Original source: eMedicine Medscape
Accelerated Idioventricular Rhythm
Accelerated idioventricular rhythm (AIVR) was first described by Sir 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, 2] Importantly, there is potential rate overlap between AIVR and some slow ventricular tachycardia. AIVR should not be diagnosed solely based on ventricular rate; context is important. 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. [3, 4, 5]
In most cases, the mechanism of AIVR appears to be related to the enhanced automaticity in His-Purkinje fibers and/or myocardium, [6] sometimes accompanied with vagal excess and decreased sympathetic activity. [7] 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). [8] 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. [9]
Most AIVRs originate from a single focus. Occasionally, in patients with acute myocardial ischemia and myocarditis, AIVR can originate from multiple foci. [10, 11] The ventricular rate of AIVR is generally between 40 and 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 the ventricular rate.
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. [12] 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. [8, 13, 14]
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, [13] although the mortality rates are similar in patients with and without AIVR.
Accelerated idioventricular rhythm (AIVR) can occur in people with and without apparent heart diseases. [15] The most common cause of AIVR is myocardial ischemia-reperfusion. Other causes include the following:
Congenital heart disease [17]
Dilated cardiomyopathy [5]
Drugs: Digoxin toxicity, [4] cocaine toxicity, [18] and various anesthesia agents [19, 20, 21]
Beach et al reported on the case of a boy aged 4 years who appeared to have developed AIVR from the administration of inhaled albuterol to treat his status asthmaticus. [23]
The true prevalence of accelerated idioventricular rhythm (AIVR) is unknown.
The true prevalence of AIVR is unknown.
Hingorani et al analyzed drug-free ambulatory ECG recordings from 1273 healthy volunteers (who had normal screening ECGs) from 22 phase 1 studies that were analyzed in a core ECG laboratory. AIVR was observed in 0.3% of healthy volunteers, and other types of arrhythmias were observed in a higher percentage of healthy volunteers. The results suggest that some cardiac arrhythmias may be due to chance in early-phase studies. [24]
No racial preponderance exists, and men and women are equally affected.
No age predilection exists.
Accelerated idioventricular rhythm (AIVR) is a mostly self-limiting rhythm and typically has a benign prognosis when AIVR rather than a slow(ed) VT is the true underlying entity. [25] The prognosis of patients with AIVR largely depends on their underlying conditions.
In general, AIVR does not significantly affect the patients’ morbidity and mortality, which reflects that of the underlying condition causing the AIVR. In a very small retrospective observation study, AIVR was found to be associated with a lower 7-day survival rate in postresuscitation patients. [22]
Rarely, AIVR can result in hemodynamic instability, especially in patients with severe cardiomyopathy. Rarely, AIVR may degenerate into ventricular tachycardia or ventricular fibrillation.
Reassure patients that accelerated idioventricular rhythm (AIVR) per se does not significantly affect their prognosis. Educate patients that some of the underlying etiologies for AIVR should be treated accordingly.
For patient education, see the Heart Health Center as well as Heart Rhythm Disorders.
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Nayereh G Pezeshkian, MD Assistant Professor of Medicine, Division of Cardiology and Electrophysiology, University of California, Davis, School of Medicine
Nayereh G Pezeshkian, MD is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography, Heart Rhythm Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, American Thoracic Society
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Actelion, Bayer, Gilead, United Therapeutics<br/>Received research grant from: Actelion, Arena, Gilead, GSK, Liquidia, Reata, United Therapeutics<br/>Received income in an amount equal to or greater than $250 from: Actelion, Complexa, Gilead, Medtronic, Reata, United Therapeutics.
Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society
Disclosure: Nothing to disclose.
Robert E Fowles, MD Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.
Rakesh K Sharma, MD, FACC Adjunct Associate Professor of Medicine and Cardiology; University of Arkansas for Medical Sciences, Medical Center of South Arkansas
Disclosure: Nothing to disclose.
Vibhuti N Singh, MD, MPH, FACC, FSCAI Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine; Director, Cardiology Division and Cardiac Catheterization Lab, Chair, Department of Medicine, Bayfront Medical Center, Bayfront Cardiovascular Associates; President, Suncoast Cardiovascular Research
Vibhuti N Singh is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association
Disclosure: Nothing to disclose.
Source: eMedicine Medscape
This article is provided for informational purposes only and is not a substitute for professional medical advice. Always consult with a qualified healthcare provider for diagnosis and treatment.
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