Faculty Bibliography

OBJECTIVES/OBJECTIVE:Patients with low left ventricular ejection fraction (LVEF) undergoing high-risk coronary artery bypass grafting (CABG) are at increased risk for postcardiotomy cardiogenic shock. This report describes planned concomitant microaxial temporary mechanical support (MA-TMS) device placement as a viable bridge-to-recovery strategy for high-risk patients receiving surgical revascularization. METHODS:A retrospective review was performed for all patients from October 2017 to May 2019 with low LVEF (<30%), New York Heart Association Class III or IV symptoms, and myocardial viability who underwent CABG with prophylactic MA-TMS support at a single institution (n = 13). RESULTS:Mean patient age was 64.8 years, and 12 patients (92%) were male. Eight patients (62%) presented with acute coronary syndrome. Mean predicted risk of mortality was 4.6%, ranging from 0.6% to 15.6%. An average of 3.4 grafts were performed per patient. Greater than 60% of patients were extubated within 48 hours and out-of-bed within 72 hours, and the average duration of MA-TMS was 5.7 days. Mean postoperative length of stay was 16.7 days. There were no postoperative myocardial infarctions or deaths. CONCLUSIONS:Prophylactic MA-TMS may allow safe and effective surgical revascularization for patients with severe left ventricular dysfunction who may otherwise be offered a durable ventricular assist device.

Epinephrine, a non-specific adrenergic agonist, is one of the most commonly used inotropes perioperatively. Recent studies have shown that inflammatory response in cardiac surgery could result in hypoperfusion, dysrhythmias, myocardial ischemia, and other pathophysiological alterations in the postoperative period. These alterations might be contributing to the adverse clinical outcome. Although epinephrine has been shown to have effects on the immune system, how epinephrine affects inflammatory response is unclear. We hypothesized that epinephrine exposure may alter the inflammatory response which may potentially contribute to the adverse clinical outcomes. We used cultured rat cardiomyocytes (H9C2) with epinephrine exposure in this study. The expression of mRNA for inflammation-related genes was quantitated for the comparison of experimental group (with epinephrine) and control group (without epinephrine). The results demonstrated significant changes of inflammation-related gene expressions in cardiomyocytes after epinephrine administration. The clinical implications of the gene expression changes in cardiomyocytes are unclear.