The physiological basis of essential hypertension is a continuing rise in the systemic vascular resistance (SVR) over time, a process which does not appear to be halted by drug treatment that normalizes diastolic blood pressure (BP). 1 Since SVR is a major determinant of BP in the absence of left ventricular (LV) systolic dysfunction, BP rises in parallel with the SVR. This can easily be demonstrated with drugs such as phenylnephrine or cyclosporin that increase the SVR. It was previously thought that peripheral vasoconstriction was a ‘protective’ response to an early hyperkinetic circulation. However, this hypothesis has largely been discounted. 2 Hypertension is thus the response to an increased SVR, the aetiology of which is still unclear. The increased pressure generated within the left ventricle to maintain a high level of systemic arterial BP has an inherent tendency to cause cardiac dilatation. To prevent this from happening, the natural adaptive response is to dissipate the excess pressure through LV wall thickening. We now know that reversing hypertensive LV hypertrophy (LVH) with treatment may improve prognosis. 3 However, resting BP, the measure currently used to manage hypertension, is not a good predictor of LVH. Perhaps this partly explains why control of resting BP does not normalize cardiac mortality 4 or stroke risk. 5 Furthermore, it has been noted that in some patients with apparently well‐controlled resting BP, LVH may persist 6 or even continue to increase. 7