3.16) is an automatic rhythm, independent of the sinus node, that originates in the ventricle and competes with sinus rhythm. More rarely (see Fig. Accelerated Idioventricular Rhythm (AIVR) AIVR results when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node. Warren Smith, Margaret Hood, in Cardiothoracic Critical Care, 2007. Similarly, AIVR may terminate abruptly because the sinus rate increases or because the ventricular escape rate slows. In contrast to the reentrant idiopathic fascicular VT, focal Purkinje VTs are most likely related to abnormal automaticity. In addition, these VTs are transiently suppressed by adenosine and with overdrive pacing.11. Rarely, the loss of AV synchrony may produce a symptomatic reduction in cardiac output (lightheadedness, breathlessness), especially in patients with diastolic dysfunction (e.g., left ventricular hypertrophy [LVH]). Copyright © 2020 Elsevier B.V. or its licensors or contributors. It can also occur in normal athletic hearts and during return of spontaneous circulation (ROSC) following cardiac arrest. AIVR is a generally benign rhythm. Often associated with increased vagal tone and decreased sympathetic tone. In conjunction with thrombolytic therapy, reperfusion ventricular arrhythmias were considered as a noninvasive marker of successful infarct artery recanalization; however, current evidence suggests that those arrhythmias are neither specific nor sensitive. The arrhythmia occurs with equal frequency in patients with anterior or inferior MI and may be provoked by spontaneous or induced coronary reperfusion.71,72 AIVR may begin with a premature ventricular beat or may occur as a result of sinus slowing or an increase in the ventricular “escape” rate. AIVR is defined by its rate (60 to 100 beats/min) and is sometimes referred to as slow VT. AIVR occurs in 8% to 20% of patients, usually during the first 2 days after MI. AIVR is particularly common with acute MI, and may be a sign of reperfusion after the use of thrombolytic agents or after interventional coronary artery procedures, or it occur spontaneously. It is associated with a heart rate of between 50 and 100 beats per minute and is usually self-terminating. AIVR is often short lived and has no hemodynamic consequences. Patients are generally asymptomatic, and the rhythm is discovered only incidentally.
Idiopathic focal VTs can arise from the Purkinje system in either ventricle and can present as PVCs, accelerated idioventricular rhythm, or VT. Focal Purkinje VTs arising from the left Purkinje network exhibit an RBBB pattern with either left- or right-axis deviation and can be difficult to distinguish from fascicular VT. Ventricular arrhythmias upon reperfusion typically manifest as bursts of PVCs with long coupling intervals and accelerated idioventricular rhythms occurring at the moment of reperfusion, and are hemodynamically well tolerated. Alteration of the EP substrate and, in particular, intracellular Ca2+ overload combined with increased catecholamines, likely play a central role in reperfusion arrhythmias. Accelerated idioventricular rhythm (AIVR) is a slow ventricular rhythm that captures the heart because the sinus rate is even slower. None is indicated unless symptomatic (rare) (Table 3.7). AIVR is defined by its rate, under 100 beats/min.
Other conditions in which AIVR is observed include myocardial ischemia, digoxin toxicity, hypokalemia, and cardiac surgery, but these are not causative factors.
Ziad F. Issa MD, ... Douglas P. Zipes MD, in Clinical Arrhythmology and Electrophysiology (Third Edition), 2019. Figs.
21-17). AIVR is classically seen in the reperfusion phase of an acute ST-segment-elevation myocardial infarction (STEMI; post thrombolytic therapy or primary percutaneous coronary intervention). 16.15), AIVR is initiated by premature beats rather than escape beats. Fusion complexes in which the ventricles are depolarized by both the sinus and ventricular impulses often occur. When AIVR is sustained and hypotension is observed, an agent such as atropine may be useful in overdriving the AIVR by accelerating the sinus node.
These VTs are sensitive to autonomic tone and frequently display chronotropic properties. These arrhythmias originate within the reperfusion zone and likely reflect myocellular reperfusion injury. 16.20 and 16.21 present examples of a distinctive arrhythmia called accelerated idioventricular rhythm (AIVR), sometime referred to as slow VT. Recall that with typical VT the heart rate is more than 100 beats/min. Similarly, AIVR may terminate abruptly because the sinus rate increases or because the ventricular escape rate slows. There is AV dissociation, with the atrial and ventricular rates typically being relatively similar. When the sinus rate slows, AIVR appears; when the sinus rate speeds up, the arrhythmia disappears. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. URL: https://www.sciencedirect.com/science/article/pii/B9780323529938000163, URL: https://www.sciencedirect.com/science/article/pii/B9781416037736100205, URL: https://www.sciencedirect.com/science/article/pii/B9780323399685000032, URL: https://www.sciencedirect.com/science/article/pii/B9780323478700000374, URL: https://www.sciencedirect.com/science/article/pii/B9780750675727500242, URL: https://www.sciencedirect.com/science/article/pii/B9780323401692000160, URL: https://www.sciencedirect.com/science/article/pii/B9780323523561000220, URL: https://www.sciencedirect.com/science/article/pii/B9780750675840000136, URL: https://www.sciencedirect.com/science/article/pii/B9780323523561000244, Goldberger's Clinical Electrocardiography (Ninth Edition), 2018, Supraventricular and Ventricular Arrhythmias in Acute Myocardial Infarction, Ventricular and Supraventricular Arrhythmias in Acute Myocardial Infarction, Brian Olshansky MD, ... Nora Goldschlager MD, in, Ary L. Goldberger MD, FACC, ... Alexei Shvilkin MD, PhD, in, Goldberger's Clinical Electrocardiography (Ninth Edition), Ventricular Arrhythmias in Ischemic Heart Disease, Ziad F. Issa MD, ... Douglas P. Zipes MD, in, Clinical Arrhythmology and Electrophysiology (Third Edition), Ventricular arrhythmias upon reperfusion typically manifest as bursts of PVCs with long coupling intervals and, Electrocardiographic Technology of Cardiac Arrhythmias. Accelerated idioventricular rhythm (AIVR) results when the rate of an ectopic ventricular pacemaker causes a wide QRS rhythm that is faster than the sinus node but not fast enough to cause tachycardia (<100 bpm) (Fig. AIVR is usually self-limited. The ventricular rate is generally between 70 and 100 bpm (near the sinus rate) but should not be considered to be “slow VT.” AIVR is distinguished from VT by its slower rate (< 100 bpm). Ary L. Goldberger MD, FACC, ... Alexei Shvilkin MD, PhD, in Goldberger's Clinical Electrocardiography (Ninth Edition), 2018. Underlying sinus rhythm with AV dissociation or retrograde ventriculo-atrial (VA) activation may be present. This latter type is more likely to be associated with faster ventricular tachyarrhythmias.
In this setting, it does not require treatment.
It is commonly seen during MI, occurring in 30% of inferior MIs and 5% of anterior MIs; it may or may not represent a reperfusion injury rhythm. Jose L. Baez-Escudero, in Cardiology Secrets (Fifth Edition), 2018. From: Goldberger's Clinical Electrocardiography (Ninth Edition), 2018, Dina M. Sparano, Judith A. Mackall, in Cardiac Intensive Care (Third Edition), 2019. P waves may be absent, retrograde (following the QRS complex and negative in ECG leads II, III, and aVF), or independent of them (AV dissociation). A proposed mechanism is enhanced automaticity of a ventricular natural pacemaker, although triggered activity may play a role, especially in ischemia and digoxin toxicity.
AIVR is often associated with increased vagal tone and decreased sympathetic tone.
In humans, AIVR is the most common arrhythmia following coronary reperfusion.63,74 Most cases of AIVR probably occur as a result of enhanced automaticity in Purkinje fibers on the endocardial surface near or within the infarction zone.74 In vitro studies, using a model of coronary artery reperfusion, have shown AIVRs that were caused by triggered activity associated with delayed afterdepolarization.75 Rapid VT with a rate twice that of the AIVR has been observed in some patients, suggesting re-entry with episodic exit block as another possible mechanism for the arrhythmia.76,77, Brian Olshansky MD, ... Nora Goldschlager MD, in Arrhythmia Essentials (Second Edition), 2017. The classic onset of AIVR is with mild slowing of sinus rate with emergence of the ventricular rhythm via fusion complexes; its classic offset is the reverse, via fusions with a mild increase in sinus rate.