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Year : 2021  |  Volume : 11  |  Issue : 4  |  Page : 201-204

Simultaneous presence of atrial arrhythmia and hypocalcemia in dilated cardiomyopathy: A series of two cases

1 Department of Pediatric Cardiology, Medica Super Specialty Hospital, Kolkata, West Bengal, India
2 Department of Cardiology, Medica Super Specialty Hospital, Kolkata, West Bengal, India
3 Department of Paediatric Cardiology, Amrita Institute of Medical Sciences, Kochi, Kerala, India

Date of Submission06-Oct-2020
Date of Decision01-Nov-2020
Date of Acceptance01-Nov-2020
Date of Web Publication25-Oct-2021

Correspondence Address:
Dr. Anil Kumar Singhi
Senior Consultant, Department of Pediatric Cardiology, Medica Super Specialty Hospital, Mukundapur, Kolkata - 700 099, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_70_20

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Dilated cardiomyopathy in young children has varied etiological factors. Some cases have correctable causes such as incessant arrhythmia, correctable metabolic abnormality, and left ventricular obstructive lesions. Two 4-month-old infants presented with severe left ventricular dysfunction and ectopic atrial tachycardia. Biochemical profile of the infants showed low ionic and total calcium, elevated serum phosphate, elevated alkaline phosphatase, and elevated serum lactate. The parathyroid hormone was elevated and 25-hydroxyvitamin D3 was reduced. The patients were treated with beta-blocker, calcium, and Vitamin D supplementation, along with antifailure therapy. The tachycardia resolved over a 12-h period and calcium normalized in the next few days. The left ventricular function returned to normal over a 5–16-month period. In 6–8 years of follow-up, patients were in sinus rhythm doing very well with normal cardiac function with normal calcium-related biochemical parameters. The presence of incessant atrial arrhythmia in a case of hypocalcemic cardiomyopathy is rare and can have link with hypocalcemia-induced electrical changes in the cardiomyocyte in selected cases. Thorough and protocol-based treatment approach helps in correct diagnosis and treatment. Further study and molecular research can shed more light on the complex interaction of hypocalcemia and arrhythmia.

Keywords: Atrial arrhythmia, dilated cardiomyopathy, hypocalcemia, Vitamin D deficiency

How to cite this article:
Singhi AK, Mukherjee SS, Shine Kumar K H, Kumar RK. Simultaneous presence of atrial arrhythmia and hypocalcemia in dilated cardiomyopathy: A series of two cases. J Indian coll cardiol 2021;11:201-4

How to cite this URL:
Singhi AK, Mukherjee SS, Shine Kumar K H, Kumar RK. Simultaneous presence of atrial arrhythmia and hypocalcemia in dilated cardiomyopathy: A series of two cases. J Indian coll cardiol [serial online] 2021 [cited 2022 Sep 24];11:201-4. Available from: https://www.joicc.org/text.asp?2021/11/4/201/329150

  Introduction Top

Children presenting with severe left ventricular dysfunction can have treatable causes. Rarely, more than one correctable cause may be present in a given case. We report a series of two young infants presenting with clinical features of severe left ventricular dysfunction in a tertiary care pediatric cardiac unit.

  Clinical Course of the Cases Top

Case 1

The first infant aged 4 months and 9 days weighing 5.3 kg presented with a 1-week history of breathing difficulty and poor feeding. The baby had tachycardia and tachypnea with intercostal retraction. Cardiac evaluation revealed left ventricular third heart sound, with no significant murmur. Electrocardiogram (ECG) showed regular narrow complex tachycardia at 190/min. The P wave morphology was varying along with varying RP interval, suggestive of atrial arrhythmia [Figure 1]. Echocardiogram showed severe left ventricular dysfunction with mild mitral regurgitation (MR). The coronary arteries were normal in origin. The provisional diagnostic was tachycardiomyopathy. Intravenous adenosine bolus was given which slowed the tachycardia transiently. He was started on intravenous metoprolol infusion. He had low serum total and ionic calcium and high serum phosphate. The alkaline phosphatase was high. The parathyroid hormone (PTH) level was significantly elevated [Table 1]. This feature suggested possibility of pseudohypoparathyroidism. Intravenous calcium gluconate was given along with Vitamin D3 for the correction of hypocalcemia. On detailed clinical evaluation, subsequently, rickety rosary was found. There was no evidence suggesting cataract and dysmorphism. He was developmentally normal for age. The X-ray of the wrist was normal. The tachycardia reverted to normal sinus rhythm on the same day evening. The serum calcium is normalized by the 4th day of admission. The parental therapy was changed subsequently to oral supplementation of calcium and calcitriol (Vitamin D3). The QTc interval was 540 ms initially which subsequently returned to normal [Supplemental Figure 1]. He received oral diuretic, angiotensin-converting enzyme inhibitor (ACEI), beta-blocker, calcium, and Vitamin D supplementation. The metoprolol was changed to carvedilol after arrhythmia reverted to sinus rhythm. The presence of rickety rosary and complete remission of biochemical anomaly on Vitamin D3 and calcium supplementation along with the improvement of cardiac function lead to final diagnosis of Vitamin D-deficient rickets with secondary hyperparathyroidism. 25-hydroxyvitamin D level sample was sent on 3 months of follow-up not at the time of admission as calcium and bolus dose of Vitamin D supplementation was already given. The patient had complete normalization of the left ventricular function and resolution of metabolic abnormality at 5 months of follow-up. He had a normal growth and development of 6-year follow-up.
Table 1: Biochemical parameters

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Figure 1: Electrocardiogram of the patient-1 on admission revealed regular narrow complex tachycardia with a rate of 190/min. The P wave morphology was varying. The RP interval was prolonged and varying suggestive of ectopic atrial arrhythmia

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Case 2

The second infant aged 4½ months weighing 5.2 kg had a 2-day history of respiratory distress. He presented with cardiac failure in sick state and was mechanically ventilated on admission. The ECG showed regular narrow complex long RP tachycardia with a rate of 200 per minute. The P wave morphology and RP interval appeared varying suggestive of ectopic atrial tachycardia (EAT) [Figure 2]. Initial echocardiogram showed evidence of severe left ventricular dysfunction and moderate-to-severe MR. The coronary arteries were normal and there was no evidence of any left ventricular outflow tract obstruction. Intravenous bolus of adenosine slowed the tachycardia transiently and then tachycardia continued. The patient was started on intravenous metoprolol. Initial cardiomyopathy workup showed low serum total and ionic calcium. The alkaline phosphatase was high and phosphate was high normal. Taking clue from our first patient, we sent serum Vitamin-D (25 OH Vitamin D3) and PTH samples sent before starting any calcium supplement. Vitamin-D (25 OH Vitamin D3) was significantly low and the PTH level was elevated [Table 1]. There was no evidence of cataract, dysmorphism, or rickety rosary. The X-ray of the wrist was normal. Initially, intravenous calcium gluconate was given for correction of hypocalcemia which subsequently was changed to oral calcium supplementation. The patient received Vitamin D3 parenterally, and then, oral calcitriol (Vitamin D3) supplementation was started. The tachycardia reverted to normal sinus rhythm the next day morning. The QTc interval was 520 ms initially which returned to normal on follow-up. The patient developed one episode of seizure on day 4 which was attributed to hypocalcemia and treated accordingly. Computed tomographic scan of the brain and electroencephalogram were normal. The serum calcium normalized by the 5th day of admission. The infants received oral diuretic, ACEI, carvedilol, in addition to calcium and Vitamin D supplementation. Calcium and Vitamin D supplementation was discontinued after 6 months. The patient required 16 months for normalization of ventricular function and resolution of MR after which and cardiac medications tapered off. He had normal growth and development in 8-year follow-up.
Figure 2: Electrocardiogram of the patient-2 showing regular narrow complex long RP tachycardia with a rate of 200/min. The P wave morphology and RP interval appeared varying suggestive of ectopic atrial tachycardia

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  Discussion Top

Dilated cardiomyopathy (DCM) is a group of disorders with diverse etiology characterized by myocardial dysfunction. The causes for DCM can be postinfectious, metabolic, drug induced, nutritional deficiency, arrhythmia, genetic, and structural cardiac causes or idiopathic. Among the correctable causes, hypocalcemia is relatively common in infancy and childhood. Different series reported up to 10%–16% of pediatric cohorts of DCM having significant calcium deficiency.[1] Vitamin D deficiency is a common cause of hypocalcemia in childhood, and it has high prevalence in developing countries, especially in very young breastfed babies.[2],[3] The Vitamin D level below 25 nmol/l is considered insufficient and below 15 nmol/l is considered significantly deficient.[3] Our first patient had high or high normal serum phosphate which created diagnostic confusion in the first case as a possible case of pseudohypoparathyroidism. The infants in our case series were exclusively breastfed. Jain et al. found that Vitamin D deficiency is associated with significantly elevated PTH suggestive of secondary hyperparathyroidism.[2]

EAT is a well-established cause of tachycardiomyopathy, which is potentially partially or fully correctable. Apparently, the presence of two potentially correctable causes of the left ventricular dysfunction such as hypocalcemia and significant atrial arrhythmia is rare. Recently, some case reports described significant atrial arrhythmia and hypocalcemia in cases with cardiomyopathy and explained the atrial arrhythmia induced by hypocalcemia-related cellular changes.[4],[5] Calcium exerts its most prominent effect on the duration of Phase “2” (plateau) of the action potential (AP) in cardiomyocytes. Reduced calcium ion-dependent inactivation of calcium channels keeps the calcium channels open for a longer period, thereby allowing late inflow of calcium ion.[6] Grandi et al. found L-type Ca2 + channels responsible for the dependency of AP duration on calcium ions in experimental models.[7] The increased duration of Phase “2” of the ventricular AP results in an increased duration of the S-T segment and of the Q-T interval as well as duration of effective refractory period.[6],[7] Hypocalcemia-induced prolongation of the repolarization interval may promote AP instability with increased beat-to-beat variability. This may result in activation of premature inward depolarization current, the early after depolarization (EAD). Hypocalcemia-induced prolonged repolarization in the atrial fibers makes them vulnerable for EAD and different types of atrial arrhythmia such as supraventricular tachycardia, extrasystole ventricular beats, atrial fibrillation, and supraventricular extrasystole.[6],[8] The degree of QT interval prolongation is related to degree of hypocalcemia. Hence, more severely affected infants will be more vulnerable to develop hypocalcemia-induced arrhythmia. Vitamin D deficiency independently contributes to atrial arrhythmia.[9] Hypoxia and acidosis also induce EAD in a patient, which may be present in a case of severe left ventricular dysfunction making the child susceptible to electrical and rhythm abnormality. Possibly, hypocalcemia-induced electrophysiological changes which are clinically significant are more prone to be seen in patients with severe hypocalcemia. [10] All patients with hypocalcemia do not develop manifest atrial arrhythmia possibly in a background of severe hypocalcemia; other factors play a role to induce arrhythmia in some of the cases. Atrial arrhythmia could be one of its manifestations in hypocalcemia in selected cases. Further research in this field can shed more light on the relationship of atrial arrhythmia with hypocalcemia.

  Conclusion Top

Significant hypocalcemia and incessant atrial tachycardia both are independently very important causes of correctable cardiomyopathy. Coexistence of both in a given patient is rare. The hypocalcemia-induced electrical changes in cardiomyocyte may induce ectopic atrial arrhythmia in some cases of hypocalcemia and aggravates left ventricular dysfunction. Correction of hypocalcemia along with antiarrhythmic therapy restores electromechanical function and cardiac rhythm. The relationship of atrial arrhythmia in selected cases of hypocalcemia causing left ventricular dysfunction merits further studies and molecular research.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for 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.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Sanyal D, Raychaudhuri M. Infants with dilated cardiomyopathy and hypocalcemia. Indian J Endocrinol Metab 2013;17:S221-3.  Back to cited text no. 1
Jain V, Gupta N, Kalaivani M, Jain A, Sinha A, Agarwal R. Vitamin D deficiency in healthy breastfed term infants at 3 months & their mothers in India: Seasonal variation & determinants. Indian J Med Res 2011;133:267-73.  Back to cited text no. 2
[PUBMED]  [Full text]  
Kutilek S, Vracovska M, Pecenkova K, Brozikova H, Rondzikova E, Boskova E, et al. Three cases of transient neonatal pseudohypoparathyroidism. Sudan J Paediatr 2018;18:42-7.  Back to cited text no. 3
Jindal A. Hypocalcemia and tachycardia induced cardiomyopathy. Indian Pediatr 2012;49:930.  Back to cited text no. 4
Fernando MP, Perera PJ, Muthukumarana OJ, Uyangoda K. Hypocalcaemia leading to supra ventricular tachycardia in a three-month old Sri Lankan infant with vitamin D deficient rickets: A case report. Ceylon Med J 2017;62:242-43.  Back to cited text no. 5
Nijjer S, Ghosh AK, Dubrey SW. Hypocalcaemia, long QT interval and atrial arrhythmias. BMJ Case Rep 2010;2010:bcr0820092216.  Back to cited text no. 6
Grandi E, Pasqualini FS, Pes C, Corsi C, Zaza A, Severi S. Theoretical investigation of action potential duration dependence on extracellular Ca2+in human cardiomyocytes. J Mol Cell Cardiol 2009;46:332-42.  Back to cited text no. 7
Wang Y, He K, Wang O, Lin X, Chen S, Jiang Y, et al. Manifestations of left ventricular dysfunction and arrhythmia in patients with chronic hypoparathyroidism and pseudohypoparathyroidism: A preliminary study. BMC Endocr Disord 2020;20:61.  Back to cited text no. 8
Bansal B, Bansal M, Bajpai P, Garewal HK. Hypocalcemic cardiomyopathy-different mechanisms in adult and pediatric cases. J Clin Endocrinol Metab 2014;99:2627-32.  Back to cited text no. 9
Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by after depolarizations. Role of M cells in the generation of U waves, triggered activity and torsade de pointes. J Am Coll Cardiol 1994;23:259-77.  Back to cited text no. 10


  [Figure 1], [Figure 2]

  [Table 1]


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