question.
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