EP 101: Case Studies (Part 2)

In another installment of EP Lab Digest’s EP 101 series, the authors present three new case overviews, then ask readers to test their knowledge in EP by answering questions about each case. Case #1: A 27-year-old female underwent electrophysiology (EP) study for symptomatic palpitations. During the EP study, a single high right atrial premature extrastimulus (S1S2 coupling interval = 300 msec) following a 400 msec drive train demonstrated a “jump” in the AV nodal function curve and initiated a narrow complex tachycardia. Diagnostic maneuvers confirmed AV nodal reentry tachycardia (AVNRT) of the slow-fast variety. No other tachyarrhythmias were inducible. Slow pathway ablation was performed, and a tracing from the EP study performed post-ablation is shown (Figure 1). Figure 1 shows single atrial premature extrastimulus testing (S1S2 coupling interval = 230 msec) in the presence of 2 mcg/min of isoproterenol. AH interval at S1S2 coupling interval of 240 msec was 110 msec. Atrial activity (as noted in the high right atrial catheter [hRA]) following extrastimulus testing is denoted by arrows. Shown are recordings from surface leads (I, aVF, V1, V6) and intracardiac recordings from the high right atrium (hRA, hRA d), His bundle (His p, His m, His d), and right ventricular apex (RVa, RVa d). Question: Which of the following statements is true regarding the success of the ablation procedure? A. Further ablation is required as non-sustained AVNRT is induced, suggesting viable antegrade-conducting slow pathway. B. Further ablation is required, as more than one echo beat is induced with isoproterenol. C. Further ablation is required, as there is still a “jump” in the AV nodal function curve with isoproterenol. D. No further ablation is required, as this is a non-sustained atrial tachycardia induced by atrial premature extrastimulus and is not of AV nodal origin. E. No further ablation is required, as the induced AVNRT is non-sustained and isoproterenol was required for induction. The answer is D. Figure 1 shows single atrial premature extrastimulus testing (S1S2 coupling interval = 230 msec) in the presence of 2 mcg/min of isoproterenol following slow pathway ablation. Careful evaluation of the figure demonstrates three beats of narrow complex tachycardia following the premature atrial extrastimulus. AH interval with S1S2 =230 msec is 130 msec, which does not meet criteria for a “jump” as it only increased 20 msec when compared to S1S2 = 240 msec. Evaluation of atrial activity during the three beats of tachycardia demonstrates that the atrial signal in hRA is near-simultaneous or even earlier than the atrial signal in the His bundle electrogram, showing that this is a non-sustained atrial tachycardia and not atrial echoes from retrograde AV nodal fast pathway conduction. Case #2: A 65-year-old female undergoes electrophysiology testing for evaluation of syncope. Shown in Figure 2 are recordings from surface leads (I, aVF, V1, V6) and intracardiac recordings from the high right atrium (hRA, hRA d), His bundle (His p, His m, His d), and right ventricular apex (RVa, RVa d). Question: The second stimulus in this tracing (figure 2, see arrow) is most consistent with: A. VA block. B Loss of ventricular capture. C. Premature ventricular contraction. D. Attainment of ventricular effective refractory period. The answer is B. Figure 2 demonstrates RV apical pacing at 600 msec. The first beat demonstrates VA conduction through the AV node (earliest atrial activity noted in the distal His bundle electrogram). The second stimulus shows a ventricular spike, but this is not followed by a ventricular electrogram either at the RV apex electrode or in the His bundle electrode. This is loss of ventricular capture. It is not VA block, as no ventricular electrogram is seen in the RV apical electrode following the pacing spike. Ventricular effective refractory period is defined as the longest S1S2 coupling interval that captures the ventricle and is demonstrated using extrastimulus testing, which is not the case here. A solution to this problem might be to check pacing thresholds and to make sure there is adequate output while pacing. One should also make sure that the electrode catheter is located in a stable position in the RV apex. If not, repositioning the catheter might resolve this problem. Case #3: A 19-year-old male without any past cardiac history presents for evaluation of paroxysmal episodes of rapid palpitations with minimal activity, which was associated with chest discomfort and near-syncope. One documented spontaneous episode lasted for five minutes before terminating. There is no family history of sudden death. A 12-lead electrocardiogram at baseline is shown in Figure 3: Panel A. Echocardiogram showed mildly enlarged left ventricular size with a left ventricular ejection fraction of 45%. No valvular or segmental wall motion abnormalities were noted. The patient underwent a Bruce protocol treadmill test, and approximately two minutes into recovery, a wide complex tachycardia similar to the previously documented episode was noted (Figure 3: Panel B). The patient was hypotensive and dizzy, but did not pass out. The tachycardia spontaneously terminated. Endomyocardial biopsy was negative for myocarditis or infiltrative diseases. Cardiac MRI showed moderate diffuse left ventricular hypokinesis, but no fatty infiltrations were seen. An electrophysiology study is planned. Question: Which of the following statements is most accurate? A. This patient has idiopathic left ventricular tachycardia; ablation will be curative and an ICD is not indicated. B. This patient has outflow tract ventricular tachycardia; if ablation is successful, an ICD is not indicated. C. The mechanism of the tachycardia is uncertain; this patient has a class 1 indication for an ICD irrespective of whether the tachycardia can be successfully ablated. D. This mechanism of the tachycardia is uncertain; if ablation is successful, an ICD is not indicated as the cardiomyopathy is most likely tachycardia mediated. The answer is C. The baseline electrocardiogram shows normal sinus rhythm with indeterminate axis. QRS morphology is abnormal with low voltage in the limb leads. PR interval is normal without evidence of pre-excitation. QT interval is relatively short at 340 msec (corrected QT interval - 410 msec). A rapid, wide complex tachycardia with a RBBB, left axis morphology is induced following peak stress. This is most likely ventricular tachycardia and the RBBB, left axis morphology resembles idiopathic left ventricular tachycardia with origin from the inferoapical septum. However, the patient does have structural heart disease by the echocardiographic and MRI evaluation. One cannot be certain whether his cardiomyopathy is tachycardia mediated. He definitely needs an electrophysiology study to prove the mechanism of the tachycardia and to assess whether the tachycardia is amenable to ablation. In spite of this, his clinical profile fits a class 1 indication for an ICD per the 2008 ACC/AHA/HRS guidelines.1 The guidelines state that ICD therapy is indicated in patients “with structural heart disease and spontaneous sustained ventricular tachycardia, whether hemodynamically stable or unstable.” Thus, choice ‘C’ is the most accurate answer. See next month’s issue for another EP 101 installment!