Related Experiment Videos
Does acute-phase beta blockade reduce left atrial appendage function in patients with chronic nonvalvular atrial
1Departments of Cardiology, Medical Faculty, Yüzüncü Yil University, Van, Turkey.
Insights
Acute beta-blocker therapy may harm left atrial appendage (LAA) function in patients with atrial fibrillation. This study found reduced LAA emptying velocities and new thrombi formation after metoprolol administration.
Area of Science:
- Cardiology
- Pharmacology
- Medical Imaging
Background:
- Chronic nonvalvular atrial fibrillation (AF) often requires rate control.
- Left atrial appendage (LAA) dysfunction is a risk factor for thromboembolism in AF.
- Beta-blockers are commonly used for rate control in AF.
Purpose of the Study:
- To evaluate the effect of acute beta-blocker therapy on LAA function in patients with chronic AF.
- To assess changes in LAA emptying velocities and thrombus formation.
- To investigate potential risks of beta-blockers in this patient population.
Main Methods:
- Transesophageal echocardiography (TEE) was used to assess 21 patients with chronic AF.
- Measurements included heart rate, blood pressure, LAA emptying velocities, and echo contrast.
- Patients received a metoprolol bolus, followed by 1 week of oral therapy, with serial TEE assessments.
Main Results:
- Metoprolol significantly reduced heart rate and blood pressure.
- LAA emptying velocities decreased significantly after metoprolol administration (P <.001).
- New LAA thrombi developed in 2 patients post-treatment.
Conclusions:
- Acute beta-blocker therapy may impair LAA function in patients with chronic AF.
- Reduced LAA emptying velocity and thrombus formation are potential adverse effects.
- Caution is advised when initiating beta-blockers in AF patients with normal LV function and rapid ventricular rates.
Abstract:
To investigate whether acute-phase beta-blocker therapy has a harmful effect on left atrial appendage (LAA) function in patients with chronic nonvalvular atrial fibrillation by transesophageal echocardiography (TEE), we evaluated 21 patients with normal left ventricular systolic function and a poorly controlled ventricular rate, despite the use of digoxin. Baseline parameters that were obtained included heart rate, blood pressure, LAA emptying velocities, and left atrial spontaneous echo contrast intensity. Then, each patient was given a bolus dose of 5 mg metoprolol. Ten minutes later, a second set of assessments was performed. After the first TEE studies, each patient began treatment with metoprolol (50 mg orally twice daily for 1 week). A second TEE study was performed after 1 week of continuous oral metoprolol therapy at maintenance dose, and values were again determined. The average resting apical heart rate was 91 +/- 7 bpm. As expected, beta-blocker therapy showed a marked decrease in heart rate at 10 minutes (79 +/- 6 bpm, P <.001) and at 1 week (71 +/- 4 bpm, P <.001). Beta-blocker therapy caused a significant reduction in systolic and diastolic blood pressures (144 +/- 16 / 93 +/- 6 mm Hg at baseline, 137 +/- 16 / 87 +/- 9 mm Hg at 10 minutes, and 135 +/- 12 / 86 +/- 8 mm Hg at 1 week, P <.001). With the beta-blocker therapy, the baseline transesophageal Doppler parameter of LAA emptying velocities (at baseline 24 +/- 7 cm/s) fell significantly at 10 minutes (19 +/- 7 cm/s, P <.001) and at 1 week (17 +/- 6 cm/s, P <.001) after initiation of beta-blocker therapy. After a bolus of metoprolol, spontaneous echo contrast intensity did not change in any patients, but 1 week later, it increased in 1 patient. In 2 patients who had not been found to have an LAA thrombus at baseline TEE study, the second TEE examination demonstrated new thrombi in the LAA. In conclusion, our findings suggest that in patients with chronic nonvalvular atrial fibrillation who have normal left ventricular systolic function and a poorly controlled ventricular rate despite the use of digoxin, acute-phase beta blockade may have a harmful effect on LAA function.