Atenolol treatment in hypertensive patients significantly reduced left ventricular mass from 144 to 127 g/m2 (p<0.05), with wall thickness reductions seen as early as 4 weeks.
Observational (n=12)
p-value: p=<.05
Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.
Dunn et al. (Sat,) conducted a observational in previously untreated essential hypertension (n=12). atenolol vs. baseline was evaluated on Left ventricular mass (p=<.05). Atenolol treatment in hypertensive patients significantly reduced left ventricular mass from 144 to 127 g/m2 (p<0.05), with wall thickness reductions seen as early as 4 weeks.