A 38-year-old European woman with type I diabetes mellitus and corrected hypothyroidism and negative family history of dysrhythmias or cardiomyopathies was first noted to have a persistent asymptomatic tachycardia ∼110–120 b.p.m. during the third trimester of her first pregnancy. The 12-lead electrocardiogram (ECG) at the time confirmed P-wave morphology consistent with a sinus tachycardia with normal intrinsic atrioventricular conduction and narrow QRS complex. Reversible causes were ruled out and the tachycardia was attributed to the pregnant state. After delivery of her first son, the tachycardia persisted postpartum over several months and she was referred to Cardiology for suspected inappropriate sinus tachycardia. Apart from the elevated heart rate the physical exam was normal. A transthoracic echocardiogram (TTE) 8 months after delivery demonstrated a dilated left ventricle (LV) with severely impaired function [ejection fraction (EF) 15%], presence of an apical thrombus and an interatrial shunt. A cardiac magnetic resonance imaging (MRI) confirmed the echocardiographic findings and additionally diagnosed an ischaemic scar in the apex () but coronaries were unobstructed on ECG-gated computed tomography coronary angiogram. A genetic screen within the 100 000 Genomes project did not reveal any abnormalities in the 84 genes associated with dilated cardiomyopathy known at the time. The main differential diagnosis was a late diagnosis of peripartum cardiomyopathy with secondary LV thrombus formation complicated by embolic myocardial infarction, or myocarditis and a paradoxical coronary embolic event facilitated by the interatrial defect. With optimal medical heart failure therapy and Warfarin the left ventricular function fully recovered, the left ventricular thrombus resolved completely, and heart rate normalized within 6 months. A persistent foramen ovale closure was performed after recovery of LV function and thrombus resolution based on the differential diagnosis of paradoxical embolism. Warfarin was ceased. An attempt to wean the heart failure medication resulted in progressive LV dilatation (as documented in a routine follow-up cardiac MRI) within 3 months after stopping her betablocker and angiotensin-converting enzyme-inhibitor (ACEI) and were therefore reinstituted. The patient remained asymptomatic throughout.\nThree years later the patient became pregnant with her second child, requiring suspension of ACEI therapy. Bisoprolol was continued and she was closely monitored with clinical and echo surveillance by the Pregnancy Heart Team. Towards the beginning of the third trimester, the patient noted palpitations and a repeated TTE found a mildly impaired left ventricular EF of 46% (compared to previously 57%) and a heart rate of 120 b.p.m. No overt clinical signs of heart failure were present. The 12-lead ECG () demonstrated a regular organized atrial rhythm with 1:1 conduction to the ventricles with discrete monomorphic P waves separated by isoelectric intervals with upright P waves in the inferior leads, negative in aVL and I, and biphasic negative–positive in V1–V2. The electrocardiographical features were consistent with a left-sided FAT with suspected origin from the superior mitral annulus using the Kistler algorithm. A further up-titration of Bisoprolol to maximum dose failed to control her heart rate, worsened her fatigue, and caused loss of hypoglycaemia awareness.\nGiven the deterioration in LV function in the context of a persistent atrial tachycardia and the previous cardiomyopathy during her first pregnancy, treatment to rate control the arrhythmia was mandated; however, options in this circumstance were limited by the safety profile of commonly used antiarrhythmic drugs. Ivabradine was discussed considering the higher incidence of autonomic FATs during pregnancy and the recent evidence of its efficiency in this particular subset of arrhythmias. In view of the limited available data regarding the teratogenic risk of ivabradine, this option was reviewed with the Pregnancy Heart Team and pharmacists, as well as the patient. It was felt that the benefits would outweigh the risks and ivabradine was started at a dose of 5 mg twice daily. A three-lead 24 h Holter ECG was fitted and recording started parallel to commencing the treatment. The effect was observed ∼6 h after the first dose with a successful reduction of the average heart rate to ∼100 b.p.m. (). Ivabradine was further increased to the target dose of 7.5 mg twice daily. A repeated TTE under improved rate control demonstrated an improved left ventricular function (LV EF 55%).\nThe patient was scheduled for obstetric foetal ultrasound scans at gestation Weeks 28, 32, and 36, which revealed no abnormalities, and had an uncomplicated vaginal delivery of a 3900 g healthy male infant at term. A 12-lead ECG 1 month postpartum showed spontaneous resolution of the atrial tachycardia and confirmed normal sinus rhythm. Ivabradine was stopped and her betablocker continued. The ACEI has been reinstituted after the pregnancy. She has been symptom free since delivery.
A 30 day old boy weighing 3 kg was referred to our pediatric intensive care unit in view of significant respiratory distress and cardiogenic shock. Physical examination revealed tachycardia (200bpm), and tachypnoea with decreased pulses and poor peripheral perfusion. Blood gas showed severe metabolic acidosis (pH 6.9; HCO3 3.6 mol/L; PCO2 15mmHg). The baby was resuscitated with intravenous fluid and sodium bicarbonate correction.The 12-lead electrocardiogram (ECG) showed a regular narrow QRS tachycardia with a rapid ventricular rate of 187 bpm with long RP interval and abnormal peaked P wave morphology.The P waves were biphasic in V1 and positive in leads II, III and aVF suggestive of EAT []. Chest radiograph showed a cardiothoracic ratio of 75%. Echocardiography showed severe left ventricular (LV) dysfunction [ejection fraction (EF) 19%] with significant LV dilatation [LVIDd 2.5cm (Z score +3.18)]. SARS-CoV-2 PCR was negative and antibodies levels were normal. Adenosine given during the tachycardia, resulted in transient termination of the tachyarrhythmia followed by reappearance []. Enteral ivabradine (0.15mg/kg) was given resulting in gradual reduction of heart rate one hour after initiation and the rhythm became sinus after 4 hours. Enteral digoxin (10mcg/kg/day) was added one hour after ivabradine. There was significant improvement in the hemodynamics and perfusion (mean BP 25 mmHg). Blood gas after stabilization revealed improvement in the metabolic acidosis (pH 7.49; HCO3 16.6 mol/L; PCO2 22mmHg). However the respiratory distress and LV dysfunction persisted. Supportive care including bubble continuous positive airway pressure, milrinone and furosemide infusion were provided for the LV dysfunction. He symptomatically improved with supportive care and it was weaned off after 24 hours. LV dimension [LVIDd 1.6cm (Z score -1.29)] and function (EF 55%) improved significantly after 72 hours. He was discharged after 5 days of hospitalization on oral ivabradine (0.15mg/kg twice a day), and digoxin (5mcg/kg twice a day). The timeline of events which happened during the first 72 hours isshown in the .