Left ventricular hypertrophy (LVH) is present in the majority of patients with type 2 diabetes, since it affects 70%. It is a strong independent predictor of cardiovascular deaths and events and is even worse than triple vessel coronary disease. The reason why LVH is so adverse is because it predates so many different cardiovascular events i.e. LVH is intrinsically arrhythmogenic and causes sudden death, it impedes left ventricular (LV) filling and leads to diastolic heart failure, it reduces coronary perfusion reserve and causes ischaemia and it causes left atrial enlargement, atrial fibrillation (AF), and cardio-embolic strokes. Controlling blood pressure (BP) and using a drug that blocks the renin-angiotensin system (RAS) are the standard approaches to the management of LVH but this approach is only partially effective since 44% of all patients with type 2 diabetes are normotensive patients with LVH. Thus "normotensive LVH" is very common. Indeed, BP only contributes 25% to the variability in LV mass seen in a population. (This is important since LVH is the same thing as a high level of LV mass). Despite a "normal" BP, normotensive LVH is just as risky as is hypertensive LVH. Nevertheless, we do know that regressing LVH irrespective of BP changes is an effective way to reduce the incidence of all major cardiovascular (CV) events including specifically sudden deaths, heart failure hospitalisations, new onset AF and strokes. The Losartan Intervention For Endpoint reduction in hypertension study (LIFE) provides conclusive proof that in diabetes, LVH regression per se reduces future cardiovascular events (by 24%), reduces CV deaths (by 37%) and reduces total deaths (by 41%) irrespective of BP.