To address the coronavirus (Covid-19) pandemic,¹ strict social containment measures have been adopted worldwide, and health care systems have been reorganized to cope with the enormous increase in the numbers of acutely ill patients.^2,3 During this same period, some changes in the pattern of hospital admissions for other conditions have been noted. The aim of the present analysis is to investigate the rate of hospital admissions for acute coronary syndrome (ACS) during the early days of the Covid-19 outbreak.

Nephropathy induced by exposure to radiocontrast agents, a possible complication of percutaneous coronary interventions, is associated with significant in-hospital and long-term morbidity and mortality. Patients with preexisting renal failure are at particularly high risk. We investigated the role of hemofiltration, as compared with isotonic-saline hydration, in preventing contrast-agent–induced nephropathy in patients with renal failure.

The authors hypothesized that the cytokine storm described in COVID-19 patients may lead to consistent cell-based tissue factor (TF)-mediated activation of coagulation, procoagulant microvesicles (MVs) release, and massive platelet activation. COVID-19 patients have higher levels of TF+ platelets, TF+ granulocytes, and TF+ MVs than healthy subjects and coronary artery disease patients. Plasma MV-associated thrombin generation is present in prophylactic anticoagulated patients. A sustained platelet activation in terms of P-selectin expression and platelet–leukocyte aggregate formation, and altered nitric oxide/prostacyclin synthesis are also observed. COVID-19 plasma, added to the blood of healthy subjects, induces platelet activation similar to that observed in vivo. This effect was blunted by pre-incubation with tocilizumab, aspirin, or a P2Y12 inhibitor.