Atrial Tachycardias

John A. Kalin, MD and Ann C. Garlitski, MD Tufts Medical Center, Boston, Massachusetts
John A. Kalin, MD and Ann C. Garlitski, MD Tufts Medical Center, Boston, Massachusetts
In this article, the authors describe a brief case on atrial tachycardia, which can sometimes be a challenging arrhythmia to identify, treat and ablate.


The patient is a 64-year-old female with a past medical history of hypertension who is referred to an electrophysiologist for evaluation of palpitations. Her symptom of rapid heartbeat is associated with dizziness and difficulty concentrating. Her blood pressure is 130/90. A 12-lead electrocardiogram reveals an atrial tachycardia (AT) with an average ventricular rate of 92 beats per minute. A transthoracic echocardiogram reveals normal chamber sizes and left ventricular function.


Within the broad scope of supraventricular tachycardias (SVTs), AT remains a challenging arrhythmia in clinical practice. While ablation of tachyarrhythmias such as typical atrial flutter, resulting from a large macroreentrant circuit, have a well-defined target such as the cavotricuspid isthmus, a focal AT can arise from any location in the supraventricular space, from the crista terminalis to the pulmonary veins. The possible mechanisms include automaticity, triggered activity or microreentry. Atrial tachycardia represents 5–15% of all SVTs, and while it is frequently seen in structurally normal hearts, it can also be seen in association with congestive heart failure, valvular heart disease and congenital heart disease. There is no particular predilection for age, gender, race or ethnicity. Common symptoms include palpitations, lightheadedness, anxiety and fatigue, and rarely, syncope. Of note, when incessant and untreated, AT may lead to the development of a tachycardia-induced cardiomyopathy. The 12-lead electrocardiogram reveals atrial rates that may vary widely from approximately 140 to 220 beats per minute. Close examination of the P-waves suggest the location of the focus. Atrial activity from the high right atrium is reflected by P-waves that are upright in leads II, III, and aVF as well as leads I, aVL and V1; this morphology suggests forces moving from the superior aspect of the heart downward and leftward to activate both the right and left atria. P-waves that are negative in leads II, III, and aVF suggest an area of activation from the inferior aspect of the atrium, while P-waves that are positive in leads I and aVL reflect activity originating from the left atrium. Atrial tachycardias may start or stop abruptly and often accelerate quickly when initiated, often referred to as a ‘warm-up’. Occasionally sensitive to adenosine, ATs may slow with beta blockers or calcium channel blockers and may be abruptly terminated with cardioversion, if necessary. However, the response of ATs to therapy is more variable than other SVTs and may require more definitive therapy such as an electrophysiology study and radiofrequency ablation. The decision to proceed with an invasive approach over medical therapy is made on a case-by-case basis depending on symptoms, response to therapy, and comorbidities. The patient was in an incessant tachycardia with an atrial cycle length of 280 milliseconds when she underwent an invasive electrophysiology study. Diagnostic catheters were positioned in the coronary sinus, His position, and right ventricle. We chose to use a three-dimensional mapping system in order to perform simultaneous acquisition of anatomic and electrical data. In addition, we chose to use a multipolar, single-plane, double-loop diagnostic catheter (with an outer loop of 20 mm and 20 electrodes) in order to obtain data efficiently. A three-dimensional mapping system in combination with a multipolar diagnostic catheter may greatly aid the process of identifying the site of a focal AT. Colors which correspond to timing are displayed on a three-dimensional model of the chamber of interest. In this case, the right atrium, superior vena cava and inferior vena cava were initially mapped and the earliest site of activation was noted to be along the interatrial septum. Given the suspicion of breakthrough from a left-sided origin (isoelectric P waves in I and negative P-waves in aVL), a transseptal puncture was performed in order to map the left atrium. Activation mapping of the left atrium and all four pulmonary veins identified a focal site of earliest activation along the junction of the roof and left superior pulmonary vein. Radiofrequency energy was delivered via an externally irrigated 3.5 mm ablation catheter. Following ablation, the tachycardia could not be reinduced despite pacing and the infusion of isoproterenol.


AT may be a challenging arrhythmia to identify, treat and ablate. However, the use of a three-dimensional mapping system and advanced diagnostic catheters allows for safe and effective ablation. Disclosures: The authors have no conflicts of interest to report.