QT prolongation due to aortic aneurysm rupture and amiodarone in a patient with a H558R polymorphism in the cardiac sodium channel gene SCN5A

Minerva Cardioangiol. 2006 Aug;54(4):503-6.

Abstract

The duration of the QT interval is influenced by many pathologic processes and drugs. We report a 74-year-old man who was admitted after syncope. His electrocardiogram (ECG) showed a QT interval of 0.44 s (QTc 0.53 s). After 10 h a ruptured abdominal aortic aneurysm was diagnosed and the patient underwent implantation of an aorto-bi-iliac Y-prosthesis. After surgery QT interval normalized. Under therapy with amiodarone, given because of atrial fibrillation, QT prolongation occurred again and disappeared after discontinuation of amiodarone. The postoperative course was complicated by critical illness polyneuropathy and plexopathy. Whereas amiodarone is a well recognized cause of QT prolongation, aortic aneurysm rupture has not been described previously. Vegetative mechanisms and sudden decrease of cardiac afterload due to the ruptured aneurysm may have altered myocardial repolarisation and thus prolonged QT interval duration. In conclusion in a patient with syncope and QT prolongation, extracardiac causes like rupture or an aortic aneurysm have to be included into the differential diagnosis.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Amiodarone / adverse effects*
  • Anti-Arrhythmia Agents / adverse effects*
  • Aortic Aneurysm, Abdominal / complications*
  • Aortic Rupture / complications*
  • Arrhythmias, Cardiac / etiology*
  • Arrhythmias, Cardiac / physiopathology
  • Electrocardiography
  • Humans
  • Male
  • Muscle Proteins / genetics*
  • NAV1.5 Voltage-Gated Sodium Channel
  • Polymorphism, Genetic*
  • Sodium Channels / genetics*

Substances

  • Anti-Arrhythmia Agents
  • Muscle Proteins
  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Sodium Channels
  • Amiodarone