The unpredictable nature and potentially catastrophic consequences of ventricular arrhythmias (VAs) have obligated physicians to search for therapies to prevent sudden cardiac death (SCD). At present, a low left ventricular ejection fraction (LVEF) has been used as a risk factor to predict SCD in patients with structural heart disease and has been consistently adopted as the predominant, and sometimes sole, indication for implantable cardioverter defibrillator (ICD) therapy. Although the ICD remains the mainstay life-saving therapy for SCD, it does not modify the underlying arrhythmic substrate and may be associated with adverse effects from perioperative and long-term complications. Preventative pharmacological therapy has been associated with limited benefits, but anti-arrhythmic medications have significant side effects profiles. Catheter ablation of VAs has greatly evolved over the last few decades. Substrate mapping in sinus rhythm has allowed haemodynamically unstable VAs to be successfully treated. Both LVEF as an indication for ICD therapy and electro-anatomical mapping for substrate modification identify static components of underlying myocardial arrhythmogenicity. They do not take into account dynamic factors, such as the mechanisms of arrhythmia initiation and development of new anatomical or functional lines of block, leading to the initiation and maintenance of VAs. Dynamic factors are difficult to evaluate and consequently are not routinely used in clinical practice to guide treatment. However, progress in the treatment of VAs should consider and integrate dynamic factors with static components to fully characterize the myocardial arrhythmic substrate.
The flowchart shows clinical pathways for prevention of sudden cardiac death in patients with structural heart disease. Blue boxes and arrows show current clinical practice. Green boxes and arrows describe potential future directions. *Cardiac magnetic resonance imaging, T wave alternans, high-resolution voltage substrate mapping, electrophysiological evaluation of anatomical and functional components of potential arrhythmia circuits and patterns of VT initiation.