Treatment of Diastolic Dysfunction in Hypertensive Left Ventricular Hypertrophy

The relation of hypertension and left ventricular hypertrophy (LVH) to diastolic dysfunction are well described.1 Diastolic dysfunction has been shown to be associated with higher all-cause and cardiac mortality, even in patients without significant systolic dysfunction or symptoms of congestive heart failure, independently of covariates.1 Thus, the identification of asymptomatic patients with diastolic dysfunction by Doppler echocardiography is essential and identifies patients at risk of adverse outcome. The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study was the first to indicate that about 10% reduction in LV mass was associated with improvement in diastolic function, most notably those related to active relation (shortening of isovolumic relaxation time, IVRT) and passive chamber stiffness (prolongation of deceleration time, DT) after treatment with either a losartan- or atenolol-based regimen.2 The present report from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) study extends the LIFE study results by showing that improvement in diastolic function with antihypertensive treatment was detected earlier (at 48 weeks) and more consistently using tissue velocity echocardiography than conventional Doppler echocardiography.3 Tissue velocity echocardiography allows for noninvasive measurement of intramyocardial systolic and diastolic velocities directly and has been shown to correlate with interstitial fibrosis and myocyte β-adrenergic receptor density in humans.4