To the Editor—Response

To the Editor—Response

LETTERS TO THE EDITOR To the Editor: I read with interest the article by Suleiman and Asirvatham,1 which was published in the “Hands On” section of th...

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LETTERS TO THE EDITOR To the Editor: I read with interest the article by Suleiman and Asirvatham,1 which was published in the “Hands On” section of the October 2008 issue of Heart Rhythm. The authors’ discussion of the topic, including the anatomical relationship of the semilunar valves, clearly helps the electrophysiologist to further understand the complexities involved with the ECG manifestations and mapping and ablation of outflow tract premature ventricular complexes (PVCs) and ventricular tachycardias arising from the region close to the pulmonic and aortic semilunar valves. As such, I am looking forward to reading Part II of the series. However, I would like to point out that the details shown in Figure 3 of the article require further clarification. As described by the authors, the second complex as seen on the surface ECG leads is, indeed, a PVC. However, the recorded intracardiac ventricular electrogram on the ablation catheter does not appear to be earlier by 46 ms to the surface QRS, nor is it significantly earlier than the ventricular electrogram recorded in the distal coronary sinus (CS). It appears that although the right timing caliper is in line with the onset of QRS, the left caliper is, in fact, in line with the atrial electrogram of the sinus beat (or perhaps a premature atrial beat originating in the high right atrium). The atrial electrograms and the activation sequence in the CS catheter are identical to the preceding sinus beat. Indeed, the ventricular electrograms and the activation sequence in the CS catheter are different. This has occurred because the ventricular electrograms recorded are of the critically timed outflow tract PVC that has occurred almost simultaneously with the atrial beat. I would be most interested to learn whether the authors agree with my interpretation of the electrograms shown in the figure. Bharat K. Kantharia, MD, FRCP, FAHA, FACC, FESC [email protected] University of Texas-Health Science Center at Houston Houston, Texas

Reference 1.

Suleiman M, Asirvatham SJ. Ablation above the semilunar valves: when, why, and how? Part I. Heart Rhythm 2008;5:1485–1492.

To the Editor—Response: We thank Dr. Kantharia for his letter regarding our article on ablation above the semilunar valve.1 We thank him for his general comments and, importantly, for pointing out the need for clarification of the details shown in Figure 3 of our article.

As Dr. Kantharia points out, the electrograms on the ablation catheter that we used to measure the timing in relation to the onset of the surface QRS may well be the onset of an atrial electrogram from either a sinus beat or a right atrial premature beat, and the fact that ablation was successful at this site may not have been related to this measured electrogram. The ventricular electrograms and activation sequence in the coronary sinus for the premature ventricular complexes (PVCs) are, of course, different and reflect the change in activation from the patient’s clinical PVC. The PVC has occurred nearly simultaneously with the atrial beats. Although we completely agree with the possibility that the electrogram being measured is atrial cannot be excluded from the tracing shown in Figure 3, we would like to discuss the following observations and make a few general comments on the difficulties created when mapping PVCs rather than ventricular tachycardia as a result of ongoing atrial activity dissociated from PVCs. 1. Although the atrial activation sequence apposed on the PVC is similar to the atrial activation sequence of the sinus beat, there are some differences. For example, the initial electrogram of note on the ablation distal catheter occurs 12 ms earlier than expected when compared to the onset of the electrogram on the HARA catheter in sinus rhythm and 15 ms earlier than the proximal coronary sinus when compared to the sinus beat. All these changes may be the result of the second atrial sequence being the serendipitous PAC, which suggests that the earliest part of the electrogram may be ventricular in origin. 2. Appreciating and accepting the difficulties with interpreting the morphology of electrograms with bipolar recordings, the near-field nature and notching of the electrogram noted as the early electrogram that we measured are similar to those seen with the ventricular electrogram of the sinus beat. Again, this suggests to us that the ventricular electrogram may have started early along with the atrial electrogram. 3. With continued mapping of subsequent beats of arrhythmia the morphology of the local electrogram was constant. Further the timing of this electrogram with care not to move the ablation distal electrode, was consistently 40 to 50 ms ahead of the onset of the QRS complex. 4. Ablation at this site promptly resulted in termination of the PVCs and subsequently did not recur. We would like to take this opportunity to point out this and other pitfalls with PVC mapping during sinus rhythm.

1547-5271/$ -see front matter © 2009 Published by Elsevier Inc. on behalf of Heart Rhythm Society.

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Heart Rhythm, Vol 6, No 1, January 2009

Figure 1 Intracardiac electrograms showing the difficulties and the potential solutions to discerning atrial and left ventricular electrograms during supravalvar premature ventricular complex (PVC) mapping. A: With a fused PVC and sinus beat, it becomes impossible when viewing sequences in isolation to determine whether the large electrogram seen on the ablation distal electrode, particularly the early deflection, is part of the atrial electrogram or the ventricular electrogram. In this instance, however, regardless of the nature of the electrogram, there is no early activation when compared to the onset of the QRS. B: In this patient, with mapping above the aortic valve in the left coronary cusp, the situation is somewhat easier because few or no atrial electrograms typically are recorded in the left coronary cusp. The earliest sharp deflection is taken and noted to be earlier than the surface QRS by 40 ms. C: The nature of the electrogram often is clarified when more than one PVC occurs in sequence or ventricular tachycardia because the atrial activation times will vary and the true ventricular electrogram can be identified.

1. When performing an activation map either beats where no fusion is occurring or where there is a fixed degree of fusion should only be included. Even a single beat of ventricular arrhythmia with fused AV conduction can completely change the activation sequence in the map and give misleading results. 2. Preferably, only PVCs of a relatively fixed coupling interval should be included.2

3. When trying to distinguish whether a given electrogram is atrial or ventricular (which can be very difficult when fractionated signals are present in the right or noncoronary cusp),3 either observing two consecutive beats of tachycardia or performing the mapping and measurement of activation times during atrial pacing at varying rates may be required (Figure 1).

Figure 2 Recordings obtained from a different patient with supravalvar (pulmonic valve) outflow tract mapping. A: Another feature that can make electrogram identification and mapping easier is the observation of diastolic potentials in sinus rhythm that are clearly different from either the regular ventricular electrogram or the atrial electrogram (arrows). When premature ventricular complexes (PVCs) occur, the timing between the local electrogram and the onset of PVC is constant, suggesting the earliest activity of PVC that exits to the ventricle from above the valve originates at this time. B: Close-up view of mid-diastolic signals and their fixed relationship prior to ventricular and surface ECG activation during the clinical PVCs.

Letters to the Editor

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4. PVC mapping may be easier to perform from the left coronary cusp or anterior right coronary cusp because the atrial electrogram tends to be far-field or is not recorded in these areas (Figure 2). Again, we thank Dr. Kantharia for pointing out the lack of clarity in Figure 3 of the article and appreciate the opportunity to provide a few additional points of explanation. Samuel J. Asirvatham, MD [email protected] Mayo Clinic Rochester, Minnesota

References 1. 2.

3.

Suleiman M, Asirvatham SJ. Ablation above the semilunar valves: when, why, and how? Part I. Heart Rhythm 2008;5:1485–1492. Srivathsan K, Gami AS, Ackerman M, et al. Treatment of ventricular fibrillation in a patient with prior diagnosis of long QT syndrome: importance of precise electrophysiologic diagnosis to successfully ablate the trigger. Heart Rhythm 2007;4:1090 –1093. Gami AS, Venkatachalam KL, Friedman PA, et al. Successful ablation of atrial tachycardia in the right coronary cusp of the aortic valve in a patient with atrial fibrillation: what is the substrate? J Cardiovasc Electrophysiol 2008;19:982– 986.

To the Editor: It appears that the implantable cardioverter-defibrillator (ICD) industry uses electrical measurements, such as lead electrical impedance, to determine that an implanted ICD

Figure 1

lead has failed.1 However, two recent publications in Heart Rhythm report that electrical impedance monitoring has only limited effectiveness in preventing adverse clinical events, specifically inappropriate shocks, resulting from fracture of ICD leads.2,3 This letter supports these findings by pointing out that electrical impedance has been found to be an insensitive measure of the imminent structural failure of an electrical connection. Supporting evidence is the result of constantdeflection mechanical cycling tests (at ⫺55°C, 35°C, and 125°C) of a solder joint by Solomon.4,5 The test setup and the 35°C test data are shown in Figure 1. As the crack grew from under the chip carrier through the fillet, the load required to deflect the joint dropped. The load drop and electrical resistance increase were measured as functions of the number of cycles. The load drop began at the first few cycles, but the resistance began to increase significantly only after the load dropped more than 50%. At 35°C and 125°C, the resistance increased by 0.1% or more only when the load dropped by 60%. At ⫺55°C, a resistance increase was observed only when the load dropped by more than 80%. The explanation is that the crack grows from under the chip carrier through the fillet, and the resistance increase is local and insignificant until the crack penetrates through the fillet. Furthermore, once the resistance increase became observable, the resistance increased rapidly thereafter. For

Constant-deflection mechanical cycling test of a solder joint.4 A: Setup, B: Data. (© IEEE 1989.)