Abstract 11912: Glycocalyx Shedding is Markedly Increased During Acute Phase of Takotsubo Cardiomyopathy
Introduction: Acute myocardial infarction (AMI) and other forms of myocardial acute oxidative stress are associated with variable “shedding” of vascular and other glycocalyx. This glycocalyx shedding (GCS) can be quantitated by release into plasma of glycocalyx components such as Syndecan-1 (SD1), which is the most prevalent proteoglycan. Previous in vitro studies have implicated both catecholamines and BNP release as potential accentuating factors in GCS: since these are prominent aspects of the pathogenesis of Takotsubo cardiomyopathy (TTC), we hypothesised that TTC (i) would be associated with increased GCS both acutely and during subsequent 3 months of continued myocardial inflammation and (ii) extent of GCS would be predictable on the basis of NT-proBNP and catecholamine releases.
Methods: SD1 concentrations were measured in 49 TTC patients acutely and after 3 months in comparison with 12 normal age-matched controls and 10 myocardial infarct patients. Correlations between SD1 and (i) acute LV function, (ii) lowest BP on admission, (iii) peak catecholamine release, and (iv) extent of systemic and myocardial inflammatory activation [measured by high sensitive C-reactive protein (hsCRP), NT-proBNP concentrations, and myocardial T2 signal intensity on cardiac MRI] were sought.
Results: Acute SD1 concentrations in TTC patients were significantly elevated compared to 3 month and control values (2-way ANOVA) (Figure). However, there was no significant difference between acute TTC and MI levels. In addition, there were no correlations between SD1 concentrations and extent of severity of acute episode.
Conclusions: 1. TTC, despite minimal associated myocardial necrosis, is associated with marked increase in GCS.
2. Extent of GCS in TTC is not closely related to either release of NT-proBNP or normetanephrine.
We postulate that GCS may contribute to some of the clinical features of TTC, such as development of pulmonary oedema without marked increases in PCWP.
Author Disclosures: T.H. Nguyen: None. S. Liu: None. G. Ong: None. I. Stafford: None. M. Frenneaux: None. J.D. Horowitz: None.
- © 2016 by American Heart Association, Inc.