Abstract 16300: Endothelial Dysfunction and Inflammation in Stress Cardiomyopathy
Introduction: Stress cardiomyopathy (SCM) is characterized by reversible left ventricular dysfunction. SCM has an identical acute presentation as acute myocardial infarction (AMI). The mechanism of SCM has not been completely elucidated. As patients with chest pain and normal coronary arteries are known to have endothelial dysfunction, we tested the hypothesis that endothelial dysfunction might be different in SCM and AMI.
Method: To evaluate endothelial function, we performed brachial artery flow mediated dilation (FMD) on 11 patients with SCM, 8 patients with AMI and 6 control patients with no CAD. Briefly, the diameter of the brachial artery is measured by high-resolution vascular ultrasound in response to an increase in blood flow after five minutes occlusion of the brachial artery. Measurements were made at 1, 5 and 10 minutes post blood pressure cuff release to induce reactive hyperemia. Furthermore, blood from 15 patients with SCM, 12 patients with AMI and 6 patients without CAD were collected and serum proteins were subsequently analyzed using the SOMAscan™ assay.
Results: We found that patients with SCM have decreased FMD compared to patients with AMI as well as patients without CAD. At 1 minute, FMDs were 11.60%, 11.03% and 3.97% (p ≤ 0.002) in the control, AMI and SCM groups, respectively. At 5 minute, FMDs were 17.40%, 8.46% and 5.60% (p ≤ 0.006) in the control, AMI and SCM groups, respectively (Figure 1). SOMAscan™ assay revealed that canonical inflammatory markers such as CRP, GFD15, SAA, and IL-2 are elevated in the patients with SCM and AMI as compared to controls. IL-10, an anti-inflammatory cytokine, is decreased in both the SCM and AMI groups.
Conclusion: We demonstrate that stress cardiomyopathy is a heightened inflammatory state associated with endothelial dysfunction similar to acute myocardial infarction. Inflammation and endothelial dysfunction at the microvascular level may play an important role in reversible left ventricular dysfunction.
Author Disclosures: I. Kassas: None. K. Tran: None. T. Fitzgibbons: None. K. Chen: None. S. Craige: None. S. Kant: None. J. Bote: None. S. Girgis: None. G. Aurigemma: None. J. Keaney: None.
- © 2016 by American Heart Association, Inc.