Accelerated idioventricular rhythm (AIVR) is a form of ectopic or automatic ventricular arrhythmia usually noted in the acute care setting during cardiac rhythm monitoring. This condition is characterized by a ventricular rate that is slower than traditionally defined ventricular tachycardia (VT). Generally, the heart rate is less than 100 beats per minute (bpm), but some authors have used heart rate less than 120 bpm. It is often, but not always, slightly faster than the underlying sinus rhythm; therefore, the ventricular rate takes over as the predominant rhythm.
AIVR may also be defined as an ectopic rhythm with 3 or more consecutive premature ventricular beats and a rate faster than the normal ventricular intrinsic escape rate of 30-40 bpm but slower than VT.
AIVR is an electrocardiographic diagnosis and does not generally produce any particular symptoms. Making a correct diagnosis remains one of the most important concerns because the usual treatments for patients with the more common form of ventricular arrhythmia, such as VT, may not apply.
Pathophysiology
Enhanced automaticity appears to be the likely electrophysiologic mechanism behind the genesis of AIVR. Enhanced automaticity generally is ascribed to phase-4 depolarization of the action potential of the myocardial cell. AIVR can occur in the His-Purkinje fibers or myocardium under certain abnormal metabolic conditions.
AIVR arises from subordinate or second-order pacemakers and manifests itself when the patient's prevailing sinus rate becomes lower than the accelerated rate (AIVR) of the otherwise suppressed focus. Sinus bradycardia combined with enhanced automaticity of the subordinate site is the common pathophysiology.
Several conditions, including myocardial ischemia (especially inferior wall ischemia or infarction), digoxin toxicity, electrolyte imbalance (eg, hypokalemia), and hypoxemia may accentuate the phase-4 depolarization in the subordinate pacemaker tissues of the atrioventricular (AV) junction or His-Purkinje system, thus increasing the rate of impulse generation. Frequently, when inferior wall ischemia is present, the subordinate pacemaker acceleration coexists with sinus node depression. The latter permits escape and domination of the pacemaker function, which may occur with AV junctional or ventricular rates of only 60-70 bpm. The ectopic mechanism also can begin after a premature ventricular complex or, as described above, when the ectopic ventricular focus simply can accelerate sufficiently enough to overtake the intrinsic rhythm.
The onset of AIVR is gradual (nonparoxysmal). The ventricular rhythm can be regular or irregular and, occasionally, can show sudden doubling, suggesting the presence of exit block. The ventricular rate, commonly 60-110 bpm, usually stays within 10-15 beats of the sinus rate; therefore, the control of the cardiac rhythm occasionally passes back and forth between these 2 competing pacemaker sites.
Fusion beats often develop at the onset and termination of arrhythmia, which occurs when the pacemakers are competing for control of ventricular depolarization. Because of the slow rate, capture beats also are common. Due to the slow rate and nonparoxysmal onset, precipitation of more rapid ventricular arrhythmias rarely is observed. Rhythm termination generally occurs gradually, while the underlying sinus rhythm accelerates or the AIVR slows down.
Accelerated idioventricular rhythm in the reperfusion era
Ever since the beginning of the thrombolytic era, the occurrence of AIVR in patients with acute MI has been considered a specific marker of successful reperfusion following the infusion of the lytic agents.
Whether such association exists with reperfusion through direct percutaneous coronary intervention was investigated in a recent study of 125 consecutive patients undergoing direct percutaneous coronary intervention for a first acute MI. 24-hour Holter monitoring revealed that AIVR appeared in 15.2% of the patients. The incidence of AIVR was not different between patients with TIMI grade 2 flow and those with TIMI grade 3 flow (13% vs 16%). No differences were reported in the incidence of major cardiac events within 12-month follow-up in patients with and without AIVR. However, AIVR was associated with higher vagal tone and lower sympathetic activity, the occurrence of AIVR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion following percutaneous coronary intervention.
AIVR may also be defined as an ectopic rhythm with 3 or more consecutive premature ventricular beats and a rate faster than the normal ventricular intrinsic escape rate of 30-40 bpm but slower than VT.
AIVR is an electrocardiographic diagnosis and does not generally produce any particular symptoms. Making a correct diagnosis remains one of the most important concerns because the usual treatments for patients with the more common form of ventricular arrhythmia, such as VT, may not apply.
Pathophysiology
Enhanced automaticity appears to be the likely electrophysiologic mechanism behind the genesis of AIVR. Enhanced automaticity generally is ascribed to phase-4 depolarization of the action potential of the myocardial cell. AIVR can occur in the His-Purkinje fibers or myocardium under certain abnormal metabolic conditions.
AIVR arises from subordinate or second-order pacemakers and manifests itself when the patient's prevailing sinus rate becomes lower than the accelerated rate (AIVR) of the otherwise suppressed focus. Sinus bradycardia combined with enhanced automaticity of the subordinate site is the common pathophysiology.
Several conditions, including myocardial ischemia (especially inferior wall ischemia or infarction), digoxin toxicity, electrolyte imbalance (eg, hypokalemia), and hypoxemia may accentuate the phase-4 depolarization in the subordinate pacemaker tissues of the atrioventricular (AV) junction or His-Purkinje system, thus increasing the rate of impulse generation. Frequently, when inferior wall ischemia is present, the subordinate pacemaker acceleration coexists with sinus node depression. The latter permits escape and domination of the pacemaker function, which may occur with AV junctional or ventricular rates of only 60-70 bpm. The ectopic mechanism also can begin after a premature ventricular complex or, as described above, when the ectopic ventricular focus simply can accelerate sufficiently enough to overtake the intrinsic rhythm.
The onset of AIVR is gradual (nonparoxysmal). The ventricular rhythm can be regular or irregular and, occasionally, can show sudden doubling, suggesting the presence of exit block. The ventricular rate, commonly 60-110 bpm, usually stays within 10-15 beats of the sinus rate; therefore, the control of the cardiac rhythm occasionally passes back and forth between these 2 competing pacemaker sites.
Fusion beats often develop at the onset and termination of arrhythmia, which occurs when the pacemakers are competing for control of ventricular depolarization. Because of the slow rate, capture beats also are common. Due to the slow rate and nonparoxysmal onset, precipitation of more rapid ventricular arrhythmias rarely is observed. Rhythm termination generally occurs gradually, while the underlying sinus rhythm accelerates or the AIVR slows down.
Accelerated idioventricular rhythm in the reperfusion era
Ever since the beginning of the thrombolytic era, the occurrence of AIVR in patients with acute MI has been considered a specific marker of successful reperfusion following the infusion of the lytic agents.
Whether such association exists with reperfusion through direct percutaneous coronary intervention was investigated in a recent study of 125 consecutive patients undergoing direct percutaneous coronary intervention for a first acute MI. 24-hour Holter monitoring revealed that AIVR appeared in 15.2% of the patients. The incidence of AIVR was not different between patients with TIMI grade 2 flow and those with TIMI grade 3 flow (13% vs 16%). No differences were reported in the incidence of major cardiac events within 12-month follow-up in patients with and without AIVR. However, AIVR was associated with higher vagal tone and lower sympathetic activity, the occurrence of AIVR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion following percutaneous coronary intervention.
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