AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

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.

Frequency

United States

No definite frequency can be determined. Because AIVR mostly occurs following reperfusion in some patients after acute myocardial infarction or digitalis toxicity, its incidence would parallel that of coronary disease but with a much lower order of frequency. In a recent study, AIVR was observed in 15.2% of patients after reperfusion was established through direct percutaneous coronary intervention for acute MI.

International

International prevalence is similar to that in the United States.

Mortality/Morbidity

AIVR typically does not affect the patient's clinical course or prognosis seriously. Morbidity and mortality depends on the inciting and/or underlying condition.

Race

No racial differences in AIVR are noted.

Sex

AIVR apparently does not have a sex predilection.

Age

No age predilection can be described.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Patients may report symptoms or exhibit signs related to the following clinical presentations:

• Presence of acute myocardial infarction: Patients with AIVR most commonly have a history of recent or concomitant chest pain or other features of evolving acute myocardial infarction.
• Thrombolytic therapy for the management of acute myocardial infarction: More often than not, such patients have a history of therapeutic interventions aimed at revascularization, eg, thrombolytic therapy or percutaneous revascularization.
• Percutaneous coronary intervention: A history of reperfusion of the occluded infarct-related artery with percutaneous interventions, such as angioplasty, percutaneous transluminal coronary angioplasty (PTCA), or intracoronary stenting may be present.
• Often present with spontaneous recanalization of the coronary artery: Sometimes, a history of thrombolytic therapy or percutaneous interventions may not be present. However, passage of time since the onset of chest pain and the history of relief from pain and improvement in the electrocardiographic changes may reflect spontaneous recanalization of the infarct-related coronary artery.
• Other symptoms: Patients may have history of treatment with digoxin in the setting of ischemic cardiomyopathy, atrial fibrillation, or myocardial ischemia, and they may present with digoxin toxicity, which can manifest as AIVR.

Physical

Physical findings are consistent with the underlying illness.

• Patients with AIVR may present with a slow pulse rate (bradycardia). Hypotension may be present, caused by the bradycardia itself or a loss of atrial contraction ("kick") in patients with compromised left ventricular function.
• Due to AV dissociation, patients may present with cannon a waves. These are accentuated venous waves observed over the external jugular veins in the neck, and they are due to right atrial contraction when the tricuspid valve is closed because of synchronous right ventricular contraction.
• An irregular heart rhythm may be noted. Occasionally, an irregular heart rhythm develops because of the alternating predominance of the sinus rate and idioventricular rate.
• Due to AV dissociation and variation of dominant rhythm, the intensity of heart sounds on auscultation may vary. This relates to varying atrial-ventricular coupling times.

Causes

As a rule, arrhythmia occurs in patients with the following:

• Heart disease (eg, acute myocardial infarction, digitalis toxicity, at reperfusion of a previously occluded coronary artery)
• Possibly during resuscitation
• Drugs (eg, digoxin)
• Dilated cardiomyopathy
• Outpatient procedures (due to spinal anesthesia)

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Supraventricular rhythm or arrhythmia with aberrant conduction

Junctional rhythm with intraventricular conduction defects

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Blood tests
• • Cardiac enzymes establish the diagnosis of patients with acute myocardial infarction.
  • Assessment of renal status, achieved by measuring BUN and creatinine, is essential for patients presenting with digoxin toxicity.
• Other laboratory tests
• • Chemistry panel, including electrolytes
  • Magnesium level
  • Digoxin level

Imaging Studies

• Echocardiography often is used to evaluate myocardial and valvular function to rule out underlying cardiac disease.
• Cardiac catheterization and angiography may become necessary for patients with continued evidence of ischemia.

Other Tests

• Electrocardiographic recognition
• • The ventricular rate, commonly 60-100 (or 120) bpm, usually remains within 10 beats of the sinus rate.
  • The control of the cardiac rhythm switches back and forth between the 2 competing pacemaker sites (ie, normal or sinus and idioventricular), which leads to fusion beats at the onset and termination of the arrhythmia. Because of the slow rate, capture beats also are common.
  • The usual ECG pattern includes shortening of the PR interval that occurs as the PP intervals prolong, leading to emergence of the subordinate QRS complexes as they assume the pacemaker function. After a brief period, the PP interval shortens, P waves reappear before the QRS complex, and ventricular capture by atrial impulse is reestablished.
• Signal-averaged ECG (SAECG) is of uncertain prognostic value in this setting.
• Holter monitoring may reveal the duration, frequency, and rate of the AIVR.
• Inpatient telemetry monitoring

Procedures

• Coronary angioplasty or stent implantation may be required if the patient has significant coronary obstruction.
• If the patient develops more complex or recurrent ventricular arrhythmias, electrophysiology studies (EPS) may be required. Cardiac EPS is an invasive method for assessing the heart's electrical function. It allows physicians to locate abnormal sites inside the heart that may be causing serious arrhythmias. During an EPS, physicians insert flexible catheters (electrodes or wires) into veins and guide them into the cardiac chambers. Once inside, the catheters can sense electrical impulses in various areas of the heart; they also can be used to stimulate different parts of the heart.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Rarely, pharmacological or electrical suppressive therapy is necessary because the ventricular rate generally is less than 100 bpm. If the following conditions exist, further therapy may be considered:

• AV dissociation results in loss of sequential AV contraction and hemodynamic benefits of atrial contribution to ventricular filling.
• AIVR occurs with a more rapid VT.
• AIVR begins with a premature ventricular complex that has a short coupling interval and causes discharge in the vulnerable period of the preceding T wave.
• The ventricular rate is too rapid and produces symptoms.
• VT or fibrillation can develop from AIVR. This appears to be fairly rare. When indicated, therapy should be administered, as already noted, for patients with VT or ventricular fibrillation. Often, by simply increasing the sinus rate with atropine or atrial pacing, the AIVR suppresses.

Surgical Care

Patients with AIVR usually do not require surgical treatment; however, in certain circumstances, surgery may become an option. These circumstances include the following:

• AIVR with fast ventricular response, frequent recurrence, or ventricular fibrillation
• If the patient develops more complex or recurrent ventricular arrhythmias, EPS may be required. Cardiac EPS allows physicians to locate abnormal sites inside the heart that may be causing serious arrhythmias.
• Optimal revascularization with angioplasty or coronary bypass surgery may become necessary for management of the underlying ischemic heart disease.
• If the patient is symptomatic or hemodynamically compromised, increasing the atrial rate with atropine, isoproterenol, or atrial pacing will overdrive the AIVR.

Consultations

In certain cases, the following consultations may be necessary:

• Cardiologist
• Electrophysiologist
• Cardiovascular surgeon
• Pharmacist/pharmacologist
• Nephrologist

Diet

Patients with AIVR often present during or immediately following acute myocardial infarction. They frequently exhibit AIVR after thrombolytic therapy or percutaneous revascularization. Usually, these patients should have nothing by mouth (NPO) until their hemodynamic condition is stabilized.

• Diet should be advanced slowly, beginning with a liquid or soft diet. The diet should be low in fat. Sodium should be curtailed in patients with concomitant hypertension or congestive heart failure.
• Careful electrolyte balance should be achieved, especially in patients who are intubated. In these patients, enteral or parenteral nutrition should be instituted once the patient is hemodynamically stabilized.
• Patients with acute coronary syndromes do not always have to be NPO, and all patients with AIVR do not need such cautious management. Thus, advancing diet generally is reserved for patients who are hemodynamically unstable.

Activity

AIVR may develop in patients who are acutely or critically ill. Activity recommendations for critically ill patients are as follows:

• Complete bed rest is prescribed for patients in the initial stage. Continuous ECG monitoring is essential.
• Once patients are stable enough to be moved from the intensive care unit (coronary care unit) to an ECG-monitored step-down or progressive care unit, gradual progression in activity should be prescribed in concert with the institution of phase-1 cardiac rehabilitation and assessment.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Accelerated AV junctional and ventricular rhythms generally require no specific antiarrhythmic therapy.

In patients with ischemia, AIVR usually is self-limited and of no major consequence hemodynamically.

When associated with digitalis intoxication or electrolyte disturbances, AIVR promptly reverses with control of toxic or metabolic influences.

Specific antiarrhythmic drugs (including lidocaine) may suppress a subordinate pacemaker that is needed to maintain cardiac output in the presence of dysfunction of a normal sinus node.

If a faster ventricular rate or AV synchrony is desirable for hemodynamic benefits, attempts to enhance cardiac rates may be achieved pharmacologically or by pacing, as follows:

• Atropine (0.6-1.2 mg IV) may increase the sinus rate and allow the sinus to resume its normal pacemaking function if AV conduction is intact. Atropine has little or no influence on the rate of the accelerated AV junction focus. Intravenous isoproterenol (0.5-2.0 mcg/min) also can be used.
• Temporary atrial or ventricular pacing may be used to support the heart rate if it is slow enough to impair hemodynamics, but it rarely is necessary.

Drug Category: Beta-adrenergic receptor blocking agents

Compete with beta-adrenergic agonists for available beta-receptor sites. Inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.

Drug Category: Antiplatelet agents

Inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality rates by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of transient ischemic attacks.

Drug Category: Anticholinergics

The goal is to improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. This only is effective if the site of block is within the AV node. For patients with infranodal block, this therapy is ineffective.

Drug Category: Angiotensin-converting enzyme (ACE) inhibitors

Cause vasodilatation and improved ventricular remodeling. Used for the underlying diseases often associated with AIVR, eg, dilated cardiomyopathy and coronary artery disease

Drug Category: Anticholesterol agents

Cause LDL cholesterol lowering and reduction in recurrent cardiovascular events due to atherosclerosis, which may be present inpatients with AIVR. They are not specific for the therapy of AIVR.

Drug Category: Antiarrhythmic agents

Alter the electrophysiologic mechanisms responsible for ventricular arrhythmias. Used if arrhythmias are recurrent.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• AIVR does not require any particular treatment because it is a self-limited arrhythmia.
• In patients with bradycardia that is significant enough to cause hemodynamic derangements, the following measures may be required:
• • Administration of atropine (anticholinergic agent) to accelerate the underlying sinus rate
  • Insertion of temporary atrial pacemaker
  • Careful management of electrolyte imbalance, including potassium levels, and assessment of renal function (In the latter situation, patients with digoxin toxicity may manifest increased propensity to develop ventricular arrhythmias.)
• Appropriate management of the underlying disease process may be required, as follows:
• • In patients with acute myocardial infarction, treatment may include an aggressive medical regimen, including aspirin, intravenous antithrombotic therapy (unfractionated or low molecular weight heparins), intravenous nitroglycerine, and oral beta-blocking agents. Patients with compromised left ventricular function should receive ACE inhibitor therapy. These patients also may need appropriate revascularization in the form of angioplasty or bypass surgery.
  • Even though AIVR is a self-limiting arrhythmia, its genesis (automatic depolarization) reflects the presence of ischemic myocardium with hypoxic or reperfusion injury. Such myocardium may aid in the development of early or late after-depolarizations, leading to ventricular arrhythmias. In such cases, further assessment through EPS may be needed. Patients exhibiting inducible ventricular arrhythmias during EPS may require therapy with an automatic implantable cardioverter defibrillator (AICD).
  • Patients presenting with digoxin toxicity require careful monitoring of heart rhythm and rate, as well as hemodynamic parameters. If the patient's heart rate becomes too slow, temporary pacemaker insertion may be necessary. Daily digoxin levels should be checked until the level falls within the reference range. Digoxin should be withheld until such time and then reinstituted at a lower dose. Renal function and potassium levels also should be monitored carefully. Some patients with high digoxin levels may require its antibody antidote (ie, Digibind).
• Patients presenting following resuscitation from sudden cardiac arrest form another subset of patients who may exhibit AIVR. If ischemic etiology is not found, aggressive workup involving EPS should be performed. Such patients frequently benefit from AICD implantation.

Further Outpatient Care

• AIVR is a self-limited arrhythmia and does not require any particular form of outpatient therapy; however, the underlying conditions require comprehensive medical and risk factor management.
• Patients discharged after acute myocardial infarction require the following:
• • Appropriate medical regimen
    • Aspirin
    • Beta-blockers
    • ACE inhibitors for patients with compromised left ventricular function, (ie, left ventricular ejection fraction [LVEF] <40%)
    • Statin drugs in the presence of hyperlipidemia
  • Comprehensive cardiac rehabilitation
    • Cardiac rehabilitation, along with risk factor modification, reportedly improves survival rates in such patients; however, it is an underused modality.
    • Patients should be enrolled in the phase-1 rehabilitation program before discharge. The phase-2 rehabilitation program and exercise prescription should be individualized.
    • ECG monitoring may be necessary during the first few weeks of exercise training.
  • Aggressive risk reduction strategies
    • Dietary discretion and weight management
    • Lipid control, preferably with statin drugs in addition to dietary therapy
    • Smoking cessation
    • Control of hypertension (goal blood pressure [BP] <135/85 mm Hg and <125/85 mm Hg if patient has diabetes)
    • Diabetes management
• Patients with underlying diagnosis of digoxin toxicity require the following:
• • Downward dose adjustment of digoxin
  • Pulse or heart rate count prior to each digoxin dose (Avoid digoxin administration when bradycardia exists.)
  • Careful monitoring and assistance for pill intake because of the possibility of medication errors in patients with memory or visual impairment
  • Frequent monitoring of renal function and potassium levels
• Patients with postresuscitation AIVR who received an AICD before discharge require close follow-up care with a cardiovascular specialist.

In/Out Patient Meds

• Aspirin
• Beta-blockers
• ACE inhibitors
• Statin drugs
• Amiodarone (occasionally)
• Diuretics
• Antihypertensives (for patients with hypertension)
• Antidiabetic medications (for patients with diabetes)
• Carvedilol (for patients with poorer left ventricular function)

Transfer

• Transfer to another hospital for advanced evaluation and management may be necessary.
• Patients require routine high-level monitoring that is appropriate for the underlying disease (eg, acute myocardial infarction) during transfer in an advanced cardiac life support (ACLS)–equipped ambulance. Monitoring should include continuous telemetry and oxygen.
• No additional transfer requirements are needed for patients with AIVR.

Deterrence/Prevention

• AIVR usually is a transient arrhythmia, and it usually occurs after reperfusion in the territory of an occluded coronary artery caused by increased automaticity. AIVR manifests during ECG monitoring when the ventricular rate exceeds the prevailing sinus rate.
• Prevention is not necessary because AIVR usually is inconsequential. Careful observation is all that is necessary.
• In some instances, the overall ventricular rate may be too low, and the patient may experience hemodynamic compromise. Additionally, in patients with significant left ventricular dysfunction, the absence of the atrial kick during AIVR may cause diminished cardiac output. In such situations, acceleration of the underlying sinus rhythm with intravenous atropine administration may prevent recurrence of AIVR.

Complications

• AIVR usually is a self-terminating condition, but it can cause hypotension and the recurrence of more complex ventricular arrhythmias occasionally.

Prognosis

• AIVR generally has a good prognosis, and it usually is a transient and self-terminating arrhythmia.
• Prognosis depends primarily on the underlying disease process.

Patient Education

• AIVR does not commonly recur after discharge; therefore, patient educational requirements are minimal.
• Patient education should focus on the recovery from myocardial infarction. Comprehensive rehabilitation, exercise, diet, and risk reduction strategies should be discussed with patients through a team approach. Discussion of follow-up requirements; knowledge about medication and its side effects; and monitoring of blood levels for medicines, metabolites, and lipids, as well as any implanted defibrillators, are paramount.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Heart Rhythm Disorders.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• AIVR may be the patient's only rhythm. No underlying sinus rhythm may be present. For this reason, AIVR should not be treated with antiarrhythmic therapy (eg, lidocaine) until the presence of a reliable underlying rhythm is confirmed. Otherwise, the antiarrhythmic drug may eliminate AIVR, which may be the only rhythm, leading to an absence of any rhythm (or asystole). Remember this precautionary statement.
• Assess the patient carefully in an effort to determine potential causes for AIVR.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  ECG showing acute inferior wall myocardial infarction. An accelerated idioventricular rhythm (AIVR) frequently is observed in such patients following reperfusion.
	View Full Size Image
Media type:  ECG

Media file 2:  Accelerated idioventricular rhythm (AIVR). ECG showing complete heart block and slow escape ventricular rhythm (nonaccelerated idioventricular rhythm).
	View Full Size Image
Media type:  Rhythm Strip

Media file 3:  Accelerated idioventricular rhythm (AIVR). A 12-lead ECG from a patient presenting with acute myocardial infarction. Patient shows sinus bradycardia (heart rate is 44 beats per min [bpm]).
	View Full Size Image
Media type:  ECG

Media file 4:  Accelerated idioventricular rhythm (AIVR) in the patient described in Image 3 recorded 2 minutes after the previous ECG (Image 3) and 1 hour after intravenous thrombolytic therapy with Retavase. Idioventricular rate is 76 beats per minute (bpm), which dominates the underlying sinus bradycardia at 44 bpm.
	View Full Size Image
Media type:  ECG

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Bigger JT, Fleiss JL, Kleiger R. The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction. Circulation. Feb 1984;69(2):250-8. [Medline].
• Bonnemeier H, Ortak J, Wiegand UK, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann Noninvasive Electrocardiol. Apr 2005;10(2):179-87.
• Coven G, Arpesella R, Ciceri M, et al. Accelerated idioventricular rhythm during spinal anesthesia for cesarean section. Int J Obstet Anesth. Apr 2003;12(2):121-5.
• Flaker GC, Singh VN. Prevention of myocardial reinfarction. Recommendations based on results of drug trials. Postgrad Med. Nov 1 1993;94(6):94-8, 102-4. [Medline].
• Friedman PL, Stevenson WG. Unsustained ventricular tachycardia--to treat or not to treat?. N Engl J Med. Dec 26 1996;335(26):1984-5. [Medline].
• Grimm W, Marchlinski FE. Accelerated idioventricular rhythm, bidirectional ventricular tachycardia. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. 2nd ed. Philadelphia, Pa:. WB Saunders Co;1994:920.
• Ilia R, Amit G, Cafri C, et al. Reperfusion arrhythmias during coronary angioplasty for acute myocardial infarction predict ST-segment resolution. Coron Artery Dis. Sep 2003;14(6):439-41.
• Lerman BB, Stein K, Engelstein ED. Mechanism of repetitive monomorphic ventricular tachycardia. Circulation. Aug 1 1995;92(3):421-9. [Medline].
• Pepe PE, Levine RL, Fromm RE. Cardiac arrest presenting with rhythms other than ventricular fibrillation: contribution of resuscitative efforts toward total survivorship. Crit Care Med. Dec 1993;21(12):1838-43. [Medline].
• Sharma RK, Singh VN, Flaker GC. Signal-Averaged Electrocardiogram: A Non-invasive Diagnostic Tool for Arrhythmia Management. Developments in Cardiology. 1994;175-192.
• Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulation. Aug 1981;64(2):235-42. [Medline].
• Thomas JE, Katapadi M. Accelerated idioventricular rhythm in a healthy teenager post circumcision. Conn Med. Oct 2004;68(9):555-7.
• Zipes DP. Unwitting exposure to risk. Cardiol Rev. 1993;1:1.

Article Last Updated: Jun 22, 2006