Hypertensive left ventricular hypertrophy: pathophysiology, assessment and treatment

Left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular morbidity and mortality. LVH is associated with coronary events, and there is an association between cerebrovascular disease and increased left ventricular mass (LVM). Experimental studies have elucidated the importance of non-myocytic cells inducing increased perivascular and interstitial fibrosis along with thickening of the media of intramyocardial coronary arteries in hypertensive LVH. M-mode echocardiography is the most accepted standard for the diagnosis and quantification of LVH, but some controversies exist regarding the ideal methodology for serial assessment of LVM. It is still a matter of debate whether 2-dimensional echo measurements represent a more accurate method. Hopefully, both the introduction of 3-dimensional echo and new Doppler techniques can provide more accurate measurements of LVM and additional information on changes in myocardial fibrosis and stiffness. Experimental studies have shown that normalization of hypertensive myocardial and coronary artery remodelling take place with drugs like angiotensin converting enzyme (ACE)-inhibitors and calcium antagonists. Two meta-analyses suggest that ACE-inhibitors may be the most efficient drugs in reducing LVM, but a clinical correlate to this assumption is at present not available. There are some indications that regression or progression of LVH assessed by ECG and echocardiography may in fact be related to the incidence of cardiovascular events. But large-scale controlled studies of various treatment regimens are still needed to establish whether drug induced regression can improve the prognosis of hypertensive LVH independent of the antihypertensive effect.