A 9-year-old female, with a known medical history of severe dilated cardiomyopathy secondary to ectopic atrial tachycardia, presented to our clinic for a regular check-up. Echocardiography was significant for severe left ventricular (LV) dilatation, markedly reduced LV systolic function reflected by an ejection fraction of 30%, and severe mitral regurgitation. ECG revealed a regular sinus rhythm. Despite being on several medications including aspirin, carvedilol, digoxin, enalapril, and spironolactone, the patient's cardiac condition failed to improve. A gradual worsening in the systolic function of LV and the degree of mitral regurgitation was noted over the last few visits.\nUpon follow up, echocardiography findings were similar to the previous findings. However, ECG was significant for ectopic atrial tachycardia. We placed a 24-h Holter monitor a week after to evaluate appropriately her heart rhythm. Holter revealed an incessant atrial tachycardia interrupted by a few sinus beats.\nConsequently, the patient was admitted to the pediatric intensive care unit (PICU) for observation and initiation of appropriate anti-arrhythmic medications. Upon admission, carvedilol and digoxin were stopped and she was started on ivabradine at a dose of 0.025 mg/kg/day. Two hours after this first dose, she reverted to sinus rhythm (). The dose of ivabradine was increased gradually to 0.1 mg/kg/day. Reversal from atrial to sinus rhythm was observed a few hours after each dose. The effect of ivabradine was sustained for around 4–6 h. Given the suboptimal response to ivabradine, ivabradine was stopped and amiodarone was started for rhythm control. Nonetheless, during this hospital stay, a mild improvement in LV systolic function was noted on echocardiography (see ). Similarly, no side effects were attributed to the use of ivabradine. Her blood pressure remained within normal range, and she had no bradycardia or QT interval prolongation.\nThe patient cardiomyopathy was believed to be secondary to her incessant atrial tachyarrhythmia. Optimal control of rate and rhythm through medical or interventional therapies is the mainstay of DCM management in this case.
A 2-year-6-month-old girl was transferred to our hospital from a primary care center for the management of tachyarrhythmia. Eight months prior to her presentation, she was found to have an increased heart rate (HR) of around 200 bpm on routine physical examination. At that time she was asymptomatic and her echocardiography was normal. Nevertheless, a week prior to her presentation to our center, an increased HR of 190 bpm was noted again on routine exam. Repeat echocardiography revealed LV dilatation along with a reduced LV systolic ejection fraction of 35%. ECG showed supraventricular tachycardia (SVT), namely atrial tachycardia. She failed a trial of adenosine and responded weakly to metoprolol. The patient was discharged on metoprolol 25 mg/day divided into two doses. She presented 2 days later to the same hospital. She had a HR of 250 bpm. She received two doses of adenosine, one dose of amiodarone and several doses of flecainide during her admission. However, no improvement was noted after 5 days of treatment, and also after direct current cardioversion. She was then transferred to our center for adequate rate control and appropriate investigation.\nUpon admission to our PICU, HR was 190 bpm. On examination, she was pale, tachypneic and hypoactive, but responsive to verbal stimulation. A third heart sound was noted on cardiac auscultation. Additionally, she had cool extremities and palpable hepatomegaly. Echocardiography was repeated, it showed worsened LV dilatation and severe LV systolic dysfunction (EF was around 20%), and moderate mitral regurgitation (see ). ECG revealed an atrial tachycardic rhythm. Patient was given adenosine. She received a second higher dose of adenosine and an infusion of amiodarone. She failed to respond adequately to these medications. Consequently, the patient was started on ivabradine at 0.15 mg/kg/day. An adequate response was noted few hours after the first dose of ivabradine. HR decreased to 90 bpm and she reverted to sinus rhythm. shows the patient's ECG pre- and post-ivabradine. The dose of ivabradine was adjusted to 0.033 mg/kg thrice daily. Adequate response was noted and the patient was discharged on ivabradine.\nOne month after the discharge, she presented to our clinic and was found to have a normocardic sinus rhythm on ECG, and an improved cardiac function on echocardiography (EF of 50%). In short, this is a case of SVT-induced DCM managed appropriately with ivabradine.