Left ventricular (LV) hypertrophy may reflect physiological adaptation to an increased work load of the heart following intense physical training. However, LV hypertrophy often represents a pathophysiologic condition, and can develop due to intrinsic stimuli (cardiomyopathy), or secondary to extrinsic stimuli, such as pressure or volume overload accompanying hypertension and valvar disease (fig 1). Myocardial hypertrophy is also part of the remodelling process following an acute myocardial infarction, and is a common finding in patients with congestive heart failure caused by systolic and/or diastolic LV dysfunction.

The presence of LV hypertrophy is a strong independent risk factor for future cardiac events and all cause mortality.¹ The risk for sudden cardiac death is increased in subjects with LV hypertrophy, independent of the aetiology, and this event occurs also in individuals with no or only mild prior symptoms related to cardiovascular disease. Intense animal and human research has identified some common features and provided a framework within which some crucial components can be explained. Thus, whether the focus is haemodynamic or electrophysiologic, there seems to be consensus as to the initiation of a fetal-like gene programme in myocardial hypertrophy.^2,3 The insights into its consequences can be applied in the clinical management of individual patients.

During recent years, experts with different backgrounds within cardiovascular medicine have aimed to create a united picture of cardiac hypertrophy and sudden cardiac death, and to present it in such a way that in can be integrated and applied into clinical cardiovascular practice. This article is an attempt to pursue this ambition. We focus on LV hypertrophy in human hypertension as a model of cardiac hypertrophy, and myocardial hypertrophy as a condition with “reduced repolarisation reserve”,^w1 and thus a latent …