A 59-year-old woman with a history of hypothyroidism and dyslipidemia treated with diet and levothyroxine.
Since the age of 42, she had episodes of recurrent episodes of recurrent, sudden onset episodes, mostly self-limiting, associated with syncope on two occasions.
On one occasion, it was possible to document a regular narrow complex tachycardia of approximately 320 milliseconds, which seemed to be a PR wave of approximately 80 milliseconds, with a round PS cycling included in the PS segment.
The differential diagnosis of VRNAT vs ventricular atrial reentry tachycardia by a hidden paraspecific beam was proposed.
On that occasion, he became sinus rhythm with the administration of a bolus of intravenous adenosine (6 mg).
She failed to prevent episodes of tachycardia with amiodarone, atenol and flecainide.
Physical examination was within normal limits.
His baseline electrocardiogram was normal.
Two years ago, she underwent an electrophysiological study (EFS) in another center where tachycardia could not be induced.
Given the persistence of symptoms, malaise, despite drug treatment, it was decided to perform a new EPS.
Under biannual conditions, an increasing frequency was observed with a 500 ms cycle and less, there was constriction compaction ms-concentric coupling until a 450 ms cycle was programmed. The non-recognition phase was 250 ms.
Under these conditions, arrhythmias could not be induced.
Subsequently, atrial stimulation was performed at increasing frequency up to a cycle of 360 ms cycle associated with anterograde conduction with Wenckebach-type block.
Subsequently, programmed auricular stimulation was performed with stimulation cycles of 700/550 ms and less, the AH interval was linearly prolonged up to a coupling interval of 290 ms and the non-echo 280 ms time was observed.
Because tachycardia could not be induced by auricular stimulation, an infusion of isoproterenol (1-2 mcg/mln) was initiated, which accelerated the rhythm to 110 bpm.
Under these conditions, auricular stimulation was repeated at increasing frequency and programmed auricular stimulation.
The prolongation of the new HA interval was linear and arrhythmias were not detected.
Ventricular stimulation was repeated, and with a 270 ms cycle, a typical VRNAT was induced with a 262 ms cycle (228 beats per minute).
A long curved Mansfield fulguration catheter (slow color mango) was advanced through the right femoral vein. Seven radiofrequency pulses were not applied in the region of obtaining abundant non-contrast pathway.
cable 3A failed to demonstrate residual dual-way physiology and tachycardia could not be induced by atrial or ventricular stimulation at increasing frequency (with an infusion cycle of 220ms), or after induction (within 30ms).
