International Journal of Cardiology 190 (2015) 256–259
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Repetitive, incessant supraventricular tachycardia: Noninvasive determination of the electrophysiologic mechanism Laszlo Littmann a,⁎,1, Sherry J. Saxonhouse b a b
Department of Internal Medicine, Carolinas Medical Center, Charlotte, NC, USA Sanger Heart and Vascular Institute, Carolinas Medical Center, Charlotte, NC, USA
a r t i c l e
i n f o
Article history: Received 20 April 2015 Accepted 21 April 2015 Available online 23 April 2015 Keywords: Supraventricular tachycardia Incessant tachycardia Concealed accessory pathway Retrograde preexcitation Bundle branch block Activation mapping
In patients with supraventricular tachycardia (SVT), clinical electrophysiologic studies utilize programmed atrial and ventricular stimulation and electrical activation mapping to decipher the mechanism of the tachycardia. In cases of repetitive SVT, electrocardiographic (ECG) monitoring provides a unique opportunity to noninvasively investigate the effects of spontaneous premature atrial and ventricular complexes (PACs and PVCs) on the initiation and termination of the SVT [1,2]. In addition, analyzing the QRS and P-wave morphologies during ventricular preexcitation and during SVT, respectively, can be viewed as rudimentary forms of electrical activation mapping [3]. The following report describes a patient with repetitive SVT where careful analysis of telemetry recordings led to an accurate diagnosis of the tachycardia mechanism. It also offered a logical explanation for paradoxical responses of the SVT to conventional antiarrhythmic medications. The patient underwent successful catheter ablation. A 58-year-old woman with chronic left bundle branch block (LBBB) was hospitalized for acute respiratory failure. During her hospital course, she had several episodes of SVT. On each occasion, intravenous adenosine transiently terminated the tachycardia but frequently, the SVT quickly returned. The patient was then treated with repeat ⁎ Corresponding author at: Department of Internal Medicine, Carolinas Medical Center, P. O. Box 32861, Charlotte, NC 28232, USA. E-mail address: [email protected] (L. Littmann). 1 This author takes full responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
http://dx.doi.org/10.1016/j.ijcard.2015.04.181 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
intravenous boluses of metoprolol and diltiazem after which the tachycardia became repetitive and almost incessant. When all cardioactive medications were turned off, the SVT paradoxically subsided. Fig. 1 illustrates the 12-lead ECG during sinus rhythm (panel A) and during SVT (panel B). Fig. 2 shows the heart rate trend curves with (panel A) and in the absence of repeat administration of IV metoprolol and diltiazem (panel B). Over a 3-day observation period, more than 30 spontaneous initiations and terminations of the SVT were documented in telemetry. Fig. 3, panels A–D are representative examples of initiation of the SVT. Fig. 3, panels E–H are examples of spontaneous terminations. Based on analysis of the 12-lead ECGs and telemetry recordings, we concluded that the patient had repetitive orthodromic atrioventricular macroreentrant SVT utilizing a concealed left-sided accessory pathway. She underwent an electrophysiologic study which confirmed this ECG diagnosis (Fig. 4). Successful radiofrequency ablation was performed. The following simple observations helped establish the tachycardia mechanism. First, each episode of the SVT was triggered by a PAC with a relatively long P-R interval (Fig. 3, panels A–D). The P-wave morphology during SVT was different from the morphology of the triggering PAC (Fig. 3D). These observations were consistent with a reentrant mechanism [4]. Second, both the administration of adenosine and spontaneous PVCs was able to terminate the tachycardia (Fig. 3, panels E–H). These findings suggested that the tachycardia circuit involved both anterograde and retrograde A-V conduction. Third, spontaneous PVCs that occurred at a time when the His bundle was refractory consistently and markedly preexcited the atria. Note that in Fig. 3H, a PVC that was inscribed about 40 ms before the expected onset of the next QRS complex of the SVT resulted in a P-P interval of 380 ms, 110 ms shorter than the other P-P intervals during the tachycardia. This finding can only be explained by the presence of an accessory pathway capable of retrograde conduction [4,5]. Finally, during SVT the retrograde P waves were negative in the left-sided leads and were upright in lead V1, indicating a left-to-right atrial activation sequence and thus, retrograde conduction over a left free wall accessory pathway (Fig. 1B) [6]. Uncovering the electrophysiologic mechanism of the SVT also helped explain the paradoxical response of the SVT to conventional antiarrhythmic medications. In patients with concealed Wolff–Parkinson– White syndrome two important elements of reentry, namely two conduction pathways and unidirectional block in one of the pathways, are always present. Under these circumstances, initiation and maintenance of reentry depends on a delicate balance between conduction time
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
257
A
B
I
V1
V5
Fig. 1. A: Twelve-lead electrocardiogram (ECG) during sinus rhythm. B: Twelve-lead ECG during supraventricular tachycardia. Note the retrograde P waves that follow the onset of the QRS complexes by about 220 ms. The enlarged inserts demonstrate that the retrograde P waves are negative in the left-sided leads and are upright in V1.
A
06:00
12:00
06:00
12:00
18:00
24:00
B
18:00
24:00
Fig. 2. A: 24-hour heart rate trend curve demonstrates repetitive, incessant supraventricular tachycardia at a time when the patient was receiving repeat intravenous boluses of metoprolol and diltiazem. B: 24-hour heart rate trend curve after all cardioactive medications were discontinued.
258
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
A
E
B
F
C
G
D
H SP
PAC
RP
RP
RP
470
470
380
Fig. 3. A, B and C: Representative episodes of spontaneous initiations of the SVT. D: Enlarged rhythm strip. SP indicates sinus P wave; PAC indicates premature atrial complex; and RP indicates retrograde P waves. See text. E, F and G: Representative episodes of spontaneous terminations of the SVT by premature ventricular complexes. H: Enlargement of one of the spontaneous terminations. Arrows point to the retrograde P waves. Numbers indicate the P-P intervals in milliseconds. See text.
RIGHT VENTRICULAR APICAL PACING
SUPRAVENTRICULAR TACHYCARDIA
Fig. 4. Intracardiac recordings during right ventricular apical pacing and during induced SVT demonstrated eccentric retrograde atrial activation. Earliest activation was in the distal coronary sinus (CS) and latest activation was in the high right atrium (HRA). D indicates distal; P indicates proximal. “CS P” was positioned in the ostium of the coronary sinus.
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
within the reentrant loop and refractory periods of the reentrant substrates. With bundle branch block that is ipsilateral to the accessory pathway, such as in our patient who had LBBB and a left-sided accessory pathway, intraventricular conduction during SVT is baseline prolonged [7]. All supraventricular complexes had to go down the right bundle and then cross the intraventricular septum before reaching the left ventricular insertion of the accessory pathway. Any further prolongation in conduction time such as with beta blockers or calcium-channel blockers, or a shortening of atrial refractory period as with intravenous adenosine [8], may actually enhance the initiation or perpetuation of SVT. In the case presented, repeat intravenous boluses of metoprolol and diltiazem resulted in the SVT becoming repetitive and incessant (Fig. 2A). When metoprolol and diltiazem were discontinued, the runs of SVT actually subsided (Fig. 2B). It was also interesting to note that PVCs with a right bundle branch block morphology, probably arising from the left ventricle, were not only associated with much shorter RP intervals than the R-P intervals during SVT, but they also consistently resulted in termination of the tachycardia (Fig. 3, panels E–H). This finding further confirmed that prolonged interventricular conduction associated with LBBB was an important factor in maintaining a relatively slow macroreentrant tachycardia. It has been previously shown that the combination of LBBB and leftsided concealed accessory pathway can result in incessant SVT [9]. In that study, however, invasive electrophysiologic evaluation was required to elucidate the tachycardia mechanism [9]. Our case demonstrates that in patients with repetitive SVT, meticulous analysis of surface ECGs and telemetry recordings can help uncover even relatively complex electrophysiologic phenomena and their therapeutic implications even before definitive diagnosis and cure are achieved with catheter ablation.
259
Conflict of interest statement The authors declare no conflicts of interest or financial disclosures. Acknowledgment The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.
References [1] L. Littmann, J.J. Gallagher, Incessant supraventricular tachycardia due to a right free wall concealed accessory pathway: electrocardiographic diagnosis and clinical implications, J. Noninvas. Cardiol. 2 (1998) 27–30. [2] L. Littmann, The power of PACs, J. Electrocardiol. 33 (2000) 287–290. [3] S.J. Asirvatham, W.G. Stevenson, Electrocardiogram mapping — reentry: final frontier? Circ. Arrhythm. Electrophysiol. 7 (2014) 760–761. [4] M.E. Josephson, J.A. Kastor, Supraventricular tachycardia: mechanisms and management, Ann. Intern. Med. 87 (1977) 346–358. [5] W.M. Miles, R. Yee, G.J. Klein, D.P. Zipes, E.N. Prystowsky, The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways, Circulation 74 (1986) 493–500. [6] R. Garcia Civera, J.A. Ferrero, R. Sanjuan, L. Insa, M. Rodriguez, J. Segui, V. Lopez Merino, J. Llavador, Retrograde P wave polarity in reciprocating tachycardia utilizing lateral bypass tracts, Eur. Heart J. 1 (1980) 137–145. [7] C.R. Kerr, J.J. Gallagher, L.D. German, Changes in ventriculoatrial intervals with bundle branch block aberration during reciprocating tachycardia in patients with accessory atrioventricular pathways, Circulation 66 (1982) 196–201. [8] G. Kabell, L.V. Buchanan, J.K. Gibson, L. Belardinelli, Effects of adenosine on atrial refractoriness and arrhythmias, Cardiovasc. Res. 28 (1994) 1385–1389. [9] A. Stanke, C. Storti, R. De Ponti, J.A. Salerno-Uriarte, Spontaneous incessant AV reentrant tachycardia related to left bundle branch block and concealed left-sided accessory AV pathway, J. Cardiovasc. Electrophysiol. 5 (1994) 777–781.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Repetitive, incessant supraventricular tachycardia: Noninvasive determination of the electrophysiologic mechanism Laszlo Littmann a,⁎,1, Sherry J. Saxonhouse b a b
Department of Internal Medicine, Carolinas Medical Center, Charlotte, NC, USA Sanger Heart and Vascular Institute, Carolinas Medical Center, Charlotte, NC, USA
a r t i c l e
i n f o
Article history: Received 20 April 2015 Accepted 21 April 2015 Available online 23 April 2015 Keywords: Supraventricular tachycardia Incessant tachycardia Concealed accessory pathway Retrograde preexcitation Bundle branch block Activation mapping
In patients with supraventricular tachycardia (SVT), clinical electrophysiologic studies utilize programmed atrial and ventricular stimulation and electrical activation mapping to decipher the mechanism of the tachycardia. In cases of repetitive SVT, electrocardiographic (ECG) monitoring provides a unique opportunity to noninvasively investigate the effects of spontaneous premature atrial and ventricular complexes (PACs and PVCs) on the initiation and termination of the SVT [1,2]. In addition, analyzing the QRS and P-wave morphologies during ventricular preexcitation and during SVT, respectively, can be viewed as rudimentary forms of electrical activation mapping [3]. The following report describes a patient with repetitive SVT where careful analysis of telemetry recordings led to an accurate diagnosis of the tachycardia mechanism. It also offered a logical explanation for paradoxical responses of the SVT to conventional antiarrhythmic medications. The patient underwent successful catheter ablation. A 58-year-old woman with chronic left bundle branch block (LBBB) was hospitalized for acute respiratory failure. During her hospital course, she had several episodes of SVT. On each occasion, intravenous adenosine transiently terminated the tachycardia but frequently, the SVT quickly returned. The patient was then treated with repeat ⁎ Corresponding author at: Department of Internal Medicine, Carolinas Medical Center, P. O. Box 32861, Charlotte, NC 28232, USA. E-mail address: [email protected] (L. Littmann). 1 This author takes full responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
http://dx.doi.org/10.1016/j.ijcard.2015.04.181 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
intravenous boluses of metoprolol and diltiazem after which the tachycardia became repetitive and almost incessant. When all cardioactive medications were turned off, the SVT paradoxically subsided. Fig. 1 illustrates the 12-lead ECG during sinus rhythm (panel A) and during SVT (panel B). Fig. 2 shows the heart rate trend curves with (panel A) and in the absence of repeat administration of IV metoprolol and diltiazem (panel B). Over a 3-day observation period, more than 30 spontaneous initiations and terminations of the SVT were documented in telemetry. Fig. 3, panels A–D are representative examples of initiation of the SVT. Fig. 3, panels E–H are examples of spontaneous terminations. Based on analysis of the 12-lead ECGs and telemetry recordings, we concluded that the patient had repetitive orthodromic atrioventricular macroreentrant SVT utilizing a concealed left-sided accessory pathway. She underwent an electrophysiologic study which confirmed this ECG diagnosis (Fig. 4). Successful radiofrequency ablation was performed. The following simple observations helped establish the tachycardia mechanism. First, each episode of the SVT was triggered by a PAC with a relatively long P-R interval (Fig. 3, panels A–D). The P-wave morphology during SVT was different from the morphology of the triggering PAC (Fig. 3D). These observations were consistent with a reentrant mechanism [4]. Second, both the administration of adenosine and spontaneous PVCs was able to terminate the tachycardia (Fig. 3, panels E–H). These findings suggested that the tachycardia circuit involved both anterograde and retrograde A-V conduction. Third, spontaneous PVCs that occurred at a time when the His bundle was refractory consistently and markedly preexcited the atria. Note that in Fig. 3H, a PVC that was inscribed about 40 ms before the expected onset of the next QRS complex of the SVT resulted in a P-P interval of 380 ms, 110 ms shorter than the other P-P intervals during the tachycardia. This finding can only be explained by the presence of an accessory pathway capable of retrograde conduction [4,5]. Finally, during SVT the retrograde P waves were negative in the left-sided leads and were upright in lead V1, indicating a left-to-right atrial activation sequence and thus, retrograde conduction over a left free wall accessory pathway (Fig. 1B) [6]. Uncovering the electrophysiologic mechanism of the SVT also helped explain the paradoxical response of the SVT to conventional antiarrhythmic medications. In patients with concealed Wolff–Parkinson– White syndrome two important elements of reentry, namely two conduction pathways and unidirectional block in one of the pathways, are always present. Under these circumstances, initiation and maintenance of reentry depends on a delicate balance between conduction time
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
257
A
B
I
V1
V5
Fig. 1. A: Twelve-lead electrocardiogram (ECG) during sinus rhythm. B: Twelve-lead ECG during supraventricular tachycardia. Note the retrograde P waves that follow the onset of the QRS complexes by about 220 ms. The enlarged inserts demonstrate that the retrograde P waves are negative in the left-sided leads and are upright in V1.
A
06:00
12:00
06:00
12:00
18:00
24:00
B
18:00
24:00
Fig. 2. A: 24-hour heart rate trend curve demonstrates repetitive, incessant supraventricular tachycardia at a time when the patient was receiving repeat intravenous boluses of metoprolol and diltiazem. B: 24-hour heart rate trend curve after all cardioactive medications were discontinued.
258
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
A
E
B
F
C
G
D
H SP
PAC
RP
RP
RP
470
470
380
Fig. 3. A, B and C: Representative episodes of spontaneous initiations of the SVT. D: Enlarged rhythm strip. SP indicates sinus P wave; PAC indicates premature atrial complex; and RP indicates retrograde P waves. See text. E, F and G: Representative episodes of spontaneous terminations of the SVT by premature ventricular complexes. H: Enlargement of one of the spontaneous terminations. Arrows point to the retrograde P waves. Numbers indicate the P-P intervals in milliseconds. See text.
RIGHT VENTRICULAR APICAL PACING
SUPRAVENTRICULAR TACHYCARDIA
Fig. 4. Intracardiac recordings during right ventricular apical pacing and during induced SVT demonstrated eccentric retrograde atrial activation. Earliest activation was in the distal coronary sinus (CS) and latest activation was in the high right atrium (HRA). D indicates distal; P indicates proximal. “CS P” was positioned in the ostium of the coronary sinus.
L. Littmann, S.J. Saxonhouse / International Journal of Cardiology 190 (2015) 256–259
within the reentrant loop and refractory periods of the reentrant substrates. With bundle branch block that is ipsilateral to the accessory pathway, such as in our patient who had LBBB and a left-sided accessory pathway, intraventricular conduction during SVT is baseline prolonged [7]. All supraventricular complexes had to go down the right bundle and then cross the intraventricular septum before reaching the left ventricular insertion of the accessory pathway. Any further prolongation in conduction time such as with beta blockers or calcium-channel blockers, or a shortening of atrial refractory period as with intravenous adenosine [8], may actually enhance the initiation or perpetuation of SVT. In the case presented, repeat intravenous boluses of metoprolol and diltiazem resulted in the SVT becoming repetitive and incessant (Fig. 2A). When metoprolol and diltiazem were discontinued, the runs of SVT actually subsided (Fig. 2B). It was also interesting to note that PVCs with a right bundle branch block morphology, probably arising from the left ventricle, were not only associated with much shorter RP intervals than the R-P intervals during SVT, but they also consistently resulted in termination of the tachycardia (Fig. 3, panels E–H). This finding further confirmed that prolonged interventricular conduction associated with LBBB was an important factor in maintaining a relatively slow macroreentrant tachycardia. It has been previously shown that the combination of LBBB and leftsided concealed accessory pathway can result in incessant SVT [9]. In that study, however, invasive electrophysiologic evaluation was required to elucidate the tachycardia mechanism [9]. Our case demonstrates that in patients with repetitive SVT, meticulous analysis of surface ECGs and telemetry recordings can help uncover even relatively complex electrophysiologic phenomena and their therapeutic implications even before definitive diagnosis and cure are achieved with catheter ablation.
259
Conflict of interest statement The authors declare no conflicts of interest or financial disclosures. Acknowledgment The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.
References [1] L. Littmann, J.J. Gallagher, Incessant supraventricular tachycardia due to a right free wall concealed accessory pathway: electrocardiographic diagnosis and clinical implications, J. Noninvas. Cardiol. 2 (1998) 27–30. [2] L. Littmann, The power of PACs, J. Electrocardiol. 33 (2000) 287–290. [3] S.J. Asirvatham, W.G. Stevenson, Electrocardiogram mapping — reentry: final frontier? Circ. Arrhythm. Electrophysiol. 7 (2014) 760–761. [4] M.E. Josephson, J.A. Kastor, Supraventricular tachycardia: mechanisms and management, Ann. Intern. Med. 87 (1977) 346–358. [5] W.M. Miles, R. Yee, G.J. Klein, D.P. Zipes, E.N. Prystowsky, The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways, Circulation 74 (1986) 493–500. [6] R. Garcia Civera, J.A. Ferrero, R. Sanjuan, L. Insa, M. Rodriguez, J. Segui, V. Lopez Merino, J. Llavador, Retrograde P wave polarity in reciprocating tachycardia utilizing lateral bypass tracts, Eur. Heart J. 1 (1980) 137–145. [7] C.R. Kerr, J.J. Gallagher, L.D. German, Changes in ventriculoatrial intervals with bundle branch block aberration during reciprocating tachycardia in patients with accessory atrioventricular pathways, Circulation 66 (1982) 196–201. [8] G. Kabell, L.V. Buchanan, J.K. Gibson, L. Belardinelli, Effects of adenosine on atrial refractoriness and arrhythmias, Cardiovasc. Res. 28 (1994) 1385–1389. [9] A. Stanke, C. Storti, R. De Ponti, J.A. Salerno-Uriarte, Spontaneous incessant AV reentrant tachycardia related to left bundle branch block and concealed left-sided accessory AV pathway, J. Cardiovasc. Electrophysiol. 5 (1994) 777–781.
