The COVID-19 pandemic affects a large number of patients with a rapid progression of respiratory failure often requiring hospitalization or intensive care unit treatment in some patients. Survivors of severe COVID-19 suffer from persistent weakness and cardiorespiratory failure. Feasibility and potential benefit of cardiopulmonary rehabilitation (CR) after COVID-19 remains unclear. Therefore, we retrospectively analyzed a cohort of COVID-19 patients in a single center inpatient rehabilitation clinic and describe performance and outcome during CR. Patients were referred from acute care hospitals for rehabilitation after severe COVID-19. The cohort (n=28) was divided in ventilated or not ventilated patients for further analysis. 50% were female, mean age was 66 years and patients stayed in the acute hospital for 19.3±10.7 days before referral for CR. 17 patients (61%) needed previous ICU treatment in the acute care hospital. Risk factors, assessments and questionnaires on admission were comparable in both groups. Significant enhancements were observed in 6-minute walking test and Feeling Thermometer which were independent of previous ventilation status. In conclusion, comprehensive CR following COVID-19 is safe, feasible and effective. Improvements in physical performance and subjective health status were independent of previous ventilation.

Background— There is an ongoing debate as to whether the gastrointestinal safety of COX-2 inhibition compared with nonsteroidal antiinflammatory drugs (NSAIDs) may come at the cost of increased cardiovascular events. In view of the large number of patients at cardiovascular risk requiring chronic analgesic therapy with COX-2 inhibitors for arthritic and other inflammatory conditions, the effects of selective COX-2 inhibition on clinically useful surrogates for cardiovascular disease, particularly endothelial function, need to be determined. Methods and Results— Fourteen male patients (mean age, 66±3 years) with severe coronary artery disease (average of 2.6 vessels with stenosis >75%) undergoing stable background therapy with aspirin and statins were included. The patients received celecoxib (200 mg BID) or placebo for a duration of 2 weeks in a double-blind, placebo-controlled, crossover fashion. After each treatment period, flow-mediated dilation of the brachial artery, high-sensitivity C-reactive protein, oxidized LDL, and prostaglandins were measured. Celecoxib significantly improved endothelium-dependent vasodilation compared with placebo (3.3±0.4% versus 2.0±0.5%, P =0.026), whereas endothelium-independent vasodilation, as assessed by nitroglycerin, remained unchanged (9.0±1.6% versus 9.5±1.3%, P =0.75). High-sensitivity C-reactive protein was significantly lower after celecoxib (1.3±0.4 mg/L) than after placebo (1.8±0.5 mg/L, P =0.019), as was oxidized LDL (43.6±2.4 versus 47.6±2.6 U/L, P =0.028), whereas prostaglandins did not change. Conclusions— This is the first study to demonstrate that selective COX-2 inhibition improves endothelium-dependent vasodilation and reduces low-grade chronic inflammation and oxidative stress in coronary artery disease. Thus, selective COX-2 inhibition holds the potential to beneficially impact outcome in patients with cardiovascular disease.