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Background  The mechanism of inappropriate sinus tachycardia ( IST ) remains incompletely understood.    Methods and Results  We prospectively compared 3 patient groups: 11 patients with  IST  ( IST  Group), 9 control patients administered isoproterenol (Isuprel Group), and 15 patients with cristae terminalis atrial tachycardia (AT Group). P‐wave amplitude in lead  II  and  PR  interval were measured at a lower and higher heart rate ( HR 1 and  HR 2, respectively). P‐wave amplitude increased significantly with the increase in  HR  in the  IST  Group (0.16±0.07 mV at  HR 1=97±12 beats per minute versus 0.21±0.08 mV at  HR 2=135±21 beats per minute,  P =0.001). The average increase in P‐wave amplitude in the  IST  Group was similar to the Isuprel Group ( P =0.26).  PR  interval significantly shortened with the increases in  HR  in the  IST  Group (146±15 ms at  HR 1 versus 128±16 ms at  HR 2,  P <0.001). A similar decrease in the  PR  interval was noted in the Isuprel Group ( P =0.6). In contrast, patients in the atrial tachycardia Group experienced  PR  lengthening during atrial tachycardia when compared with baseline normal sinus rhythm (153±25 ms at  HR 1=78±17 beats per minute versus 179±29 ms at  HR 2=140±28 beats per minute,  P <0.01).    Conclusions  We have shown that  HR  increases in patients with  IST  were associated with an increase in P‐wave amplitude in lead  II  and  PR  shortening similar to what is seen in healthy controls following isoproterenol infusion. The increase in P‐wave amplitude and absence of  PR  lengthening in  IST  support an extrinsic mechanism consistent with a state of sympatho‐excitation with cephalic shift in sinus node activation and enhanced atrioventricular nodal conduction.

P‐Wave Amplitude and PR Changes in Patients With Inappropriate Sinus Tachycardia: Findings Supportive of a Central Mechanism