Clin Res Cardiol (2015) 104:185–188 DOI 10.1007/s00392-014-0761-8
LETTER TO THE EDITORS
Right atrial tachycardia despite silent right atrium: a case report and review of the literature Harilaos Bogossian • Gerrit Frommeyer Bernd Lemke • Markus Zarse
•
Received: 13 June 2014 / Accepted: 8 September 2014 / Published online: 12 September 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Sirs: Atrial standstill (AS) is a rare condition defined by a lack of active atrial contraction caused by an inability of the atrial myocardium to create or perpetuate electrical activity. Drugs (e.g. quinidine or digitalis), electrolyte disorder as well as structural heart diseases (hypertensive heart disease, dilated cardiomyopathy, valvular heart disease and myocarditis) and genetic predispositions may contribute to this condition [1–6]. Obstructive sleep apnea with consecutively increased right atrial pressure, underlying hypertension and paroxysms of atrial fibrillation might be further synergistically interacting contributing factors. According to the reports of Nakazato and Zipes AS seems to be a progressive disease which initially involves the high right atrium (RA) and then progresses towards the lower RA. Just the vicinity of the tricuspid valve, the lower interatrial septum and the region of the ostium of the coronary sinus remain excitable [5, 7]. As the main right atrium is not excitable, patients with AS and symptomatic bradycardia were often treated by implantation of a VVI pacemaker [5]. We present the case of a patient suffering from severe palpitations despite AS.
H. Bogossian (&) B. Lemke M. Zarse Department of Cardiology and Angiology, Klinikum Lu¨denscheid, Ma¨rkische Kliniken GmbH, Paulmannsho¨herstr. 14, 58515 Lu¨denscheid, Germany e-mail: [email protected]; [email protected] H. Bogossian M. Zarse Witten/Herdecke University, Witten, Germany G. Frommeyer Division of Electrophysiology, Department of Cardiovascular Medicine, University of Mu¨nster, Mu¨nster, Germany
We saw a 62-year-old male DDDR pacemaker (PM) patient, implanted due to intermittent AV-Block III° in another hospital. Currently the patient suffered from severe palpitations during his atrial driven tachycardia with a heart rate of 105 bpm with 1:1 ventricular stimulation (cycle length 575 ms) for 8 weeks (Fig. 1a). Coronary heart disease had already been ruled out previously via coronary angiogram. Echocardiographic examination showed an only slightly reduced systolic left ventricular function (EF 48 %) without any major valvular dysfunction. Cardiac risk factors were hypertension, hyperlipidemia and diabetes mellitus. Additionally, the patient suffered from obstructive sleep apnea and paroxysmal atrial fibrillation. To better study tachycardia during the EP Study, PM was programmed from DDDR to VVI 30/min followed by a drop in ventricular rate to 53 bpm due to 2:1 atrioventricular block (Fig. 1c). Figure 2a depicts the catheter positioning with an electrical silent right atrium (RA) along the 20 polar halo catheter which could neither sense nor evoke electrical signals even under high output stimulation (Fig. 2a). Exclusively in the coronary sinus (CS) and directly adjacent areas a remnant strand of vital right atrial myocardium displayed rapid centrifugal activity (Fig. 2b). We performed entrainment stimulation along the coronary sinus electrodes where we achieved similar post-pacing intervals (PPI) at the most proximal pair of electrodes and consecutively longer PPIs while stimulating more distally. Atrial ectopy from the pulmonary veins was excluded after transseptal puncture with a 20-polar Lasso Catheter. A CS anomaly or a CS diverticle was ruled out by CS phlebography. 3-D electroanatomical mapping was employed after pacing manoeuvres including entrainment and post-pacing
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Fig. 1 12 lead ECG during initial atrial tachycardia (a) (CL 557 ms) with consecutively right ventricular unipolar stimulation during DDD mode and after ablation (b) with depiction of the preferred AV sequential intrinsic activation of the QRS. c Atrial tachycardia documented via intracardiac signals from the coronary sinus (CS) catheter with a 2:1 intrinsic ventricular activation seen in the surface ECG after PM settings were changed to VVI 30 mode. d The electroanatomical activation of the micro-reentrant tachycardia within
the right atrium in a slight RAO view by means of the Ensite NaVXÒ (St. Jude Medical) mapping system. The blue depiction of the coronary sinus catheter marks the ostium and proximal portions of the coronary sinus. Different colours annotate the activation sequence with the earliest activation in white and red and the latter activation in green, blue and purple. Brown dots delineate the ablation from earliest activation down to the tricuspid valve
intervals were measured to closer define the area of interest (Fig. 1d). At the defined hot spot RF energy was applied. However, solely after adding a line up to an electrically isolated anchor point at the tricuspid-valve circumference tachycardia was terminated, followed by an atrial electrical standstill which required DDDR pacing (Figs. 1d, 2d). Long-AV interval allowed for intrinsic-AV conduction which immediately decreased clinical symptoms (Fig. 1b). The patient was closely followed up in our outpatient clinic for pacemaker patients for 3 years with stable parameters. Echocardiographic-PW parameters demonstrated a restrictive-ventricular filling pattern with a clearly diminished A-wave (E/A = 3.0). Due to the persistent right atrial standstill and the previously described paroxysmal
atrial fibrillation episodes life-long anticoagulation was recommended. Subsequently, the cumulative percentage of ventricular stimulation was around 40 %. However, 18 months after implantation the patient developed completely asymptomatic persistent atrial fibrillation. Therefore, the patient did not wish any further cardioversion or ablation. The pacemaker was programmed to VVIR mode. Atrial electrical standstill in one atrial chamber with the contralateral one demonstrating rather normal electrical activity is quite unusual. In this rare cohort (patients with AS) the combination of AS and tachycardia is even more seldom. Kammeraad et al. [8] described in two children an intraatrial reentrant tachycardia and coexistent AS. Duncan et al. [9] presented a case with focal right atrial tachycardia despite left atrial standstill––after extensive left atrial ablation––
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Fig. 2 An LAO view of 20 polar Halo catheter along the tricuspid valve (a), an 8 polar coronary sinus and the atrial PM lead is positioned adjacent to the coronary sinus ostium with the corresponding surface ECG and intracardiac electrograms during atrial tachycardia (b). Whereas atrial tachycardia can be seen along the coronary sinus catheter representing left atrial electrical activity, the right atrial Halo catheter displayed no electrical signals suggestive of
a silent right atrium (b). c AP view a 20 polar Lasso catheter positioned in the left atrium, an 8 polar catheter in the proximal coronary sinus and the 4 polar ablation catheter anteroseptal of the coronary sinus ostium. d The corresponding surface and intracardiac electrograms depicting termination of the atrial tachycardia during ablation
which terminated after ablation at the site of earliest activation corresponding to the low-right atrial free wall. Although the diastolic atrial contraction activity is disturbed due to the silent atrium it is possible to save the intrinsic conduction to the ventricle with a low position of the atrial lead in implanted-DDD pacemakers. If necessary a 3D Mapping System could help to find the best sensing and pacing site in the right atrium [10]. Caused by the damage progression from the high right atrium to the low and septal right atrium the remaining active myocardium must be expected––similar to our case––in the CS ostium region (Fig. 2c). At this site it is usually possible to capture the atrium but it is also the site where tachycardia can occur.
Conflict of interest
All authors declare no conflict of interest.
References 1. Wolff L, White PD (1929) Auricular standstill during quinidine therapy. Heart 14:295–303 2. White PD (1916) Auricular standstill: an unusual effect of digitalis on the heart, with especial reference to the electrocardiogram. Boston M & S J 175:233–239 3. Surawicz B (1963) Electrolytes and the electrocardiogram. Am J Cardiol 12:656–664 4. Allenthworth DC, Rice GJ, Lowe GW (1969) Persistent atrial standstill in a family with myocardial disease. Am J Med 47:775–784
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188 5. Nakazato Y et al (1995) Clinical and electrophysiological characteristics of atrial standstill PACE 18:1244–1254 6. Schroeter MR, Hasenfuß G, Zabel M et al (2013) Atrial standstill in a patient with progressive severe heart failure. Clin Res Cardiol 102:473–476 7. Zipes DP, Gaum WE, Genetos BC et al (1977) Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia. Circulation 55:253–260 8. Kammeraad J, Ramanna H, Sreeram N (2003) Ablation of atrial reentrant tachycardia in children with silent atrium. Int J Cardiol 89:91–92
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Clin Res Cardiol (2015) 104:185–188 9. Duncan E, Schilling RJ, Earley M (2013) Isolated left atrial standstill identified during catheter ablation. Pacing Clin Electrophysiol 36:120–124 10. Arimoto T, Sukekawa H, Takayama S, Ikeno E, Takeishi Y, Kubota I (2008) Electroanatomical mapping in partial atrial standstill for visualization of atrial viability and a suitable pacing site. Pacing Clin Electrophysiol 31:509–512
LETTER TO THE EDITORS
Right atrial tachycardia despite silent right atrium: a case report and review of the literature Harilaos Bogossian • Gerrit Frommeyer Bernd Lemke • Markus Zarse
•
Received: 13 June 2014 / Accepted: 8 September 2014 / Published online: 12 September 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Sirs: Atrial standstill (AS) is a rare condition defined by a lack of active atrial contraction caused by an inability of the atrial myocardium to create or perpetuate electrical activity. Drugs (e.g. quinidine or digitalis), electrolyte disorder as well as structural heart diseases (hypertensive heart disease, dilated cardiomyopathy, valvular heart disease and myocarditis) and genetic predispositions may contribute to this condition [1–6]. Obstructive sleep apnea with consecutively increased right atrial pressure, underlying hypertension and paroxysms of atrial fibrillation might be further synergistically interacting contributing factors. According to the reports of Nakazato and Zipes AS seems to be a progressive disease which initially involves the high right atrium (RA) and then progresses towards the lower RA. Just the vicinity of the tricuspid valve, the lower interatrial septum and the region of the ostium of the coronary sinus remain excitable [5, 7]. As the main right atrium is not excitable, patients with AS and symptomatic bradycardia were often treated by implantation of a VVI pacemaker [5]. We present the case of a patient suffering from severe palpitations despite AS.
H. Bogossian (&) B. Lemke M. Zarse Department of Cardiology and Angiology, Klinikum Lu¨denscheid, Ma¨rkische Kliniken GmbH, Paulmannsho¨herstr. 14, 58515 Lu¨denscheid, Germany e-mail: [email protected]; [email protected] H. Bogossian M. Zarse Witten/Herdecke University, Witten, Germany G. Frommeyer Division of Electrophysiology, Department of Cardiovascular Medicine, University of Mu¨nster, Mu¨nster, Germany
We saw a 62-year-old male DDDR pacemaker (PM) patient, implanted due to intermittent AV-Block III° in another hospital. Currently the patient suffered from severe palpitations during his atrial driven tachycardia with a heart rate of 105 bpm with 1:1 ventricular stimulation (cycle length 575 ms) for 8 weeks (Fig. 1a). Coronary heart disease had already been ruled out previously via coronary angiogram. Echocardiographic examination showed an only slightly reduced systolic left ventricular function (EF 48 %) without any major valvular dysfunction. Cardiac risk factors were hypertension, hyperlipidemia and diabetes mellitus. Additionally, the patient suffered from obstructive sleep apnea and paroxysmal atrial fibrillation. To better study tachycardia during the EP Study, PM was programmed from DDDR to VVI 30/min followed by a drop in ventricular rate to 53 bpm due to 2:1 atrioventricular block (Fig. 1c). Figure 2a depicts the catheter positioning with an electrical silent right atrium (RA) along the 20 polar halo catheter which could neither sense nor evoke electrical signals even under high output stimulation (Fig. 2a). Exclusively in the coronary sinus (CS) and directly adjacent areas a remnant strand of vital right atrial myocardium displayed rapid centrifugal activity (Fig. 2b). We performed entrainment stimulation along the coronary sinus electrodes where we achieved similar post-pacing intervals (PPI) at the most proximal pair of electrodes and consecutively longer PPIs while stimulating more distally. Atrial ectopy from the pulmonary veins was excluded after transseptal puncture with a 20-polar Lasso Catheter. A CS anomaly or a CS diverticle was ruled out by CS phlebography. 3-D electroanatomical mapping was employed after pacing manoeuvres including entrainment and post-pacing
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Clin Res Cardiol (2015) 104:185–188
Fig. 1 12 lead ECG during initial atrial tachycardia (a) (CL 557 ms) with consecutively right ventricular unipolar stimulation during DDD mode and after ablation (b) with depiction of the preferred AV sequential intrinsic activation of the QRS. c Atrial tachycardia documented via intracardiac signals from the coronary sinus (CS) catheter with a 2:1 intrinsic ventricular activation seen in the surface ECG after PM settings were changed to VVI 30 mode. d The electroanatomical activation of the micro-reentrant tachycardia within
the right atrium in a slight RAO view by means of the Ensite NaVXÒ (St. Jude Medical) mapping system. The blue depiction of the coronary sinus catheter marks the ostium and proximal portions of the coronary sinus. Different colours annotate the activation sequence with the earliest activation in white and red and the latter activation in green, blue and purple. Brown dots delineate the ablation from earliest activation down to the tricuspid valve
intervals were measured to closer define the area of interest (Fig. 1d). At the defined hot spot RF energy was applied. However, solely after adding a line up to an electrically isolated anchor point at the tricuspid-valve circumference tachycardia was terminated, followed by an atrial electrical standstill which required DDDR pacing (Figs. 1d, 2d). Long-AV interval allowed for intrinsic-AV conduction which immediately decreased clinical symptoms (Fig. 1b). The patient was closely followed up in our outpatient clinic for pacemaker patients for 3 years with stable parameters. Echocardiographic-PW parameters demonstrated a restrictive-ventricular filling pattern with a clearly diminished A-wave (E/A = 3.0). Due to the persistent right atrial standstill and the previously described paroxysmal
atrial fibrillation episodes life-long anticoagulation was recommended. Subsequently, the cumulative percentage of ventricular stimulation was around 40 %. However, 18 months after implantation the patient developed completely asymptomatic persistent atrial fibrillation. Therefore, the patient did not wish any further cardioversion or ablation. The pacemaker was programmed to VVIR mode. Atrial electrical standstill in one atrial chamber with the contralateral one demonstrating rather normal electrical activity is quite unusual. In this rare cohort (patients with AS) the combination of AS and tachycardia is even more seldom. Kammeraad et al. [8] described in two children an intraatrial reentrant tachycardia and coexistent AS. Duncan et al. [9] presented a case with focal right atrial tachycardia despite left atrial standstill––after extensive left atrial ablation––
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Fig. 2 An LAO view of 20 polar Halo catheter along the tricuspid valve (a), an 8 polar coronary sinus and the atrial PM lead is positioned adjacent to the coronary sinus ostium with the corresponding surface ECG and intracardiac electrograms during atrial tachycardia (b). Whereas atrial tachycardia can be seen along the coronary sinus catheter representing left atrial electrical activity, the right atrial Halo catheter displayed no electrical signals suggestive of
a silent right atrium (b). c AP view a 20 polar Lasso catheter positioned in the left atrium, an 8 polar catheter in the proximal coronary sinus and the 4 polar ablation catheter anteroseptal of the coronary sinus ostium. d The corresponding surface and intracardiac electrograms depicting termination of the atrial tachycardia during ablation
which terminated after ablation at the site of earliest activation corresponding to the low-right atrial free wall. Although the diastolic atrial contraction activity is disturbed due to the silent atrium it is possible to save the intrinsic conduction to the ventricle with a low position of the atrial lead in implanted-DDD pacemakers. If necessary a 3D Mapping System could help to find the best sensing and pacing site in the right atrium [10]. Caused by the damage progression from the high right atrium to the low and septal right atrium the remaining active myocardium must be expected––similar to our case––in the CS ostium region (Fig. 2c). At this site it is usually possible to capture the atrium but it is also the site where tachycardia can occur.
Conflict of interest
All authors declare no conflict of interest.
References 1. Wolff L, White PD (1929) Auricular standstill during quinidine therapy. Heart 14:295–303 2. White PD (1916) Auricular standstill: an unusual effect of digitalis on the heart, with especial reference to the electrocardiogram. Boston M & S J 175:233–239 3. Surawicz B (1963) Electrolytes and the electrocardiogram. Am J Cardiol 12:656–664 4. Allenthworth DC, Rice GJ, Lowe GW (1969) Persistent atrial standstill in a family with myocardial disease. Am J Med 47:775–784
123
188 5. Nakazato Y et al (1995) Clinical and electrophysiological characteristics of atrial standstill PACE 18:1244–1254 6. Schroeter MR, Hasenfuß G, Zabel M et al (2013) Atrial standstill in a patient with progressive severe heart failure. Clin Res Cardiol 102:473–476 7. Zipes DP, Gaum WE, Genetos BC et al (1977) Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia. Circulation 55:253–260 8. Kammeraad J, Ramanna H, Sreeram N (2003) Ablation of atrial reentrant tachycardia in children with silent atrium. Int J Cardiol 89:91–92
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Clin Res Cardiol (2015) 104:185–188 9. Duncan E, Schilling RJ, Earley M (2013) Isolated left atrial standstill identified during catheter ablation. Pacing Clin Electrophysiol 36:120–124 10. Arimoto T, Sukekawa H, Takayama S, Ikeno E, Takeishi Y, Kubota I (2008) Electroanatomical mapping in partial atrial standstill for visualization of atrial viability and a suitable pacing site. Pacing Clin Electrophysiol 31:509–512
