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Published on: June 29, 2014
Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol
Insights
Atenolol effectively treats hypertension, leading to left ventricular hypertrophy regression as early as 4 weeks. This blood pressure control improves cardiac structure without impairing systolic function.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) regression is a known effect of antihypertensive drugs.
- The precise timeline for LVH regression during treatment remains unclear.
Purpose of the Study:
- To define the time course of left ventricular hypertrophy regression in patients with essential hypertension treated with atenolol.
- To assess the impact of atenolol on cardiac structure and function over one year.
Main Methods:
- 12 patients with essential hypertension received atenolol for one year.
- Echocardiograms were performed at baseline and seven times serially.
- Blood pressure, heart rate, and cardiac structural parameters were monitored.
Main Results:
- Atenolol significantly reduced blood pressure and heart rate.
- Posterior and septal wall thicknesses decreased significantly by 4 weeks.
- Left ventricular mass showed a statistically significant reduction by 6 months.
Conclusions:
- Regression of left ventricular hypertrophy begins as early as 4 weeks with atenolol therapy.
- Atenolol-induced blood pressure control leads to sustained LVH regression without compromising left ventricular systolic function.
Abstract:
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.
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