Article Text

Download PDFPDF

Pathophysiology, diagnosis and treatment of tachycardiomyopathy
  1. Claire A Martin,
  2. Pier D Lambiase
  1. Department of Cardiology, Barts Health NHS Trust, London, UK
  1. Correspondence to Dr Pier D Lambiase, UCL Institute of Cardiovascular Science & Barts Heart Centre Cardiology Department Barts Heart Centre W. Smithfield, London EC1 7EB, UK; pierlambiase{at}, p.lambiase{at}

Statistics from

Learning objectives

  • Recognise the diagnosis of tachycardiomyopathy (TCMP)

  • Understand the pathophysiology

  • Determine treatment strategies to restore left ventricular function

  • The role of TCMP in non-responders to cardiac resynchronisation


Tachycardiomyopathies (TCMP) are an important cause of left ventricular (LV) dysfunction that should be recognised by physicians as they are potentially reversible and have a significant impact on morbidity and prognosis. They are classically defined as the reversible impairment of ventricular function induced by persistent arrhythmia. However, it is becoming increasingly evident that they can be induced by atrial and ventricular ectopy promoting dyssynchrony and indeed the term ‘arrhythmia-induced cardiomyopathy’ is emerging to describe the phenomenon.1 2 A more current proposed definition highlights aetiology: ‘Atrial and/or ventricular dysfunction—secondary to rapid and/or asynchronous/irregular myocardial contraction, partially or completely reversed after treatment of the causative arrhythmia’ 3 (figure 1). Two categories of the condition exist: the arrhythmia is the only reason for ventricular dysfunction (arrhythmia-induced), and another where the arrhythmia exacerbates ventricular dysfunction and/or worsens heart failure (HF) in a patient with concomitant heart disease (arrhythmia-mediated).4 The exclusion of underlying structural heart disease can be challenging as current imaging techniques, for example, MRI cannot easily identify diffuse fibrosis which may itself be primary or secondary to the effects of arrhythmia promoting ventricular wall dyskinesis and stretch or valvular regurgitation.

Figure 1

Arrhythmias leading to left ventricular dysfunction. AF, atrial fibrillation; LBBB, left bundle branch block; PVCs, premature ventricular complexes; RBBB, right bundle branch block; RV, right ventricular; SVT, supraventricular tachycardia.


The mechanisms of TCMP are not fully defined but include subclinical ischaemia, abnormalities in energy metabolism, redox stress and calcium overload.5 6 In animal models of persistent high rate atrial or ventricular pacing, ventricular impairment is also associated with changes in myocardial electrophysiology including prolongation of the action potential and spontaneous ventricular arrhythmias. Indeed, persistent left bundle branch block leads …

View Full Text

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.