Mechanical and other factors relating to left ventricular hypertrophy.

Although the development of left ventricular hypertrophy in hypertension is explained as a response to increases in pressure load and wall tension, the relationship between left ventricular mass and conventional blood pressure is usually weak. This may be due to the lack of standardization and the small number of blood pressure measurements in some studies. However, even 24-h blood pressure monitoring can explain only around 25% of the variation in left ventricular mass, and repeated blood pressure measurements over 30 years have not proved better in this respect. Therefore, other factors have been considered, including anthropometric and demographic characteristics; genetic influences; differences in salt intake, physical activity and alcohol consumption; neurohumoral factors; duration of hypertension; and previous antihypertensive treatment. Antihypertensive treatment may reduce left ventricular mass and a number of prospective, randomized, comparative studies have assessed whether some (classes of) drugs are more effective than others. A meta-analysis of such studies, comparing diuretics, beta-blockers, calcium antagonists and/or angiotensin-converting enzyme (ACE) inhibitors, suggests that the reduction of left ventricular mass with each of these classes is similar to the reduction obtained with the other three classes statistically combined. Of particular interest is the observation that the four studies which specifically compared an ACE inhibitor and a calcium antagonist concluded that their effects on left ventricular mass did not significantly differ. Furthermore, that agents such as minoxidil and hydralazine do not reduce left ventricular mass.