Abstract
Accelerated ventricular rhythm is well-recognized in adults and is frequently reported with reperfusion post-infarction. It is rare in newborns. We present a case of presumed neonatal myocarditis likely secondary to maternal viral infection, presenting with an accelerated idioventricular rhythm. This was diagnosed as non-sustained ventricular tachycardia. The baby was started on a beta blocker for the same, which paradoxically increased the duration and frequency of the rhythm. Once the nature of the arrhythmia was identified to be accelerated idioventricular rhythm, the beta-blocker was stopped. This, as well as the gradual resolution of inflammation, resulted in quiescence of the arrhythmia. Accelerated idioventricular rhythm can be the presentation of neonatal myocarditis. Prompt identification can help in avoiding unnecessary therapy for this generally benign and self-limiting arrhythmia.
Highlights
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Differentiating Accelerated Idioventricular Rhythm from Ventricular Tachycardia is important, given that the former is generally benign.
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Benign but Significant: While AIVR is typically self-limiting, its presence can be a sign of serious underlying conditions like myocarditis.
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This case highlights the importance of conservative management while ensuring diagnostic vigilance to avoid unnecessary interventions.
1
Case report
We describe the case of a 6-day-old male neonate, born at 37 weeks of gestation via normal vaginal delivery to a 25-year-old primigravida mother with a history of gestational diabetes mellitus (managed with oral hypoglycaemic agents). The neonate weighed 2560 g at birth and cried immediately, with APGAR scores of 8 and 9 at 1 and 5 min, respectively. The mother experienced a febrile episode with flu-like symptoms at 33 weeks gestation, for which she was treated with Oseltamivir. A week later, she developed pruritus and conjugated hyperbilirubinemia, which was treated with ursodeoxycholic acid. Irregularity in the heartbeat of the fetus was documented antenatally after the episode of maternal illness. The neonate had a smooth perinatal transition; however, at 4 h of life, he presented with asymptomatic hypoglycemia and was shifted to the intensive care unit (ICU) in a peripheral center. There, an irregular heart rate was noted, and electrocardiography (ECG) revealed frequent, non-sustained runs of broad QRS complex tachycardia. There was no hemodynamic compromise with the arrhythmia. This was diagnosed as non-sustained ventricular tachycardia (NSVT). An echocardiogram performed in the first hours of life was normal. Cardiac biomarkers were elevated, with high-sensitivity Troponin T (HS Trop T) at 67.7 ng/L and creatine phosphokinase (CPK) at 713 IU/L. The baby was referred to our facility on Day 6 for the persistence of the abnormal rhythm on ECG ( Fig. 1 ), hemodynamically stable with no evidence of heart failure. Repeat cardiac biomarkers showed HS-Troponin-T of 171 ng/L and CPK of 520 IU/L. Ventricular function was preserved. The baby was presumed to have myocarditis; an etiological workup was done. Serum electrolytes and thyroid function tests were within normal limits. IgM TORCH serology was negative. Blood counts were normal, and C-reactive protein (CRP) was negative. Inflammatory markers were notable for elevated interleukin-6 (IL-6) at 16.77 pg/mL, D-dimer >20 μg/mL, and Ferritin at 212.8 ng/mL, suggesting an underlying systemic inflammatory pathology. The mother underwent evaluation for autoimmune conditions, which included an ANA panel and rheumatoid factor assay, both of which were negative, effectively ruling out maternal autoimmune etiology. Consequently, the myocarditis was attributed to an unidentified maternal viral infection that occurred at 33 weeks of gestation.
Beta-blocker (Propranolol) was initiated on Day 2 of hospital admission because of the increased frequency and duration of the abnormal rhythm, although with no hemodynamic compromise ( Fig. 2 ). This led to the worsening of the rhythm, which was now sustained, while still maintaining hemodynamic stability ( Fig. 3 ). ECG showed a broad complex tachycardia at a rate of 150 per minute, with QRS morphology different from that of the sinus rhythm, confirming a ventricular origin ( Fig. 3 ). Mostly, VA conduction was observed, as evidenced by inverted P waves in leads II, III, and aVF. Fusion beats were noted as well ( Fig. 4 ). The relatively narrow QRS duration and slow rate for a newborn were suggestive of accelerated idioventricular rhythm (AIVR) rather than Ventricular tachycardia (VT). In order to allow the sinus node to take over, propranolol was stopped after 48 h. This resulted in a dramatic reduction in the frequency and duration of episodes within 24 h of discontinuation, gradually returning to sinus rhythm ( Fig. 5 ). Repeat inflammatory markers four days later demonstrated a declining trend, further supporting resolution of the inflammatory process. The child was discharged after a week of hospital stay. 72-Hour Holter monitoring done one month after discharge showed sinus rhythm with no evidence of arrhythmia. Ventricular function remained normal as well.
