Use of ivabradine for treatment of junctional ectopic tachycardia in post congenital heart surgery

  • PDF / 136,380 Bytes
  • 3 Pages / 595.276 x 790.866 pts Page_size
  • 52 Downloads / 208 Views

DOWNLOAD

REPORT


CASE REPORT

Use of ivabradine for treatment of junctional ectopic tachycardia in post congenital heart surgery Dhruva Sharma 1 & Ganapathy Subramaniam 2 & Neha Sharma 3 Received: 8 August 2020 / Revised: 17 August 2020 / Accepted: 7 September 2020 # Indian Association of Cardiovascular-Thoracic Surgeons 2020

Abstract Cardiac surgeries especially involving crux of the heart as performed in tetralogy of Fallot (TOF) and pulmonary stenosis are mainly responsible for junctional ectopic tachycardia (JET). Diversified antiarrhythmic agents have been used in an impressive way to treat JET but showed suboptimal efficacy and varied associated adverse effects. But, ivabradine has proved as final crusader for its treatment. We report our initial experience of 4 cases in last 6 months with ivabradine in the management of postoperative JET. Encouraged by various reports and our increasing experience with ivabradine in heart failure population, we have moved to ivabradine as the first drug of choice for postoperative JET. Bradycardia was the only significant adverse effect in our series. The availability of atrial and ventricular pacing wires or at least transvenous temporary pacing should be ensured before starting ivabradine. Keywords Postoperative junctional ectopic tachycardia . Ivabradine . Arrhythmias . Funny currents . Congenital cardiac surgery

Introduction Junctional ectopic tachycardia (JET) usually originates from atrioventricular node, atrioventricular junction, or bundle of His complex. Postoperative JET is mostly seen within 72 h after pediatric cardiac surgery. The incidence of postoperative JET is found to be 2–10% of cases [1, 2]. Risk factors for JET include sustained ischemia time and cardiopulmonary bypass (CPB) time, infants less than 6 months, hypoxia, electrolyte imbalance, surgery involving area near atrioventricular node, use of increased doses of ionotropic agents, defective filling of the ventricles, and atrioventricular asynchrony [2].

* Neha Sharma [email protected] 1

Department of Cardiothoracic and Vascular Surgery, SMS Medical College & Attached Hospitals, J L N Marg, Jaipur, Rajasthan 302001, India

2

Institute of Heart and Lung Transplant and Mechanical Circulatory Support, MGM Healthcare, No. 72, Nelson Manickam Road, Aminjikarai, Chennai, Tamil Nadu 600029, India

3

Department of Pharmacology, SMS Medical College & Attached Hospitals, J L N Marg, Jaipur, Rajasthan 302001, India

Cardiac surgeries especially involving crux of the heart as performed in tetralogy of Fallot (TOF) and pulmonary stenosis, atrioventricular canal (AV) canal, and ventricular septal defect repair, arterial switch operation, Norwood procedure, and interrupted aortic arch repair are mainly responsible for JET [3]. Plausible reason of etiopathogenesis of JET includes expanded automaticity that is caused within the bundle of His due to direct trauma or edema by sutures or infiltrative hemorrhage to bundle of His and the AV node [2, 3]. JET is typically characterized with a heart rate of more than 170 beats per min