Abstract 11265: Elevated Plasma Annexin A5 Levels in Patients after Atrial Switch Operation for Complete Transposition of the Great Arteries: Association with Impaired Systemic Ventricular Myocardial Deformation
Background: Experimental data suggest involvement of annexin A5 (AnxA5) in cardiomyocyte apoptosis. In adults with heart failure, elevated plasma AnxA5 level has been related to ventricular dysfunction.
Objective: We tested the hypothesis that plasma AnxA5 level is increased in patients after atrial switch operation for complete transposition of the great arteries and is related to serum level of tumour necrosis factor-alpha (TNF-α), a stimulant of cardiomyocyte apoptosis, systemic ventricular myocardial deformation, and subpulmonary ventricular eccentricity.
Methods: Plasma AnxA5 and serum TNF-α levels were determined in 27 patients, aged 25.2±3.1 years, and 20 age-matched controls and myocardial deformation was assessed by speckle tracking echocardiography.
Results: Compared with controls, patients had significantly higher circulating AnxA5 (p<0.001) and TNF-α (p=0.018) levels, lower systemic ventricular global longitudinal systolic strain and systolic and diastolic strain rates (SRs) (all p<0.001), and reduced subpulmonary global systolic strain and early diastolic SR (both p<0.001). For the whole cohort, plasma AnxA5 correlated with serum TNF-α (p=0.002), systemic ventricular strain and systolic and diastolic SRs (all p<0.05), and subpulmonary strain and early diastolic SR (both p<0.001). In patients, plasma AnxA5 level correlated positively with subpulmonary ventricular eccentricity (p=0.027). Multiple linear regression analysis identified systemic ventricular systolic strain (β=-0.50, p<0.001) and serum TNF-α (β=0.29, p=0.022) as significant correlates of plasma AnxA5.
Conclusion: Elevated plasma AnxA5 level in patients after atrial switch operation is associated with impaired systemic myocardial deformation and increased serum TNF-α level, implicating a possible role of cardiomyocyte apoptosis in the pathogenesis of progressive systemic ventricular dysfunction.
- © 2011 by American Heart Association, Inc.