• Users Online: 323
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 11  |  Issue : 2  |  Page : 56-59

Moderator band calcification masquerading infrahisian conduction system disease


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

Date of Submission12-Sep-2021
Date of Decision06-Apr-2022
Date of Acceptance25-May-2022
Date of Web Publication24-Jun-2022

Correspondence Address:
DM Cardiology Debasish Das
Department of Cardiology, All India Institute of Medical Sciences, Bhubaneswar - 751 019, Odisha
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcpc.jcpc_48_21

Rights and Permissions
  Abstract 

Relationship between moderator band (MB) calcification and infrahisian conduction system disease has not been described in the world literature so far. We report a case of a 74-year old male presenting with recurrent cardiogenic syncope 6 times is the last 2 months.He had echocardiographic evidence of dense moderator band calcification.Electrophysiology study revealed a His-Ventricular(HV) interval of 100 msec suggestive of significant infrahisian conduction system disease.He was put on a dual chamber pacemaker and he had no further episode of syncope during the follow up. Our description is unique and the first in the world literature that dense MB calcification in echocardiography may be an indirect clue to the presence of severe infrahisian conduction system disease.

Keywords: Band, calcification, conduction, disease, infrahisian, moderator, system


How to cite this article:
Das D, Das T, Pramanik S, Bannerjee A, Kumar A. Moderator band calcification masquerading infrahisian conduction system disease. J Clin Prev Cardiol 2022;11:56-9

How to cite this URL:
Das D, Das T, Pramanik S, Bannerjee A, Kumar A. Moderator band calcification masquerading infrahisian conduction system disease. J Clin Prev Cardiol [serial online] 2022 [cited 2022 Dec 6];11:56-9. Available from: https://www.jcpconline.org/text.asp?2022/11/2/56/348082


  Introduction Top


The moderator band (MB, also known as septomarginal trabecular[1]) is a band of cardiac muscle found in the right ventricle (RV) of the heart.[2],[3] It was first described by Leonardo da Vinci in his exploration of human anatomy. From its attachments, it was thought to prevent overdistension of the ventricle and was named the “moderator band.” It is well marked in sheep and some other animals. The MB connects the base of the anterior papillary muscles (APMs) to the ventricular septum. The MB is important because it carries part of the right bundle branch of the atrioventricular bundle of the conduction system of the heart to the APM.[1] This shortcut across the chamber of the ventricle ensures equal conduction time in the left ventricle and RV, allowing for coordinated contraction of the APM.[1] The MB is often used by radiologists and obstetricians to more easily identify the RV in prenatal ultrasound. Age-related sclerodegenerative calcification of the MB interferes with conduction across the right bundle and manifests as right bundle branch block. Although the presence of right bundle branch block presents a normal phenomenon in the elderly, the presence of bifascicular block with dense calcification of the MB may serve an indirect evidence to the presence of severe infrahisian conduction system disease as noted in our case in a 74-year-old male presenting with recurrent cardiogenic syncope, and electrophysiologic (EP) study revealed to be having severe infrahisian conduction system disease with His-ventricular (HV) interval of 101 ms with need of permanent pacing. Normal HV interval is 35–55 ms whereas HV interval more than 55 ms is known be harboring infrahisian conduction system disease, HV interval more than 70 ms with symptoms in the form of presyncope or syncope mandates pacing, and HV interval more than 100 ms warrants pacemaker implantation even in asymptomatic individuals. We implanted a dual-chamber pacemaker in the patient with no recurrence of syncope in the following 1-month postpacemaker implantation. Echocardiographic evidence of dense MB calcification may be an indirect clue to the presence of infrahisian conduction system disease, and symptomatic patients should undergo EP study always to delineate the severity of infrahisian conduction system disease and the need of permanent pacing to prevent the episode of further syncope.


  Case Report Top


A 74-year-old male presented with six episodes of cardiac syncope abrupt in onset with immediate recovery in the last 2 months, without any history of postural drop, jerky movement of limbs, uprolling of eye balls, involuntary micturition, or defecation or postepisode amnesia. He was nonsmoker, nondiabetic, nonhypertensive, and nondyslipidemic also. During presentation, he had blood pressure of 136/80 mmHg in the right arm supine position with heart rate of 95 beats per minute, with cardiovascular system and respiratory system being within normal limit. He was initially evaluated in the neurology department for recurrent syncope, and he had no focal neurological deficit and no gait instability, electrocardiography (EEG) was within normal limit, bilateral carotid Doppler was within normal limit without any obstructive atherosclerotic plaque, and computed tomography scan brain was also within normal limit and was sent for evaluation in cardiology. On clinical examination, his cardiac auscultation was within normal limit with no evidence of postural drop in blood pressure or carotid bruit. ECG revealed the presence of bifascicular block [Figure 1] in the form of right bundle branch block with the left posterior hemiblock with QRS width of 160 ms. Echocardiography revealed dense MB calcification [Figure 2] with the presence of left ventricular anteromedial papillary muscle calcification [Figure 3]. 24-h Holter analysis was within normal limit without any presence of intermittent complete heart block (CHB) or pause more than 3 s. In view of recurrent history of typical cardiogenic syncope, he was planned for EP study that revealed HV interval of 101 ms [Figure 4], suggestive of severe infrahisian conduction system disease with normal AH interval of 53 ms. In view of significant infrahisian conduction system disease with HV interval of 101 ms which stands as a Class I indication of pacing, we implanted dual-chamber pacemaker in the patient. As a routine, during HV study, we did the coronary angiogram that revealed the presence of normal coronaries. We routinely rule out the presence of severe coronary artery disease before pacing in elderly cohorts as patients with triple-vessel disease undergo epicardial pacing along with coronary artery bypass graft in the same set-up precluding prior conventional pacemaker implantation. The patient was followed up in the cardiology outpatient department after 1 and 3 months. He did not reveal any further history of syncope or presyncope. Follow-up left ventricular ejection fraction was within normal limit, there was no lead-induced tricuspid regurgitation, and he was quite asymptomatic. As we normally proceed for midseptal pacing, QRS was relatively narrow [Figure 5]. Pacing thresholds were also absolutely normal (<1 mV) in all those follow-ups.
Figure 1: ECG showing bifascicular block with QRS d of 160 m

Click here to view
Figure 2: Apical four-chamber view showing dense moderator band calcification. The yellow arrow indictates dense chunk of calcification inside the moderator band

Click here to view
Figure 3: Apical four-chamber view showing the presence of moderator band calcification along with anteromedial papillary muscle calcification. The yellow arrow indictates dense chunk of calcification inside the moderator band

Click here to view
Figure 4: Electrophysiology study revealing HV interval of 101 ms suggestive of significant infrahisian conduction system disease, HV: His-ventricular

Click here to view
Figure 5: Postpacing ECG with relatively narrow QRS suggestive of reduction in HV interval. HV: His-ventricular

Click here to view



  Discussion Top


MB or septomarginal trabecula is a band of cardiac muscle that connects the distal interventricular septum to the base of the APM in the RV. MB carries the fibers of right bundle as a part of conduction system and MB calcification occurs as a part of sclerodegenerative process of aging; calcification of the MB interferes with the normal conduction across right bundle and manifests as right bundle branch block in the ECG. Our case is a unique description of the fact that MB calcification can be an indirect evidence of severe infrahisian conduction system disease with an HV interval of 101 ms as noted in the EP study. Lee and Hur[4] classified MB into the following three types: cylindrical column, long and thin column, and wide and flat column where they described as type 2 and 3 to be more common. MB in our case was of type 3 which is the most common type with extensive calcification.

The function of the MB is to contract the APM to prevent tricuspid regurgitation through tension of the chordae tendineae, but its role as an indirect evidence to the presence of severe infrahisian conduction system disease has not been described so far in the world literature. When the MB is abnormally thick or enlarged, it might block the flow to the pulmonary trunk, and this could be the reason for a double-chamber RV or an apical ventricular septal defect.[5],[6],[7],[8] Therefore, if the MB is removed during the surgical repair of an apical ventricular septal defect, this could adversely affect the contraction of APM or the normal role of the chordae tendineae inserted into the anterior tricuspid valve leaflet causing severe tricuspid regurgitation. The RV MB is a source for Purkinje-mediated arrhythmias.[9] Premature ventricular contractions (PVCs) and ventricular tachycardia (VT) from the MB have typical morphological features with a left bundle branch block pattern and a left superior axis with positive QRS in leads I and aVL. The RV MB is a source of idiopathic ventricular fibrillation (VF) triggered by PVCs that is potentially treated with catheter ablation. PVCs from the MB presenting with syncope or presyncope needs radiofrequency catheter ablation as MB is arrhythmogenic and PVC triggers Purkinje-mediated VF and syncope.[10] Interestingly, our patient had also associated left anteromedial papillary muscle calcification which occurs in coronary artery disease, dilated cardiomyopathy, mitral valve disease, hypercalcemia, and increased calcium phosphate product in end-stage renal disease. Paradoxically, in spite of the presence of papillary muscle calcification, the patient had normal coronaries with normal left ventricular systolic function, mitral annular calcification (MAC) was not evident in echocardiography, and the patient had no imbalance in calcium phosphate ratio due to nephropathy as renal profile was normal.[11] Dense MB calcification associated with significant infrahisian conduction system disease has not been described in literature so far although arrhythmogenic substrate of the MB has been well described. Our case may be a case of senile cardiac calcification syndrome as described by Kim et al.[12] which present as extensive calcification of the left ventricular papillary muscle. The patient in this senile cardiac calcification syndrome had paradoxically no MAC or aortic valve calcification. These cohorts of patients had calcific coronary artery without obstructive coronary artery disease. Massive calcification of tricuspid valve papillary muscle has been described in endomyocardial fibrosis along with the calcification of the MB.[13] This form of idiopathic calcification of the muscles of the heart as noted in our patient is otherwise known as idiopathic cardiac osseous metaplasia which is neither dystrophic nor metastatic calcification as described by Avila-Vanzzini et al.[14] Role of MB is well described in double chambered right ventricle and its proarrythmic role in moderator band VT is well described.Our case is unique and first to describe dense moderator band calcification as an indirect evidence of significant infrahisian conduction system disease warranting pacemaker implantation. Like papillary muscle calcification points at common association of calcific coronary artery disease, MB calcification may indirectly give a clue to the presence of infrahisian conduction system disease, and symptomatic patients need an EP study for further stratification of infrahisian conduction system disease to delineate the need for a pacemaker.


  Conclusion Top


Although the role of moderator band in double chambered right ventricle and moderator band VT have been well described,dense moderator band calcification providing an indirect evidence towards significant infrahisian conduction system disease has not been described in the literature so far. Our case is unique and the first to demonstrate the role of MB behind bradyarrhythmia and syncope as dense MB calcification may be indirect evidence to the presence of significant infrahisian conduction system disease. Symptomatic patients in the form of syncope or presyncope with MB calcification in echocardiography must undergo an EP study to delineate the extent of infrahisian conduction system disease and the subsequent need of cardiac pacing.

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

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Whitaker RH. Anatomy of the heart. Medicine 2014;42:406-8.  Back to cited text no. 1
    
2.
Rocha H, Eliziario LF, Wafae GC, Silva NC, Ruiz CR, Wafae N. Anatomy of the septomarginal trabecula in Landrace pig hearts. Morphologie 2010;94:26-9.  Back to cited text no. 2
    
3.
Kosinski A, Nowinski J, Kozłowski D, Piwko G, Kuta W, Grzybiak M. The crista supraventricularis in the human heart and its role in the morphogenesis of the septomarginal trabecula. Ann Anat 2007;189:447-56.  Back to cited text no. 3
    
4.
Lee JY, Hur MS. Morphological classification of the moderator band and its relationship with the anterior papillary muscle. Anat Cell Biol 2019;52:38-42.  Back to cited text no. 4
    
5.
Alva C, Ho SY, Lincoln CR, Rigby ML, Wright A, Anderson RH. The nature of the obstructive muscular bundles in double-chambered right ventricle. J Thorac Cardiovasc Surg 1999;117:1180-9.  Back to cited text no. 5
    
6.
Wong PC, Sanders SP, Jonas RA, Colan SD, Parness IA, Geva T, et al. Pulmonary valve-moderator band distance and association with development of double-chambered right ventricle. Am J Cardiol 1991;68:1681-6.  Back to cited text no. 6
    
7.
Yoshimura N, Matsuhisa H, Otaka S, Kitahara J, Murakami H, Uese K, et al. Surgical management of multiple ventricular septal defects: The role of the felt sandwich technique. J Thorac Cardiovasc Surg 2009;137:924-8.  Back to cited text no. 7
    
8.
Stellin G, Padalino M, Milanesi O, Rubino M, Casarotto D, Van Praagh R, et al. Surgical closure of apical ventricular septal defects through a right ventricular apical infundibulotomy. Ann Thorac Surg 2000;69:597-601.  Back to cited text no. 8
    
9.
Barber M, Chinitz J, John R. Arrhythmias from the right ventricular moderator band: Diagnosis and management. Arrhythm Electrophysiol Rev 2020;8:294-9.  Back to cited text no. 9
    
10.
Fernando W, Vargas B. Pre-syncope and ablation of moderator band premature ventricular contraction. Cardiovasc Metab Sci 2020;31:131-6.  Back to cited text no. 10
    
11.
Come PC, Riley MF. M mode and cross-sectional echocardiographic recognition of fibrosis and calcification of the mitral valve chordae and left ventricular papillary muscles. Am J Cardiol 1982;49:461-6.  Back to cited text no. 11
    
12.
Kim EJ, Song BG, Sohn HR, Hong SM, Park DW, Heo SH, et al. Senile cardiac calcification syndrome: A rare case of extensive calcification of left ventricular papillary muscle. Cardiol Res 2011;2:127-9.  Back to cited text no. 12
    
13.
Rifai L, Hammoudi N, Fouret P, Acar C. Massive calcification of the tricuspid valve papillary muscles in right ventricular endomyocardial fibrosis Interactive Cardiovasc Thorac Surg 2011;12:505-6.  Back to cited text no. 13
    
14.
Avila-Vanzzini N, Trevethan-Cravioto S, Lopez-Mora E, Herrera-Bello H, Soto-Abraham V, Martínez-Rios MA. Heart calcification (idiopathic cardiac osseous metaplasia): A case report. Arch Cardiol Mex 2014;84:140-2.  Back to cited text no. 14
    


    Figures

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



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Case Report
Discussion
Conclusion
References
Article Figures

 Article Access Statistics
    Viewed699    
    Printed42    
    Emailed0    
    PDF Downloaded73    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]