Abstract:
It is well known that stretching cardiac muscle increases the force of contraction (Frank, 1895). Less well known is that sustained stretch increases Ca2+ influx (Allen & Kurihara 1982), alters the action potential waveform (Sung, Mills et al. 2003), and causes stretch-induced arrhythmias (SIA) under some conditions (Franz, Cima et al. 1992). Cardiovascular disease is the leading cause of death in New Zealand (30% annually), with heart failure patients at increased risk of sudden cardiac death from ventricular arrhythmias (Ministry of health, 2015). Understanding the cellular mechanisms underlying SIAs will potentially lead to new therapeutic targets that will improve clinical management of patients in the future.