RationaleMyocardial injury associates significantly and independently with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 remains unclear, and cardiac involvement by SARS-CoV-2 presents a major challenge worldwide.ObjectiveThis histological and immunohistochemical study sought to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury.Methods and ResultsPostmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control group (n=11). Histological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: caspase-1, caspase-9, gasdermin-d, ICAM-1, IL-1β, IL-4, IL-6, CD163, TNF-α, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also assessed for apoptotic cells by TUNEL. Histological analysis showed severe pericardiocyte interstitial edema and higher mast cells counts per high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-1β, IL-6, MMP-9, TNF-α, and other markers in the hearts of COVID-19 patients. Expression of caspase-9 did not differ from the controls, while gasdermin-d expression was less. The TUNEL assay was positive in all the COVID-19 samples supporting endothelial apoptosis.ConclusionsThe pathogenesis of COVID-19 myocardial injury does not seem to relate to primary myocardiocyte involvement but to local inflammation with associated interstitial edema. We found heightened TGF-β and interstitial collagen expression in COVID-affected hearts, a potential harbinger of chronic myocardial fibrosis. These results suggest a need for continued clinical surveillance of patients for myocardial dysfunction and arrythmias after recovery from the acute phase of COVID-19.

Rationale: Myocardial injury is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide. Objective: This histopathological and immunohistochemical study seeks to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury. Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control patient. Histopathological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also subjected to a TUNEL assay to detect potential apoptosis. The histopathological analysis showed severe pericellular interstitial edema surrounding each of the cardiomyocytes and higher mast cells count by high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. No difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. The TUNEL assay was positive in all the COVID-19 samples confirming the presence of endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 myocardial injury seems to be related with pyroptosis leading to endothelial cell injury and disfunction. The subsequent inflammation with associated interstitial edema could explain the myocardial disfunction and arrythmias in these patients. Our findings also show that COVID-19 myocardial injury may cause myocardial fibrosis in the long term. These patients should be monitored for myocardial dysfunction and arrythmias after the acute phase of COVID-19.

Introduction Pseudomonas aeruginosa respiratory infections are challenging, and the risk of recurrence is a frequent problem. The aim of this study was to investigate the risk factors associated with the presence of P. aeruginosa, and the risk factors related to the recurrence and death of lower airway infections in inpatients in a Brazilian hospital. Methods Retrospective cohort with inpatients that had a sample of airways culture (tracheal aspirate or bronchoalveolar lavage) with the detection of P. aeruginosa. The patients with clinical criteria of infection were classified as ventilator‐associated, hospital‐acquired, or community‐acquired pneumonia. P. aeruginosa in respiratory samples without symptoms was considered colonization. The antimicrobial treatment adequacy and the clinical data were evaluated. Outcome variables included mortality and recurrence. Results One hundred and fifty‐four patients were included in the study, most of them were men, and the majority (102) were considered infected. The average length of stay was superior to 30 days. Previous pulmonary disease was associated with the occurrence of colonization. Aminoglycosides were the most active drug according to susceptibility tests and were successfully used as monotherapy. Septic shock was a risk factor for death in the infected patients. The use of adequate antimicrobial therapy was associated with major survival, independent of the infection classification. Conclusion It is possible to evaluate clinical data associated with recurrence and mortality in patients with different lung infections by P. aeruginosa. Aminoglycoside monotherapy is safe and effective in P. aeruginosa respiratory infections.

Takotsubo syndrome is known for its association with psychological stress factors. Rarely, it is associated with invasive procedures. We present a case of Takotsubo induced by bronchoscopy, a procedure with a low rate of complications.

Background: Myocardial injury is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide.Aim: This histopathological and immunohistochemical study seeks to clarify the pathogenesis of myocardial injury in COVID-19.Methods: Postmortem minimally invasive autopsies were performed in two patients who died from COVID-19, and the myocardium samples were compared to a control patient. Immunohistochemistry (IHC) staining was performed using monoclonal antibodies against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen.Results: The histopathological analysis showed severe pericellular interstitial edema surrounding each of the cardiomyocytes. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. On the other hand, no difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. Conclusion: Our findings point to a pathogenesis related with pyroptosis leading to endothelial disfunction. The subsequent inflammation with associated interstitial edema could explain the myocardial disfunction and arrythmias in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis in the long term.