EP 101: Analysis of a Long RP Tachycardia

Rakesh Gopinathannair, MD, MA, Alexander Mazur, MD, and Brian Olshansky, MD, FHRS Division of Cardiovascular Medicine, University of Iowa Hospitals, Iowa City, Iowa
Rakesh Gopinathannair, MD, MA, Alexander Mazur, MD, and Brian Olshansky, MD, FHRS Division of Cardiovascular Medicine, University of Iowa Hospitals, Iowa City, Iowa
In the next installment of the EP 101 series, the authors describe a case involving a narrow complex tachycardia with a long RP interval. Case Presentation A 78-year-old male presented to the emergency room with complaints of shortness of breath, nausea, and fatigue. Past medical history was significant for abdominal aortic aneurysm repair and hypertension treated with metoprolol (75 mg twice daily) and furosemide. His 12-lead electrocardiogram showed a narrow complex tachycardia at 153 beats/min with a long RP interval and negative p-waves in the inferior leads (Figure 1). Systolic blood pressure was 95 mmHg. Adenosine administration broke the rhythm to sinus bradycardia for a minute, but the tachycardia returned. No flutter waves were noted during a 5-second pause following adenosine administration. The tachycardia broke spontaneously after a few minutes. Echocardiogram showed normal left ventricular size and function and mild aortic insufficiency. Given symptomatic narrow complex tachycardia, an electrophysiology study was performed with a plan for catheter ablation. Baseline rhythm was sinus. Baseline PR interval was 161 msec. AH and HV intervals were within normal limits. A narrow complex tachycardia (SVT) was easily inducible by ventricular decremental pacing as well as ventricular burst pacing. It was also easily inducible by atrial or coronary sinus burst pacing or atrial extrastimulus testing. During atrial extrastimulus testing, tachycardia initiation was dependent on a critical AH interval prolongation with an H-V-A initiation pattern (Figure 2). The tachycardia almost always terminated with a ventricular electrogram. The tachycardia cycle length was 395 msec and surface p-waves during tachycardia were negative in inferior leads. Earliest atrial activation during SVT was noted in the proximal coronary sinus. During tachycardia, septal VA timing was 165 msec, His-earliest A was 185 msec, QRS-earliest A was 155 msec, AH interval was 150 msec, and HV interval was 50 msec (Figure 3). Ventricular decremental pacing showed VA conduction with a progressively changing activation pattern: shift of earliest atrial activation from the distal His bundle electrode to the proximal coronary sinus electrode with decreasing pacing cycle lengths. Ventricular extrastimulus testing showed decremental atrial activation with earliest A in the proximal coronary sinus and a retrograde His deflection preceding earliest A at short V1V2 coupling intervals. There was no clear “jump” in the AV nodal function curve antegrade. There was no antegrade preexcitation. The following differential diagnoses were entertained at this point: 1. Atypical form of AV nodal reentrant tachycardia (AVNRT) 2. Orthodromic AV reciprocating tachycardia (ORT), perhaps using a slow conducting and decremental concealed posteroseptal accessory pathway 3. Atrial tachycardia. Single ventricular premature beats introduced during tachycardia when the His bundle was refractory did not advance atrial activation during tachycardia (Figure 4). Relatively early-coupled single premature ventricular beats dissociated the ventricle from the atria (no change in tachycardia cycle length in the atrium) (Figure 5). Moreover, ventricular premature beats introduced during SVT reproducibly terminated the tachycardia without conducting to the atrium (Figure 6). Spontaneous premature atrial beats arising from the left atrium during SVT did not disturb the tachycardia, ruling out the left atrium as a part of the circuit (Figure 7). During subtle tachycardia cycle length changes, the HH interval did not predict the subsequent AA interval, demonstrating lack of consistent VA linking. Taken together, the diagnostic data were most consistent with an atypical form of AVNRT and helped rule out atrial tachycardia and ORT. Using a 4-mm tip, large curve ablation catheter, mapping of earliest atrial activation during SVT was performed and found to be at the os of the coronary sinus. A number of test lesions (Discussion Narrow complex tachycardia with a long RP interval (RP interval ≥ PR interval) in an elderly patient often presents interesting diagnostic challenges. It is essential to make a correct diagnosis to enable safe and effective catheter ablation aimed at curing the problem. Once SVT is identified, further analysis and ablation of this tachycardia usually necessitates placement of 3 diagnostic catheters (coronary sinus, His bundle, and right ventricular) and an ablation catheter. In this case, the earliest atrial activity during tachycardia was at the proximal coronary sinus. The differential diagnoses to be considered in this case are atrial tachycardia arising from the region of the Triangle of Koch, atypical variety of AVNRT (fast-slow or slow-slow) with the retrograde exit site near the os of the coronary sinus, and ORT using a concealed, retrograde conducting, possibly decremental, accessory pathway. At this point, before going any further, a vigilant electrophysiologist should make sure that all the diagnostic catheters are in the proper place by checking them under fluoroscopy, at least in 2 orthogonal views. This is especially important in the case of the coronary sinus catheter, which in some cases could be positioned very deep into the coronary sinus such that the proximal electrode, instead of being at the os of the coronary sinus, is now in a location corresponding to the posterior left atrium. This simple precaution will help save valuable time and effort by not misinterpreting a left-sided atrial tachycardia or a left-sided accessory pathway-mediated ORT as one coming from the right posteroseptal location. As discussed, paying close attention to electrophysiological features at baseline and during SVT as well as employing various pacing maneuvers enables one to correctly identify the tachycardia mechanism and institute effective ablation therapy. If no diagnostic maneuvers favoring a particular mechanism are seen, attention should be paid to collect information that can conclusively exclude other mechanisms, thus making a diagnosis by exclusion. A septal VA time greater than 70 msec during tachycardia (corresponding to the long RP interval) effectively excludes typical slow-fast AVNRT.1 Retrograde activation was decremental during right ventricular apical pacing. Moreover, the switch in earliest atrial activation from the distal His-bundle electrode to proximal coronary sinus during ventricular extra-stimulus testing was, at times, preceded by a retrograde His. These findings suggest the retrograde limb during tachycardia to be AV node rather than an accessory pathway, although a decremental posteroseptal accessory pathway-mediated tachycardia (permanent junctional reciprocating tachycardia) cannot be completely excluded. The initiation of the tachycardia during single atrial extrastimuli (A1A2) requiring a critical AH interval can be consistent with atypical AVNRT and ORT. ORT using a posteroseptal accessory pathway was excluded by the following findings: a) Premature ventricular extrastimuli delivered during SVT captured the ventricle but did not disturb the tachycardia, thus effectively dissociating the right ventricle from the tachycardia circuit. This excludes a macroreentrant ORT, in which the right ventricle is an integral component. b) Contrary to what one expects in an ORT, there was no consistent VA linkage during tachycardia. During periods of tachycardia cycle length variations (“wobble”), the HH interval did not predict the subsequent AA interval. c) A His-refractory premature ventricular beat delivered during tachycardia did not pre-excite the atrium. d) Other pacing maneuvers (not done in this case) can provide supporting evidence that can help exclude an ORT. For example, if the tachycardia can be entrained from the right ventricular apex and upon cessation of pacing, a post pacing interval (PPI) – tachycardia cycle length >115 msec provides further evidence that the right ventricular apex is not involved in the tachycardia circuit and favors AVNRT. An atrial tachycardia was excluded in this case based on the following findings: a) Ventricular premature beats delivered during SVT terminated the arrhythmia without conducting to the atria (Figure 6). This effectively excludes atrial tachycardia as the mechanism. b) Tachycardia initiation dependent on critical AH interval prolongation as well as an H-V-A pattern of initiation are inconsistent with an atrial tachycardia. c) As shown in Figure 7, spontaneous initiation of left atrial premature beats during SVT did not have any effect on the tachycardia, helping exclude the left atrium as a participant in the arrhythmia. d) If the tachycardia can be entrained by right ventricular overdrive pacing, then upon cessation of pacing, one would expect a VAAV response for an atrial tachycardia. A VAV or VAHV response favors AVNRT or ORT.1 Thus, the presence of dual AV nodal pathways retrograde, critical AH prolongation initiating long RP tachycardia in an HVA fashion, along with maneuvers that excluded atrial tachycardia and ORT, establishes the mechanism of tachycardia in our patient to be an atypical variety of AVNRT. The most common strategy in radiofrequency ablation of atypical AVNRT is to target the AV nodal slow pathway location in the septal tricuspid annulus. A standard 4-mm tip ablation catheter is usually sufficient. Preformed sheaths can be helpful if catheter stability becomes a problem. Irrigated/cooled ablation is often not needed and can be counterproductive. Ablation is usually performed in sinus rhythm and at the target site, and the distal ablation catheter electrode should have an A:V ratio of 1:4. It is our practice to start at a lower power and temperature setting (30 W and 45 degrees), with slow up-titration while watching for junctional beats with preserved retrograde conduction and subsequent return to sinus rhythm upon cessation of energy delivery. Post ablation, it is essential to confirm that the tachycardia is rendered non-inducible and that AV and VA conduction are preserved. Conclusions In final analysis, this narrow complex long RP tachycardia was an atypical, perhaps slow-slow, AVNRT with a posterior retrograde exit site close to the ostium of the coronary sinus. A stepwise approach that utilizes baseline data, tachycardia characteristics including initiation, termination and AV and VA relationships during changes in tachycardia cycle length, and various pacing maneuvers, can yield crucial information, leading to the correct diagnosis and enabling effective and safe radiofrequency ablation.