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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
Published on: February 28, 2012
Digoxin use is associated with increased platelet and endothelial cell activation in patients with nonvalvular atrial
Julio A Chirinos1, Aurelio Castrellon, Juan Pablo Zambrano
1Department of Medicine, Division of Cardiology, University of Miami School of Medicine, Miami, Florida 33136, USA.
Insights
Digoxin use in atrial fibrillation patients significantly increases markers of platelet and endothelial activation. This suggests digitalis may promote thrombosis and vascular events in AF patients.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Increased intracellular calcium is crucial for platelet activation and endothelial cell function.
- In vitro studies show digitalis activates platelets.
- Endogenous digitalis-like substances influence endothelial cell processes.
Purpose of the Study:
- To investigate the association between digoxin use and markers of endothelial and platelet activation in nonvalvular atrial fibrillation (AF).
Main Methods:
- Studied 30 patients with nonvalvular AF.
- Measured platelet P-selectin (CD62P) expression and platelet microparticles (PMP).
- Assessed endothelial microparticles (EMP) using anti-CD31 (EMP31) and anti-E-selectin (EMP62E) antibodies.
Main Results:
- Digoxin users (n=16) showed no significant clinical/echocardiographic differences from non-users (n=14).
- Digoxin users had significantly elevated CD62P expression and platelet-leukocyte conjugates.
- Markedly increased endothelial activation markers (EMP62E, EMP31) were observed in digoxin users, persisting after confounder adjustment.
Conclusions:
- Digoxin use in AF patients is linked to heightened endothelial and platelet activation.
- Pharmacologic digitalis doses may activate endothelial cells and platelets.
- Digitalis use in AF could potentially increase thrombosis and vascular event risk.
Objectives:
The purpose of this study was to determine whether digoxin use is associated with increased flow cytometric markers of endothelial cell and platelet activation in patients with nonvalvular atrial fibrillation (AF).
Background:
Increased intracellular calcium is a key event in platelet activation, and several studies have demonstrated that digitalis activates platelets in vitro. Intracellular calcium also is a key regulator of endothelial cell function, and endogenous digitalis-like substances have been shown to affect biologic processes in endothelial cells.
Methods:
We studied 30 patients with nonvalvular AF. We measured the levels of (1) platelet expression of P-selectin (CD62P), (2) platelet microparticles (PMP); and (3) endothelial microparticles (EMP) identified by anti-CD31 (EMP31) and by anti-E-selectin antibodies (EMP62E).
Results:
Patients who were taking digoxin (n = 16; mean digoxin level = 0.93 ng/dL) did not demonstrate any significant differences in clinical or echocardiographic characteristics compared with patients not taking digoxin (n = 14). Patients taking digoxin had significantly increased levels of CD62P expression in platelets and platelet-leukocyte conjugates and markedly increased markers of endothelial activation: EMP62E and EMP31. After adjusting for potential confounders (including age, congestive heart failure, coronary artery disease, ejection fraction, antiplatelet, beta-blocker, and calcium channel blocker use), the differences persisted.
Conclusions:
Digoxin use in patients with AF is associated with increased levels of endothelial and platelet activation. If digitalis activates endothelial cells and platelets at pharmacologic doses, use of digitalis in conditions such as AF could predispose to thrombosis and vascular events.
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