Acute kidney injury is a common complication of acute myocardial infarction and is generally associated with adverse outcomes. We studied the incidence and clinical significance of transient versus persistent acute kidney injury in 1957 patients who survived an ST-elevation acute myocardial infarction. We divided the patients into 5 groups based on changes in serum creatinine level during hospitalization. Mild acute kidney injury (creatinine 0.3-0.49 mg/dl above baseline) occurred in 156 patients and was transient (resolved during their hospital stay) in 61. Moderate/severe acute kidney injury (creatinine more than or 0.5 mg/dl above baseline) was found in 138 patients and was transient in 60. Compared to patients without acute kidney injury, the adjusted hazard ratio for mortality was 1.2 in patients with mild, transient acute kidney injury and 1.8 in patients with mild, persistent injury where the creatinine remained elevated. Patients with persistent moderate/severe acute kidney injury had the highest mortality (hazard ratio 2.4), whereas patients with transient moderate/severe injury had an intermediate risk (hazard ratio of 1.7). A similar relationship was present between acute kidney injury and admissions for heart failure. Our study shows that dynamic changes in renal function during acute myocardial infarction are strongly related to long-term mortality and heart failure.

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Aim      Despite the regular heart damage in patients with coronavirus pneumonia caused by SARS-Cov-2, a possibility of developing lymphocytic myocarditis as a part of COVID-19 remains unsubstantiated. The aim of this study was to demonstrate a possibility of lymphocytic myocarditis and to study its morphological features in patients with the novel coronavirus infection (COVID-19) with a severe course.Material and methods   Postmortem data were studied for 5 elderly patients (74.8±4.4 years; 3 men and 2 women) with the novel coronavirus infection and bilateral, severe polysegmental pneumonia (stage 3–4 by computed tomography). COVID-19 was diagnosed based on the typical clinical presentation and positive polymerase chain reaction test in nasopharyngeal swabs. All patients were treated in different hospitals repurposed for the treatment of patients with COVID-19. A standard histological study was performed with hematoxylin and eosin, toluidine blue, and van Gieson staining. Serial paraffin slices were studied immunohistochemically with antibodies to CD3, СD68, CD20, perforin, and toll-like receptors (TLR) 4 and 9.Results In none of the cases, myocarditis was suspected clinically, added to the diagnosis or indicated as a possible cause of death. IHD and acute myocardial infarction were mentioned as error diagnoses not confirmed by the postmortem examination. The morphological examination of the heart identified signs of lymphocytic myocarditis consistent with Dallas criteria for this diagnosis. Myocardial infiltrate was characterized in detail, and a combined inflammatory damage of endocardium and pericardium was described. The immunohistochemical study with cell infiltrate typing confirmed the presence of CD3-positive Т lymphocytes and the increased expression of TLR-4. A picture of coronaritis, including that with microvascular thrombosis, was found in all cases.Conclusion      A possibility for development of lymphocytic viral myocarditis in COVID-19 was confirmed morphologically and immunohistochemically. Specific features of myocarditis in COVID-19 include the presence of coronaritis and a possible combination of myocarditis with lymphocytic endo- and pericarditis.

BACKGROUND Specific CD44 isoforms are cell surface adhesion molecules and have been shown to be associated with tumor progression and metastasis. In lung carcinoma, CD44 expression has been reported to be a feature of nonsmall cell lung carcinoma (NSCLC) but not small cell lung carcinoma. A specific variant, CD44v6, was shown to be expressed only in a subset of NSCLC, namely the squamous cell and bronchoalveolar carcinomas, suggesting that CD44 may play a role in lung carcinoma differentiation. METHODS To determine whether differential CD44 expression is an early event in the pathogenesis of lung carcinoma, the authors investigated the pattern of expression of the standard (CD44s) and variant (CD44v6) isoforms by immunohistochemistry in normal lung, nonneoplastic specimens, and bronchial biopsies of preneoplastic lesions. RESULTS In normal bronchial epithelium and all nonneoplastic cases, CD44s expression was limited to the basement membrane and adjacent lower strata of the epithelium, whereas CD44v6 was expressed within the basement membrane only. However, aberrant expression of both CD44s and CD44v6 was observed in all preneoplastic lesions examined. In cases of dysplasia, squamous metaplasia, goblet cell hyperplasia, and basal cell hyperplasia, all epithelial strata showed immunoreactivity for both isoforms, in contrast to normal epithelium, in which immunoreactivity was noted to be restricted to the basal layer cells. In contrast, CD44s and CD44v6 expression was completely absent in nearly all cases of adenomatosis. CONCLUSIONS Altered CD44s and/or CD44v6 expression appears to be a feature of all preneoplastic lesions in the lung, the precise nature of which varies according to histologic tumor type. Therefore, the authors conclude that CD44s and CD44v6 may lend themselves to be markers of preneoplastic changes in the lung. Cancer 2001;92:1231–6. © 2001 American Cancer Society.