Background Coronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19. Objectives The aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19–positive patients with STEMI compared with COVID-19–negative patients. Methods This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. Results Patients with STEMI presenting with concurrent COVID-19 infection had higher levels of troponin T and lower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly lower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated clotting times were also noted. Importantly, patients with STEMI presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission. Conclusions In patients presenting with STEMI and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMI cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases.

A combination of prolonged SAPD, advanced age, and male sex identifies patients at high risk for development of AF after CABG.

Among adults undergoing noncardiac surgery, MINS is common and associated with substantial mortality.

BACKGROUND:The association between intraoperative cardiovascular changes and perioperative myocardial injury has chiefly focused on hypotension during noncardiac surgery. However, the relative influence of blood pressure and heart rate (HR) remains unclear. We investigated both individual and codependent relationships among intraoperative HR, systolic blood pressure (SBP), and myocardial injury after noncardiac surgery (MINS).METHODS:Secondary analysis of the Vascular Events in Noncardiac Surgery Cohort Evaluation (VISION) study, a prospective international cohort study of noncardiac surgical patients. Multivariable logistic regression analysis tested for associations between intraoperative HR and/or SBP and MINS, defined by an elevated serum troponin T adjudicated as due to an ischemic etiology, within 30 days after surgery. Predefined thresholds for intraoperative HR and SBP were: maximum HR >100 beats or minimum HR <55 beats per minute (bpm); maximum SBP >160 mm Hg or minimum SBP <100 mm Hg. Secondary outcomes were myocardial infarction and mortality within 30 days after surgery.RESULTS:After excluding missing data, 1197 of 15,109 patients (7.9%) sustained MINS, 454 of 16,031 (2.8%) sustained myocardial infarction, and 315 of 16,061 patients (2.0%) died within 30 days after surgery. Maximum intraoperative HR >100 bpm was associated with MINS (odds ratio [OR], 1.27 [1.07–1.50]; P < .01), myocardial infarction (OR, 1.34 [1.05–1.70]; P = .02), and mortality (OR, 2.65 [2.06–3.41]; P < .01). Minimum SBP <100 mm Hg was associated with MINS (OR, 1.21 [1.05–1.39]; P = .01) and mortality (OR, 1.81 [1.39–2.37]; P < .01), but not myocardial infarction (OR, 1.21 [0.98–1.49]; P = .07). Maximum SBP >160 mm Hg was associated with MINS (OR, 1.16 [1.01–1.34]; P = .04) and myocardial infarction (OR, 1.34 [1.09–1.64]; P = .01) but, paradoxically, reduced mortality (OR, 0.76 [0.58–0.99]; P = .04). Minimum HR <55 bpm was associated with reduced MINS (OR, 0.70 [0.59–0.82]; P < .01), myocardial infarction (OR, 0.75 [0.58–0.97]; P = .03), and mortality (OR, 0.58 [0.41–0.81]; P < .01). Minimum SBP <100 mm Hg with maximum HR >100 bpm was more strongly associated with MINS (OR, 1.42 [1.15–1.76]; P < .01) compared with minimum SBP <100 mm Hg alone (OR, 1.20 [1.03–1.40]; P = .02).CONCLUSIONS:Intraoperative tachycardia and hypotension are associated with MINS. Further interventional research targeting HR/blood pressure is needed to define the optimum strategy to reduce MINS.