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INVASIVE AND SEMI‐INVASIVE DIAGNOSIS IN SINUS NODE DISEASE

Inuasiue electrophysiologic studies of sinus node function and dysfunction have provided much insight into possible mechanisms underlying the various ECG manifestations observed in sick sinus syndrome (SSS). Impaired sinus node automaticity as well as sinoatrial conduction disturbances are encountered and may coexist. From a clinical point of view continuous ECG monitoring is the preferred diagnostic method in patients with suspected SSS. However, invasive electrophysiologic testing may have some clinical utility in selected cases. Atrial overdrive pacing using a number of pacing rates for short periods of time has been considered a test of SN automaticity and provides a measurement of sinus node recovery time (SNRT). The result of testing is best expressed as the maximum corrected SNRT (CSNRT = SNRT mean preceding sinus CL). Sinoatrial conduction time (SACT) has been indirectly assessed by the Strauss method using single premature atrial extrastimuli and the Narula method based on low rate atrial pacing for very short periods. Clear differentiation between disturbances in automaticity and conduction is however not possible as abnormalities in one mechanism influences the evaluation of possible abnormalities in the other. This may result in false positive as well as false negative findings (1). Reference values are not universally agreed upon but CSNRTmax > 545 ms and SACT > 120 ms would be considered prolonged by most authors. Studies in SND patients and controls have shown CSNRTmax to be fairly specific but rather insensitive while both sensitivity and specificity is low for SACT. Partly for this reason attempts have been made to further evaluate the response to atrial overdrive pacing. The occurrence of secondary pauses in postpacing cycles 2-10 is a characteristic but infrequent finding in SND patients. In contrast, the observation that the paced cycle length eliciting CSNRTmax (PCLmax) is often above 600 ms in SND patients seems to have greater potential utility. For example it has been shown that 41 of 53 SND patients {11%) had either abnormal CSNRTmax (n = 13), prolonged PCLmax (n = 19) or both (n = 7) (2).