TY - JOUR T1 - Pathophysiology, diagnosis and treatment of tachycardiomyopathy JF - Heart JO - Heart SP - 1543 LP - 1552 DO - 10.1136/heartjnl-2016-310391 VL - 103 IS - 19 AU - Claire A Martin AU - Pier D Lambiase Y1 - 2017/10/01 UR - http://heart.bmj.com/content/103/19/1543.abstract N2 - Learning objectivesRecognise the diagnosis of tachycardiomyopathy (TCMP)Understand the pathophysiologyDetermine treatment strategies to restore left ventricular functionThe role of TCMP in non-responders to cardiac resynchronisationTachycardiomyopathies (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 … ER -