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[Left ventricular function in hypertension treated with beta blockers]
Insights
Atenolol, a beta-blocking agent, reduced blood pressure and heart rate in patients with essential hypertension. While initially decreasing left ventricular function, it showed improvement over 8 weeks, suggesting low risk for heart decompensation.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Essential hypertension poses risks to cardiovascular health, particularly left ventricular function.
- Beta-blocking agents are commonly prescribed for hypertension management.
Purpose:
- To assess the effects of atenolol on left ventricular function in patients with essential hypertension.
- To evaluate changes in cardiac parameters during 8 weeks of atenolol treatment.
Summary:
- 14 hypertensive patients received 100 mg/day oral atenolol.
- Significant reductions in systolic and diastolic blood pressure and heart rate were observed after 4 weeks.
- Left ventricular systolic shortening initially decreased but improved by week 8; end-diastolic diameter remained unchanged.
Impact:
- Long-term atenolol therapy shows a transient reduction in left ventricular function, which recovers over time.
- The observed functional changes are slight, indicating a low likelihood of inducing left heart decompensation.
- Findings are particularly relevant for patients with initially normal left ventricular function.
Abstract:
In 14 patients with essential hypertension, left ventricular function was assessed echocardiographically before and after 4 and 8 weeks of treatment with the betablocking agent atenolol. Atenolol was given orally in a dose of 100 mg/day. After 4 weeks of treatment systolic blood pressure decreased from 160 to 138 mm Hg(p less than 0.001) and diastolic pressure from 105 to 91 mm Hg(p less than 0.001). Heart rate decreased from 76 to 64 beats/min (p less than 0.05). Systolic shortening of the left ventricular transverse diameter declined from 41 to 36% (p less than 0.01), though in no instance did it fall below the lower limit of normality (30%). After 8 weeks of betablocking therapy, blood pressure and heart rate remained essentially unchanged. Systolic shortening increased slightly but insignificantly to 38%. The left ventricular enddiastolic diameter did not change throughout the study. It is concluded that longterm betablocking therapy is associated with a significant reduction of left ventricular function which improves in the later stage of treatment. Since the diminution of left ventricular function is slight, the induction of left heart decompensation is unlikely, at any rate in patients with initially normal left ventricular function.