A 72-year-old patient was admitted to the ICU due to acute respiratory distress syndrome caused by coronavirus disease 2019. On day 20, the patient experienced shock. The electrocardiogram showed ST segment elevation in leads V3–V6 and severe left ventricular dysfunction with an ejection fraction of 35%–40%. The left ventricle showed basal hypokinesis and apical akinesis, while the creatine kinase level was normal, indicating Takotsubo cardiomyopathy. On day 24, the patient died of multiple organ failure. In post-mortem biopsy, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigen was detected in cardiomyocytes by immunostaining. Moreover, SARS-CoV-2 RNA was detected in heart tissue. We need to further analyze the direct link between SARS-CoV2 and cardiomyocytes.

A healthy 35-year-old man was admitted to a rural hospital with coronavirus disease (COVID-19). During 14 days of hospitalization, he had no symptoms and was not given supplemental oxygen. About 3 weeks after discharge, he was re-admitted to the same hospital with new-onset continuous fever and general weakness. At the time of his second admission, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) RT-PCR was performed on a retro-nasal swab and the result was negative. Four days after admission, the patient was transferred to our intensive care unit (ICU) following deterioration of his respiratory and haemodynamic conditions, where he received mechanical ventilation, intra-aortic balloon pumping, and veno-arterial extracorporeal membrane oxygenation. A nasopharyngeal swab was obtained again at ICU admission, but RT-PCR was negative for SARS-CoV-2. All antibody titres measured against other viruses were low. Blood cultures were negative, and no bacteria were observed in sputum samples. However, SARS-CoV-2 RNA was detected by RT-PCR from sections obtained by myocardial biopsy. The patient's final diagnosis was delayed-onset SARS-CoV-2-induced fulminant myocarditis (FM). We strongly suggested that one of the proposed mechanisms of COVID-19-related myocardial injury will be the direct invasion of SARS-CoV-2 into cardiomyocytes even if delayed-onset. And this is the first case of delayed-onset FM in which diagnosis of active myocarditis was proven by pathological examination following endomyocardial biopsy and SARS-CoV-2 was detected in the myocardium by RT-PCR.

IMPORTANCE: Polymyxin B hemoperfusion (PMX-HP) is a potential therapeutic option for sepsis; however, its clinical effects remain unclear. OBJECTIVE: We explored the association between PMX-HP and clinical outcomes in patients in ICUs. DESIGN, SETTING, AND PARTICIPANTS: This is a multicenter prospective cohort study conducted in 20 ICUs in Japan between 2020 and 2022. Patients with septic shock requiring high-dose norepinephrine (≥ 0.2 µg/kg/min) were included. MAIN OUTCOMES AND MEASURES: We compared patient characteristics and outcomes between those who received PMX-HP (PMX group) and those who did not (non-PMX group). A primary outcome was 28-day mortality, with secondary outcomes including changes in mean arterial pressure (MAP) and vasoactive-inotropic score over time in the initial 48 hours, 28-day vasopressor-free days, and 90-day mortality rate. RESULTS: Among 309 patients, 175 (56.6%) were males, with a median age of 72 years and an Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 26. Overall, 82 patients underwent PMX-HP. The PMX and non-PMX groups had similar median ages (71 vs. 73 yr) and APACHE II scores (26 vs. 27). The median PMX-HP duration was 1016 minutes. The 28-day mortality was similar between the groups (PMX group: 17.1%, non-PMX group: 18.9%, p = 0.71), with an adjusted hazard ratio of 0.88 (95% CI, 0.46–1.68). MAP was maintained at a higher level with low-dose vasopressor from 8 to 32 hours following admission in the PMX group. The PMX group had fewer 28-day ICU-free days (16 vs. 18, p = 0.026). The 90-day mortality rate was similar between the groups (PMX group, 23.5%; non-PMX group, 27.1%; p = 0.62). CONCLUSIONS AND RELEVANCE: PMX-HP was not associated with the 28-day mortality improvement but was associated with higher MAP and lower vasopressor use for 8–32 hours of admission. Our findings suggested that PMX-HP requires careful adaptation.

Background/Objectives: Low-dose corticosteroids have gained popularity in the treatment of acute respiratory distress syndrome (ARDS); however, the efficacy of high-dose corticosteroids as pulse steroid therapy remains controversial. This study aimed to evaluate the efficacy of pulse steroid therapy in patients with severe ARDS requiring venovenous (V-V) extracorporeal membrane oxygenation (ECMO), where enhanced anti-inflammatory effects may be beneficial. Methods: Using data from the J-CARVE registry, which included patients with severe ARDS managed with V-V ECMO across 24 Japanese hospitals between January 2012 and December 2022, we identified 373 patients treated with corticosteroids. The patients were divided into two groups: pulse steroid therapy and non-pulse steroid therapy. Propensity score matching was performed, and all-cause hospital mortality and ECMO-free days within 28 days were compared between groups. Pulse steroid therapy was defined as methylprednisolone at a dose of 1000 mg/day. Results: After matching, 48 patients were included in each group. The all-cause hospital mortality rates were 41.7% (20/48) in the pulse steroid group and 47.9% (23/48) in the non-pulse steroid group, with no significant difference (odds ratio, 1.28; 95% confidence interval: 0.53–3.12, p = 0.68). The median ECMO-free days were 9.5 (interquartile range [IQR]: 0–17.3) in the pulse steroid group and 3 (IQR: 0–17) in the non-pulse steroid group, showing no significant difference (p = 0.69). Conclusions: Pulse steroid therapy did not improve all-cause hospital mortality or ECMO-free days in patients with severe ARDS who required V-V ECMO.