Physiological versus pathological cardiac electrical remodelling: potential basis and relevance to clinical management

Cardiac hypertrophy is an adaptive response to haemodynamic stress. Pressure and/or volume overload in hypertension, myocardial infarction (MI) and valvular heart disease are pathological stresses that lead to left-ventricular (LV) dilatation and/or wall thickening. While in the short term compensatory mechanisms maintain cardiac output, sustained hypertrophic responses can lead to maladaptive remodelling, predisposing to cardiac arrhythmias and heart failure. Physical exercise and pregnancy are examples of physiological stress. The nature of the exercise determines the balance between dilatation and increased wall thickness, producing so-called physiological hypertrophy. Although similar degrees of LV hypertrophy are achieved in pathological and physiological hypertrophy, physiological hypertrophy generally fails to produce adverse consequences like ventricular arrhythmias (Viitasalo et al. 1982; Biffi et al. 2008). So, what makes the consequences of physiological remodelling different from those of pathological remodelling?