Abstract
Stress cardiomyopathy (SCM) is a unique cardiac disorder that more often occurs in women. SCM presents in a similar fashion as acute myocardial infarction (AMI), with chest pain, ECG changes, and congestive heart failure. The primary distinguishing feature is the absence of thrombotic coronary occlusion in SCM. How this reduction in cardiac function occurs in the absence of coronary occlusion remains unknown. Therefore, we tested the hypothesis that a targeted proteomic comparison of patients with acute SCM and AMI might identify relevant mechanistic differences. Blood was drawn in normal controls (n = 6), women with AMI (n = 12), or women with acute SCM (n = 15). Two-week follow-up samples were available in AMI (n = 4) and SCM patients (n = 11). Relative concentrations of 1,310 serum proteins were measured in each of the 48 samples using the SOMAscan assay. Women with AMI had greater myocyte necrosis, as reflected by a higher peak troponin I concentration (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/ml, p < 0.05). AMI and SCM patients had equivalent reductions in left ventricular ejection fraction [LVEF (%) 39 ± 12 vs. 37 ± 12, p = 0.479]. In follow-up, women with SCM had a greater improvement in cardiac function [LVEF (%) 60 ± 7 vs. 45 ± 13, p < 0.001]. No differentially expressed proteins were detected (absolute log2-fold change >1; q < 0.05) between AMI and SCM in the acute or recovery phase. However, when we compared normal controls to patients with AMI, there was differential expression of 35 proteins. When we compared normal controls to patients with SCM, 45 proteins were differentially expressed. In comparison to normal controls, biological processes such as complement, coagulation, and inflammation were activated in both AMI and SCM. There were four proteins that showed a non-significant trend to be increased in acute SCM vs. AMI (netrin-1, follistatin-like 3, kallikrein 7, kynureninase). Despite a lesser degree of myocardial necrosis than AMI, SCM is characterized by a similar activation of inflammatory, complement, and coagulation pathways. These findings may explain reported thromboembolic complications in the short term and elevated risk of mortality in the long term of SCM.
Highlights
Stress cardiomyopathy (SCM) is a unique form of heart disease that primarily affects women
We found that women presenting with either SCM or acute myocardial infarction (AMI) have an increase in proteins related to complement, coagulation, and inflammation
Women who presented with non-ST or ST elevation myocardial infarction and had coronary angiography demonstrating either culprit LAD disease or apical variant SCM were prospectively enrolled
Summary
Stress cardiomyopathy (SCM) is a unique form of heart disease that primarily affects women. Recent studies have shown that SCM patients have increased long-term morbidity and mortality (5.6% risk of death per patient year) [6,7,8]. This disorder may not be as benign as previously thought. After almost 30 years of study, the mechanism of SCM is still not understood. Acute myocardial infarction (AMI) has greater myocyte necrosis [10]. Despite these different mechanisms of injury, cardiac function is impaired to an equivalent degree in both conditions [11]. The exact mechanism by which LV dysfunction occurs in SCM remains poorly understood
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
