Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emergent pathogen responsible for the coronavirus disease 2019 (COVID-19). Since its emergence, the novel coronavirus has rapidly achieved pandemic proportions causing remarkably increased morbidity and mortality around the world. A hypercoagulability state has been reported as a major pathologic event in COVID-19, and thromboembolic complications listed among life-threatening complications of the disease. Platelets are chief effector cells of hemostasis and pathological thrombosis. However, the participation of platelets in the pathogenesis of COVID-19 remains elusive. This report demonstrates that increased platelet activation and platelet-monocyte aggregate formation are observed in severe COVID-19 patients, but not in patients presenting mild COVID-19 syndrome. In addition, exposure to plasma from severe COVID-19 patients increased the activation of control platelets ex vivo. In our cohort of COVID-19 patients admitted to the intensive care unit, platelet-monocyte interaction was strongly associated with tissue factor (TF) expression by the monocytes. Platelet activation and monocyte TF expression were associated with markers of coagulation exacerbation as fibrinogen and D-dimers, and were increased in patients requiring invasive mechanical ventilation or patients who evolved with in-hospital mortality. Finally, platelets from severe COVID-19 patients were able to induce TF expression ex vivo in monocytes from healthy volunteers, a phenomenon that was inhibited by platelet P-selectin neutralization or integrin αIIb/β3 blocking with the aggregation inhibitor abciximab. Altogether, these data shed light on new pathological mechanisms involving platelet activation and platelet-dependent monocyte TF expression, which were associated with COVID-19 severity and mortality.

Alterations in selected respiratory gas exchange parameters have been proposed as sensitive, noninvasive indices of the onset of metabolic acidosis (anaerobic threshold (AT) during incremental exercise. Our purposes were to investigate the validity and feasibility of AT detection using routine laboratory measures of gas exchange, i.e., nonlinear increases in VE and VCO2 and abrupt increases in FEO2. Additionally, we examined the comparability of the AT and VO2 max among three modes of exercise (arm cranking, leg cycling, and treadmill walk-running) with double determinations obtained from 30 college-age, male volunteer subjects. The AT's for arm cranking, leg cycling, and treadmill walk-running occurred at 46.5 +/- 8.9 (means +/- SD), 63.8 +/- 9.0, and 58.6 +/- 5.8% of VO2 max, respectively. No significant difference was found between the leg exercise modes (cycling and walk-running) for the AT while all pairwise arm versus leg comparisons were significantly different. Using nine additional subjects performing leg cycling tests, a significant correlation of r = 0.95 was found between gas exchange AT measurements (expressed as % VO2 max) and venous blood lactate AT measurements (% VO2 max). We conclude that the gas exchange AT is a valid and valuable indirect method for the detection of the development of lactic acidosis during incremental exercise.

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In this retrospective study of SICU patients with cEEG monitoring for altered mental status, NCSz and periodic discharges were frequent and NCSz were independently associated with poor outcome. NCSz were more common when clinical seizures occurred before cEEG.