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 Table of Contents  
Year : 2021  |  Volume : 5  |  Issue : 3  |  Page : 86-89

Mid cristal atrial tachycardia and ivabradine: A Case Report

Department of Cardiology, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India

Date of Submission04-Jun-2021
Date of Acceptance03-Sep-2021
Date of Web Publication29-Sep-2021

Correspondence Address:
Dr. Debasish Das
Department of Cardiology, All India Institute of Medical Sciences, Bhubaneswar - 751 019, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/hm.hm_35_21

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We present an extreme rare case of cristal atrial tachycardia (AT) in a 23-year-old male presenting with recurrent refractory palpitation since last 1 year treated with betablocker metoprolol 50 mg twice daily. We subjected the patient for electrophysiologic study and radiofrequency ablation and A wave in the mid cristal region preceded the surface P-wave by 16 ms. Ablation here terminated the tachycardia but interestingly patient turned up with recurrent palpitation after 1 month. In view of mid cristal AT, we treated the patient with Ivabradine 5 mg twice daily after which the patient was asymptomatic in follow up. Our case is a unique demonstration of sinus node funny current inhibitor Ivabradine being effective to relieve symptoms even in failed cases of radiofrequency ablation with partial modification of mid cristal region in a case of recurrent mid cristal AT. Our take home message from this electrophysiology experience is that even in cases with partial modification of crista terminalis or failed radiofrequency ablation of Cristal atrial tachycardia Ivabradine can serve as an alternative before proceeding to 3D ablation.

Keywords: Atrial, cristal, ivabradine, tachycardia

How to cite this article:
Das D, Acharya D, Das T, Pramanik S. Mid cristal atrial tachycardia and ivabradine: A Case Report. Heart Mind 2021;5:86-9

How to cite this URL:
Das D, Acharya D, Das T, Pramanik S. Mid cristal atrial tachycardia and ivabradine: A Case Report. Heart Mind [serial online] 2021 [cited 2023 Mar 27];5:86-9. Available from: http://www.heartmindjournal.org/text.asp?2021/5/3/86/326965

  Introduction Top

Right atrial tachycardias occurring in patients without structural heart disease tend to cluster around certain anatomic sites. Approximately two thirds of these tachycardias are distributed along the long axis of the crista terminalis (CT), with an apparent gradation in frequency from superior to inferior. The CT is an area of marked anisotropy due to poor transverse cell to cell coupling.[1],[2],[3],[4] Such anisotropy, by creating a region of slow conduction, favors the development of microre-entry. In addition, the normal sinus pacemaker complex is distributed along the long axis of the CT. The presence of automatic tissue together with relative cellular uncoupling may be a requirement for abnormal automaticity. Our case is unique to demonstrate the fact that cristal atrial tachycardia (AT) even after failed radiofrequency ablation with partial modification of mid cristal region is responsive to ivabradine and it completely ameliorates the patient's symptoms due to the presence of sparingly distributed sinus complex cells along the long axis of CT.

  Case Report Top

A 23-year-old male with structurally normal heart without conventional risk factors presented to the cardiology outpatient department (OPD) with recurrent and refractory palpitation since last 1 year on metoprolol 50 mg twice daily. He narrated a gradual acceleration (warm up) and gradual deceleration (cool down) of the tachycardia suggestive of atrial tachycardia not related to exertion, spontaneous in onset, and self-terminating; also, being nonresponsive to Valsalva maneuver. He had no history of angina, presyncope, or syncope in the past. He was a college-going graduate, belonged to low socioeconomic status with no habituation to tea or coffee without any addiction to alcohol or smoking in the past. He had no history of episodes of anxiety neurosis or depression in the past. He revealed no history of such episodes in any of the family members, there was no history of familial coronary artery disease or premature death in the past. She had heart rate of 120 beats/min with blood pressure of 130/80 mm Hg in the right arm supine position. Cardiovascular system examination was within the normal limit without the presence of any organic murmur or added sound. Baseline electrocardiography (ECG) [Figure 1] revealed heart rate of 120 beats/min with negative P-wave in V1 suggestive of right atrium (RA) origin and positive P-wave in II, III, avF suggestive of superior part of RA or cristal in origin. His echocardiography revealed structurally normal heart with normal biventricular systolic function. His serum chemistry, including complete blood count, blood sugar, lipid, thyroid, and renal profile, was within the normal limit. His viral markers were negative and he was COVID-19 negative also. We subjected the patient for electrophysiologic study and radiofrequency ablation with the aid from state government health scheme due to financial constraints and low socioeconomic status. Antegrade programmed extrastimulus protocol induced the tachycardia [Figure 2], mapping revealed earliest A during the tachycardia to be in RA. We put a decapolar halo catheter in RA to localize the area of earliest activation which was found in the mid cristal region [Figure 3], a diagnosis of mid cristal atrial tachycardia was made, precise mapping with the ablation catheter revealed earliest A here preceded the surface P-wave by 16 ms [Figure 4], ablation here terminated the tachycardia [Figure 5]. Consolidation burn of 120 ms was delivered around here. The patient was discharged next day with Aspirin 75 mg once daily after food for 6 weeks and to follow-up in OPD after 1 month. Persistent atrial tachycardia in the young leads to progressive detoriation of left ventricular systolic function, development of tachycardiomyopathy with poor outcome; therefore, an early radiofrequency ablation is always warranted. The patient during follow-up presented with a history of palpitation albeit less frequent, less distressing, and less sustained than previous but he was quite symptomatic. In view of Cristal AT just below the sinus node which contains sparingly distributed sinus complex cells, the patient was treated with Ivabradine 5 mg twice daily, patient at review after 3 months in the OPD revealed no recurrence of palpitation, ECG was within normal limit and extended Holter for 7 days revealed no recurrence of atrial tachycardia. The patient was quite happy as he was quite asymptomatic. He was well tolerating and quite adherent to the drug as it made him quite asymptomatic. He had no adverse event with ivabradine in the form of profound bradycardia or blurring of vision. Our take home message from this electrophysiology experience is that even in cases with partial modification of CT or failed radiofrequency ablation of critsal atrial tachycardia ivabradine can serve as an alternative before proceeding to three-dimensional ablation.
Figure 1: Cristal atrial tachycardia

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Figure 2: Atrial tachycardia induced during antegrade pacing protocol

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Figure 3: Ablation catheter in the mid cristal region and Halo catheter in right atrium

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Figure 4: Signal in the ablation catheter preceding surface P-wave by 16 ms

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Figure 5: Termination of atrial tachycardia after ablation in mid cristal region

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  Discussion Top

Focal AT demonstrates a characteristic anatomical distribution and does not occur randomly throughout the atria. In published series, the RA is the most common location for foci, accounting for approximately 75%. Within the RA, they are most commonly observed along the CT (approximately 33%), particularly in the superior and mid-CT. Other common sites include the tricuspid annulus, the coronary sinus (CS) ostium and within the CS, the perinodal (parahisian) region and septum, and from within the right atrial appendage. In the left atrium the majority of foci originate from the pulmonary veins, the mitral annulus, left atrial appendage and left septum being less common. Banavalikar et al.[5] described Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites; strikingly our case of mid cristal AT postfailed radiofrequency ablation well responded to Ivabradine. Efficacy and safety of ivabradine was tested in 18 consecutive symptomatic patients (age 45 ± 15 years) with symptomatic inappropriate sinus tachycardia IST); 16 completed the study. There was a significant reduction of median and maximal heart rates over 6 months with small changes in minimal heart rate. There was improvement in exercise tolerance. The drug was well tolerated except for phosphene toxicity in a small number. Ivabradine, however, may precipitate bradycardia, especially in combination with beta-blockers or calcium channel antagonists and cause headaches. It should not be used with strong CYP 3A4 inhibitors or in patients with liver or severe renal dysfunction and should be avoided in patients who are hypotensive, pregnant, or breastfeeding, a substantial concern in the IST patient.[6] There is a paucity of literature report of cristal AT being sensitive to ivabradine; due to distribution of sinus complex cells along CT these form of atrial tachycardias may respond to Ivabradine along with automaticity inhibitor Metoprolol. Wellresponsiveness of Ivabradine to paroxysmal junctional reciprocating tachycardia has been well described in childhood.[7] Our case is unique and first to describe the possible role of ivabradine in Cristal ATs, the sinus complex cells carrying the funny Na + current are sparsely distributed along CT making those tachycardias ivabradine sensitive. Kalman et al.[8] described 33% of cristal AT originated from mid cristal region, i.e., they encountered six cases of mid Cristal AT out of 18 cases of atrial tachycardia and they successfully treated with radiofrequency ablation. Ivabradine has also been found to be effective in controlling the heart rate, termination of tachycardia as well as maintenance of sinus rhythm in patients with incessant atrial tachycardia.[9],[10],[11] Role of Ivabradine in controlling the heart rate in atrial fibrillation due to the fact that the if current, which is affected by ivabradine, was found to be present in the pulmonary vein myocardial sleeves, the well-recognised triggers for AF.[12] Moubarak et al. reported adequate control of heart rate (by 24-h ECG monitoring) in a patient with permanent AF and an ejection fraction of 35% who was receiving ivabradine for heart failure and no concomitant rate-lowering drugs.[13] The role of ivabradine in postural orthostatic tachycardia syndrome (POTS) has also been described; in a retrospective case series that included 22 patients, 60% of patients treated with ivabradine reported symptomatic improvement in POTS.[14] Our case is an extended indication and possible role of ivabradine in most common form of atrial tachycardia i.e., cristal AT.

  Conclusion Top

Our case is a unique demonstration of possible role of ivabradine in Cristal AT. Sparingly distribution of sinus complex cells in the cristal region in a graded manner from the superior to inferior aspect may be a plausible explanation of those cristal ATs being sensitive to ivabradine. Ivabradine was able to ameliorate symptoms in the aforesaid case of ablation failure with partial modification of mid cristal region.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Saffitz JE, Kanter HL, Green KG, Tolley TK, Beyer EC. Tissue-specificdeterminants of anisotropic conduction velocity in canine atrial and ventricular myocardium. Circ Res 1994;74:1065-70.  Back to cited text no. 1
Boineau JP, Canavan TE, Schuessler RB, Cain ME, Corr PB, Cox JL. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation 1988;77:1221-37.  Back to cited text no. 2
de Bakker JM, Hauer RN, Bakker PF, Becker AE, Janse MJ, Robles de Medina EO. Abnormal automaticity as mechanism of atrial tachycardia in the human heart – Electrophysiologic and histologic correlation: A case report. J Cardiovasc Electrophysiol 1994;5:335-44.  Back to cited text no. 3
Joyner R, Van Capelle F. Propagation through electrically coupled cells: How a small SA node drives a large atrium. Biophys J 1996;50:1157-64.  Back to cited text no. 4
Banavalikar B, Shenthar J, Padmanabhan D, Valappil SP, Singha SI, Kottayan A, et al. Clinical and electrophysiological correlates of incessant ivabradine-sensitive atrial tachycardia. Circ Arrhythm Electrophysiol 2019;12:e007387.  Back to cited text no. 5
Rubenstein JC, Freher M, Kadish A, Goldberger JJ. Diurnal heart rate patterns in inappropriate sinus tachycardia. Pacing Clin Electrophysiol 2010;33:911-9.  Back to cited text no. 6
Michel H, Heißenhuber F, Wellmann S, Melter M, Gerling S. Ectopic atrial tachycardia in a 12-month-old girl treated with ivabradine and beta-blocker, a case report. Front Pediatr 2020;8:313.  Back to cited text no. 7
Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. “Cristal tachycardias”: Origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998;31:451-9.  Back to cited text no. 8
Meles E, Carbone C, Maggiolini S, Moretti P, DE Carlini CC, Gentile G, et al. A case of atrial tachycardia treated with ivabradine as bridge to ablation. J Cardiovasc Electrophysiol 2015;26:565-8.  Back to cited text no. 9
AlMusaad A, Shaaban S, Alshuhri S, Mukhtar A. Ivabradine maintains sinus rhythm and reverses atrial tachycardia-induced cardiomyopathy. Eur Heart J Suppl 2014;16 Suppl B: B84-8.  Back to cited text no. 10
Bohora S, Lokhandwala Y, Parekh P, Vasavda A. Reversal of tachycardiomyopathy due to left atrial tachycardia by ivabradine. J Cardiovasc Electrophysiol 2011;22:340-2.  Back to cited text no. 11
Hoppe UC, Beuckelmann DJ. Characterization of the hyperpolarization-activated inward current in isolated human atrial myocytes. Cardiovasc Res 1998;38:788-801.  Back to cited text no. 12
Moubarak G, Logeart D, Cazeau S, Cohen Solal A. Might ivabradine be useful in permanent atrial fibrillation? Int J Cardiol 2014;175:187-8.  Back to cited text no. 13
McDonald C, Frith J, Newton JL. Single centre experience of ivabradine in postural orthostatic tachycardia syndrome. Europace 2011;13:427-30.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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