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Improving the prediction of long‐term readmission and mortality using a novel biomarker panel

To the Editor, The Brown et al. article, entitled “Improving the prediction of long‐ term readmission and mortality using a novel biomarker panel,” and the significant contributions it has made throughout the medical community, was met by us with deep academic interest. We concur with the authors that cardiac biomarkers should be utilized in clinical practice to accurately predict long‐term readmission rates and determine mortality rates following coronary artery bypass graft (CABG) surgery. However, we seek to highlight additional, equally effective cardiac biomarkers that were not discussed in this manuscript. First, the study failed to recognize systemic inflammation as a factor in the pathogenesis of postoperative atrial fibrillation (POAF). A paper by Harling et al. determined that patients who develop POAF express higher levels of soluble vascular endothelial cell adhesion molecule (sVCAM‐1) preoperatively than those who maintain sinus rhythm. Further, it showed that sVCAM‐1 expression decreased significantly 48 hours after the surgery. Second, the research omitted discussion on how systemic inflammatory reaction, myocardial ischemia, and reperfusion injury can stimulate a hypercoagulable state following CABG surgery. According to Men et al. and Kim et al., plasma von Willebrand factor antigen levels can be sensitively correlated with endothelial injury after CABG surgery. Therefore, this marker can measure circulation restoration's success. Third, noninvasive biomarkers of myocardial damage were not considered in the publication. Zhou et al. recognized microRNA‐1 (miR‐1) as a cardio‐specific/enriched microRNA, elevated in serum and urine after cardiopulmonary bypass open heart surgery. Their work further suggested that urinary miR‐1 could constitute a novel noninvasive biomarker of myocardial injury. Moreover, Yoshihisa et al. state that the N‐terminal fragment of titin (Titin‐N) is cleaved by calpain‐3 in damaged muscle and that urinary Titin‐N may be a marker of sarcomere damage. These cardiac biomarkers could, therefore, have provided a stronger foundation for the conclusions and results discussed in this highly valued document.