result from a decrease in coronary blood flow and stasis. Tachycardia in the presence of fixed, but severe, coronary artery stenosis is one mechanism by which a significant decrease in coronary and myocardial blood flow occurs due to the shortening of diastolic time period (28). Vasoconstriction secondary to ischemia may further decrease coronary blood flow (29,30). Hence, if coronary thrombosis occurs in the postoperative setting, it may be the result of and not necessarily the cause of prolonged ischemia and PMI. Furthermore, diabetes mellitus and LVH were the independent preoperative predictors of PMI. Both conditions are associated with reduced coronary flow reserve and microvascular dysfunction (31,32), and both predict increased cardiac risk. To what extent reduced coronary flow reserve contributes to prolonged postoperative ischemia and PMI has yet to be determined. There is only limited experimental or prospective clinical evidence for stress-induced MI. Myocardial adaptation or hibernation, rather than deterioration to infarction occurs after sustained (≤30 min) pacing-induced ischemia and norepinephrine infusion in animals with fixed coronary stenosis, provided that absolute myocardial blood flow is maintained (33). In contrast, prolonged (1 to 4 h) tachycardia-induced ischemia in the presence of a fixed, but critical, coronary stenosis leads to a progressive decline in subendocardial blood flow and diffuse subendocardial necrosis in anticoagulated dogs (34). One recent clinical study (15)showed reduced PMI and cardiac death rates from 34% to 3.4% by prophylactic bisoprolol treatment in high-risk patients undergoing major vascular surgery. This important report strongly supports our hypothesis that prolonged tachycardia and stress-induced ischemia underlie the evolution of PMI and that beta-blockade, by means of preventing prolonged postoperative ischemia, reduces PMI. Conclusions Although the mechanism of PMI remains unknown, our prospective study shows for the first time a strong temporal association between prolonged, silent, postoperative ischemia and PMI after major vascular surgery, suggesting that prolonged stress-induced ischemia may progress to MI. Whether early detection and treatment of prolonged postoperative ischemia reduce PMI has yet to be determined. Similarly, whether prolonged stress-induced ischemia may progress to non-Q-wave infarction in nonsurgical patients deserves further investigation. The impact of the COVID-19 pandemic on vascular surgery practicein the United StatesNicolas J. Mouawad, MD, MPH, MBA,a,bKaren Woo, MD, MS,cRafael D. Malgor, MD,dMax V. Wohlauer, MD,dAdam P. Johnson, MD, MPH,eRobert F. Cuff, MD,fDawn M. Coleman, MD,gSheila M. Coogan, MD,hMalachi G. Sheahan III, MD,iandSherene Shalhub, MD, MPH,jBay City, Lansing, Grand Rapids, and Ann Arbor,Mich; Los Angeles, Calif; Aurora, Colo; New York, NY; Houston, Tex; New Orleans, La; and Seattle, WashABSTRACTBackground:The coronavirus disease 2019 (COVID-19) pandemic has led to widespread postponement and cancelationof elective surgeries in the United States. We designed and administered a global survey to examine the impact ofCOVID-19 on vascular surgeons. We describe the impact of the pandemic on the practices of vascular surgeons in theUnited States.Methods:The Pandemic Practice, Anxiety, Coping, and Support Survey for Vascular Surgeons is an anonymous cross-sectional survey sponsored by the Society for Vascular Surgery Wellness Task Force disseminated April 14 to 24, 2020.This analysis focuses on pattern changes in vascular surgery practices in the United States including the inpatient setting,ambulatory, and vascular laboratory setting. Specific questions regarding occupational exposure to COVID-19, adequacyof