From the Guidelines
Accelerated junctional rhythm (AJR) is a cardiac arrhythmia originating from the atrioventricular (AV) junction that occurs at a rate of 70-130 beats per minute, which is faster than the normal junctional escape rhythm (40-60 beats per minute) but slower than junctional tachycardia (>130 beats per minute). This rhythm occurs when the SA node fails to generate impulses or when the junctional pacemaker cells become more excitable than the sinus node. On an ECG, accelerated junctional rhythm is characterized by regular QRS complexes with a normal morphology, absent or retrograde P waves (which may appear before, during, or after the QRS complex), and a consistent rate. This arrhythmia can be caused by:
- Digoxin toxicity
- Myocardial ischemia
- Myocarditis
- Electrolyte abnormalities It may also occur after cardiac surgery. Most patients with accelerated junctional rhythm are asymptomatic and require no specific treatment if hemodynamically stable. However, if the patient is symptomatic or the rhythm is caused by medication toxicity, addressing the underlying cause is essential. For digoxin toxicity, discontinuation of the medication and possibly administration of digoxin-specific antibody fragments (Digibind) may be necessary 1. Atropine may be considered if the patient is hemodynamically unstable due to the loss of atrial contribution to cardiac output. According to the 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia, there is limited evidence with regard to diagnosis and management of junctional tachycardia in adult patients, but nonparoxysmal junctional tachycardia (more commonly known as accelerated AV junctional rhythm) is far more common in adults than paroxysmal junctional tachycardia 1. The mechanism of nonparoxysmal junctional tachycardia is associated with automaticity or triggered activity, and treatment of this rhythm centers on addressing the underlying condition 1. Oral beta blockers are reasonable for ongoing management in patients with junctional tachycardia, and oral diltiazem or verapamil is also reasonable for ongoing management in patients with junctional tachycardia 1. Flecainide or propafenone may be reasonable for ongoing management in patients without structural heart disease or ischemic heart disease who have junctional tachycardia, and catheter ablation may be reasonable in patients with junctional tachycardia when medical therapy is not effective or contraindicated 1.
From the Research
Definition and Characteristics of Accelerated Junctional Rhythm (AJR)
- Accelerated junctional rhythm (AJR) is a type of abnormal heart rhythm that originates from the atrioventricular (AV) junction, which includes the AV node and the bundle of His 2.
- AJR is characterized by a faster than normal heart rate, typically between 40-120 beats per minute, and is often seen during slow pathway catheter ablation for atrioventricular nodal reentrant tachycardia 2.
- The pattern of AJR can vary, with three distinct patterns identified: continuous, alternating or "stuttering", and abrupt termination during energy delivery 2.
Mechanisms and Associations
- The mechanisms of AJR are not fully understood, but it is thought to be related to the anisotropic conduction properties of the AV junction and the slow pathway 2.
- AJR has been associated with successful slow pathway ablation sites, and its presence may indicate a high likelihood of successful ablation 2.
- The calcium clock, which refers to rhythmic spontaneous sarcoplasmic reticulum calcium release, may play an important role in AVJ automaticity and the acceleration of AVJ intrinsic rate during sympathetic stimulation 3.
Clinical Significance and Treatment
- AJR can be a marker for successful slow pathway ablation, but it can also be a nonspecific regional effect 2.
- The treatment of AJR typically involves catheter ablation, and the choice of ablation site and energy delivery protocol can affect the outcome 2.
- Calcium channel blockers, such as verapamil, may be useful in preventing or retarding the intracellular accumulation of calcium, which can cause irreversible postanoxic tissue damage 4.