Left Ventricular Hypertrophy – the Problem and Possible Solutions

Abstract

Left ventricular hypertrophy (LVH), which describes pathological changes in cardiac structure, is a powerful and reversible predictor of cardiovascular risk. There is a continuous relationship between left ventricular mass (LVM) and the likelihood of cardiovascular events, with no cut-off between the absence of such events and heightened risk. A correlation between LVH and blood pressure is well established. There is a paradox, however, that the structural changes to the heart as a result of increased workload due to high blood pressure appear to promote cardiovascular disease. This may be partially explained by the fact that ambulatory blood pressure measurements correlate more closely with LVH than resting blood pressure. Blood pressure variation throughout the day is also emerging as an important correlate of LVH, and a strong association has been identified between an early morning rise in blood pressure and increased LVM. Use of anti-hypertensive agents not only lowers blood pressure, but can also bring about LVH regression. The pathological role of angiotensin II in LVH and target-organ damage within the cardiovascular continuum suggest that agents targeting the renin angiotensin-aldosterone system (RAAS), such as the angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, may prove particularly effective and may confer beneficial effects in addition to the lowering of blood pressure. The angiotensin II receptor blockers may be very appropriate treatment options because of their placebo-like tolerability and the possibility of more complete blockade of the RAAS. Within this class of anti-hypertensive agents, pharmacological differences may mean that some agents afford greater cardioprotection than others.