Accelerated Idioventricular Rhythm

Background

Accelerated idioventricular rhythm (AIVR) was first described by Thomas Lewis in 1910.[1] AIVR is currently defined as an enhanced ectopic ventricular rhythm with at least 3 consecutive ventricular beats, which is faster than normal intrinsic ventricular escape rhythm (≤40 bpm), but slower than ventricular tachycardia (at least 100-120 bpm).[1] Importantly, there is rate overlap between AIVR and some slow ventricular tachycardia. AIVR should not be diagnosed solely based on ventricular rate. Other characteristics of AIVR are helpful for its correct diagnosis (see Differentials).

AIVR is generally a transient rhythm, rarely causing hemodynamic instability and rarely requiring treatment. However, misdiagnosis of AIVR as slow ventricular tachycardia or complete heart block can lead to inappropriate therapies with potential complications. AIVR is often a clue to certain underlying conditions, like myocardial ischemia-reperfusion, digoxin toxicity, and cardiomyopathies.[2, 3, 4]

NextPathophysiology

In most cases, the mechanism of AIVR appears to be related to the enhanced automaticity in His-Purkinje fibers and/or myocardium[5] , sometimes accompanied with vagal excess and decreased sympathetic activity.[6] Ischemia, reperfusion, hypoxia, drugs, and electrolyte abnormalities can all accelerate the phase 4 action potential depolarization rates in His-Purkinje fiber and myocardium, leading to faster spontaneous cell depolarization (enhanced automaticity).[7] When the enhanced automaticity in His-Purkinje fiber or myocardium surpasses that of sinus node, AIVR manifests as the dominant rhythm of the heart. Sinus bradycardia may facilitate the appearance of AIVR.

Under certain conditions such as acute ischemia and digoxin toxicity, triggered activity has been suggested as the mechanism for AIVR.[8]

Most AIVRs originate from a single focus. Occasionally, in patients with acute myocardial ischemia and myocarditis, AIVR can originate from multiple foci.[9, 10] The ventricular rate of AIVR is generally between 40 to 100-120 bpm.

Usually, AIVR is hemodynamically well tolerated due to its slow ventricular rate. It is self-limited and resolves as sinus rate surpasses the rate of AIVR. Rarely, AIVR can degenerate into ventricular tachycardia or ventricular fibrillation. In patients with severe myocardial dysfunction, AIVR may lead to hemodynamic instability due to the loss of AV synchrony or relatively rapid ventricular rate.

AIVR in accute myocardial infarction

Clinically, AIVR has been best studied in patients with acute ST-elevation myocardial infarction (STEMI). In the thrombolysis era, AIVR was noted to be a marker of reperfusion.[11] However, not all patients with reopened coronary artery have AIVR. In patients with acute myocardial infarction treated with primary percutaneous coronary intervention, the reported incidence of AIVR varied significantly, raging from 15-50%, depending on methods of monitoring.[7, 12, 13]

Recently, studies in patients with STEMI treated with primary percutaneous coronary intervention support that AIVR is a marker of occluded coronary artery reopening, but is not necessarily a marker for complete reperfusion. In fact, AIVR seems to be associated with more extensive myocardial damage and delayed microvascular reperfusion[12] , although the mortality rates are similar in patients with and without AIVR.

PreviousNextEpidemiologyFrequencyUnited States

The true prevalence of AIVR is unknown.

International

The true prevalence of AIVR is unknown.

Mortality/Morbidity

In general, AIVR does not significantly affect the patients’ mortality and morbidity.

In a very small retrospective observation study, AIVR was found to be associated with lower 7 days survival in postresuscitation patients.[14]

Race

No racial preponderance exists.

Sex

Men and women are equally affected.

Age

No age predilection exists.

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