Objective: Coronavirus disease 2019 (COVID-19) can infect patients in any age group including those with no comorbid conditions. Understanding the demographic, clinical, and laboratory characteristics of these patients is important toward developing successful treatment strategies. Approach and Results: In a retrospective study design, consecutive patients without baseline comorbidities hospitalized with confirmed COVID-19 were included. Patients were subdivided into ≤55 and >55yearsof age. Predictors of in-hospital mortality or mechanical ventilation were analyzed in this patient population, as well as subgroups. Stable parameters in overall and subgroup models were used to construct a cluster model for phenotyping of patients. Of 1207 COVID-19–positive patients, 157 met the study criteria (80≤55 and 77>55 years of age). Most reliable predictors of outcomes overall and in subgroups were age, initial and follow-up d -dimer, and LDH (lactate dehydrogenase) levels. Their predictive cutoff values were used to construct a cluster model that produced 3 main clusters. Cluster 1 was a low-risk cluster and was characterized by younger patients who had low thrombotic, coagulopathic, and inflammatory features. Cluster 2 was intermediaterisk that also consisted of younger population that had moderate level of thrombosis, higher inflammatory cells, and inflammatory markers. Cluster 3 was a high-risk cluster that had the most aggressive thrombotic, inflammatory, coagulopathic feature. Conclusions: In healthy patient population, COVID-19 remains significantly associated with morbidity and mortality. While age remains the most important predictor of in-hospital outcomes, thromboinflammatory interactions are also associated with worse clinical outcomes regardless of age in healthy patients.

The pathophysiology of the COVID-19 involves a systemic hypercoagulable state and systemic micro-thrombosis which can cause fatal consequences. Despite that anticoagulation seems an intuitive therapeutic option, the US National Institute of Health has issued a warning against its use in critically ill patients. We present five cases of imaging-proven or clinically suspected hypercoagulability with hemodynamic compromise despite therapeutic anticoagulation. We describe the patients with thoughts on links between pathophysiology and the laboratory values, clinical course, and imaging studies in each case. All patients presented to the hospital with symptoms and chest imaging suggestive of COVID-19 pneumonia. All patients presented with severe hypoxia requiring mechanical ventilation, and received full anticoagulation for treatment of hypercoagulable state suggested by elevated D-dimer. All but one patient received alteplase for thrombolytic therapy of suspected massive pulmonary embolism (PE). On the basis of this case series, hypercoagulability in COVID-19 is a late manifestation of the disease that persists despite anticoagulation, is cyclic in nature based on D-dimer despite thrombolysis, and is fatal if it rebounds. The use of anticoagulation and thrombolysis in these patients seemed harmful or non-beneficial. Early intervention before D-dimer elevation and hemodynamic compromise may benefit in preventing thromboembolic burden.