Electrophysiologic Characteristics

The clinical diagnosis of triggered activity is supported in part by termination ofVT with adenosine, by the Valsalva's maneuver, carotid sinus pressure, verapamil and beta-blockade. The tachycardia can also be initiated and terminated with programmed stimulation and cannot be entrained.

The ability to reproducibly initiate an arrhythmia by programmed electrical stimulation is considered a hallmark of re-entrant arrhythmias. Arrhythmias that are the consequence of automaticity, are due to spontaneous depolarization and cannot usually be initiated by programmed stimulation. Tachyarrhythmias that are due to early afterdepolarizations are brady-cardia-dependent and are not well suited for study by programmed stimulation. Under certain circumstances, triggered activity due to delayed afterdepolar-

  1. 12.3 • Receptor schema for activation and inactivation of cAMP-mediated triggered activity caused by delayed after-depolarizations (DADs). A1, receptor; A1R, adenosine; AC, adenylyl cyclase; ACH, acetylcholine; ADO, adenosine; f-AR, P adrenergic receptor;cAMP,cyclic adenosine-monophosphate; G,.,inhibitory G-protein; G,,stimulatory G-protein; Gs,stim-ulatory G-protein;ICa(L),slow inward calcium current;/SO,isoproterenol;Irl,transient inward current;M2R,muscarinic cholinergic receptor; Na-CaX, Na+-Ca2+ exchanger; PKA, protein kinase A; SR, sarcoplasmic reticulum. Reproduced from [19]
  2. 12.3 • Receptor schema for activation and inactivation of cAMP-mediated triggered activity caused by delayed after-depolarizations (DADs). A1, receptor; A1R, adenosine; AC, adenylyl cyclase; ACH, acetylcholine; ADO, adenosine; f-AR, P adrenergic receptor;cAMP,cyclic adenosine-monophosphate; G,.,inhibitory G-protein; G,,stimulatory G-protein; Gs,stim-ulatory G-protein;ICa(L),slow inward calcium current;/SO,isoproterenol;Irl,transient inward current;M2R,muscarinic cholinergic receptor; Na-CaX, Na+-Ca2+ exchanger; PKA, protein kinase A; SR, sarcoplasmic reticulum. Reproduced from [19]

izations can be initiated by programmed stimulation. The response of the triggered activity to programmed stimulation is characteristic: 1) The amplitude and coupling interval of DADs depend on the duration and rate of the preceding pacing stimuli that result in induction; 2) Pacing at progressively shorter cycle lengths is associated with a shortening of the coupling interval for the initial beats of the tachycardia (this phenomenon, termed overdrive acceleration'is typical for initiation of triggered activity); 3) Rapid burst pacing is more effective than programmed ventricular extrastimuli in inducing tachycardia.

The ability to evoke triggered activity is dependent on the autonomic status of the patient. Repro-ducibility of induction is unpredictable. A heavily sedated patient is rarely inducible. Frequently, infusion of exogenous catecholamines is necessary for initiation of the arrhyhmia. An isoproterenol infusion is started at 2 ^.g/min and the infusion rate is titrated until the heart rate is increased by at least 20% (up to 10 to 14 ^.g/min as needed). Other agents that directly or indirectly increase cAMP activity can be used to facilitate inducibility: atropine (0.04 mg/kg) and aminophylline (2.8 mg/kg). Atropine attenuates the potential effect of acetylcholine and, at this dose, amino-phylline acts as a competitive adenosine antagonist.

Induction of VT by programmed ventricular stimulation may be consistent with either reentrant excitation or triggered activity. Induction of tachycardia with programmed electrical stimulation in the presence of fragmented electrograms favors re-entry as in ARVC/D. Arrhythmia induction by isoproterenol with cycle length dependence is consistent with a cyclic AMP-mediated triggered activity and favors the diagnosis of idiopathic RVOT tachycardia [45].

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