Slow Ventricular Tachycardia in a Patient with Heart Failure on Amiodarone

A man in his 70s with a history of myocardial infarction was admitted with progressive dyspnea and findings consistent with heart failure. On admission, he had a regular tachycardia at approximately 116 bpm. ECG showed atrial tachycardia, and echocardiography revealed reduced left ventricular function with an ejection fraction (EF) of about 30%.

Atrial tachycardia, 116 beats/min

Apical 4-chamber view - The septal wall and apex are thin after previous myocardial infarction and EF i reduced

Apical 2-chamber view

Apical long-axis view

The patient received optimized heart failure therapy, and a transesophageal echocardiogram (TEE) was performed to exclude atrial thrombus before electrical cardioversion. He was started on amiodarone and underwent drainage of bilateral pleural effusions.

Restoration of sinus rythm after cardioversion

A few days later, he experienced palpitations. A new ECG demonstrated a regular, wide-complex rhythm at 98 bpm. The question arose: is this a supraventricular tachycardia (SVT) with aberrant conduction, or a ventricular tachycardia (VT)?

Slow VT - AV-dissosiation, easiest to appreciate in lead V1.

ECG Interpretation

• QRS duration: 192 ms

• Axis: Inferior (positive in leads II, III, aVF)

• Morphology: Right bundle branch block pattern (positive R in V1, deep S in V6)

• Rhythm: Regular

• AV dissociation: Present. P waves are visible and independent of QRS complexes.

  
  

The presence of AV dissociation is diagnostic of ventricular tachycardia. In such cases, the atria and ventricles beat independently, with the sinus node driving atrial activity while an ectopic ventricular focus generates the tachycardia.

Why is the Ventricular Tachycardia Slow?

Traditionally, VT is defined as a wide-complex tachycardia with a rate above 120 bpm. However, this is not an absolute requirement. In clinical practice, so-called slow VT is often observed, particularly in patients receiving antiarrhythmic therapy.

Amiodarone is known to decrease conduction velocity in both atrial and ventricular myocytes. It prolongs the action potential and refractory period, which may result in a substantially lower ventricular rate during VT episodes.

This phenomenon, commonly referred to as “slow VT,” is well recognized in patients treated with amiodarone and may lead to diagnostic confusion—especially if one expects VT to always present with a rapid rate.

Clinical Reasoning

When interpreting ECGs in patients with a history of myocardial infarction and reduced EF, VT should always be considered the most likely diagnosis for any new wide-complex rhythm, even if the tracing is difficult to classify precisely.

Medication history is crucial. Without knowledge of amiodarone use, the relatively low rate might have been misleading and prompted an incorrect interpretation.

Key Learning Points

• AV dissociation is diagnostic for VT. The presence of P waves independent of QRS complexes confirms ventricular tachycardia.

• Slow VT is most often seen with amiodarone. The drug decreases conduction velocity and lowers the tachycardia rate.

• Clinical context matters. Prior myocardial infarction and reduced EF make VT the most probable cause of a wide-complex tachycardia.

• Medication history is essential. Awareness of antiarrhythmic therapy is key to accurate ECG interpretation.

• Definitions are guides, not absolutes. Although many textbooks define VT as >120 bpm, rate alone is not diagnostic.