BackgroundInfective endocarditis (IE) is more common in patients with cancer as compared with the general population. Due to an immunocompromised state, the need for invasive procedures, hypercoagulability and the presence of indwelling catheters, patients with cancer are particularly predisposed to the development of IE.ObjectivesLimited information exists about IE in patients with cancer. We aimed to evaluate the characteristics of patients with cancer and IE at our tertiary care centre, including a comparison of the microorganisms implicated and their association with mortality.MethodsA retrospective chart review of patients with cancer who had echocardiography for suspicion of endocarditis was conducted. A total of 56 patients with a confirmed diagnosis of cancer and endocarditis, based on the modified Duke criteria, were included in the study. Baseline demographics, risk factors for developing IE, echocardiography findings, microbiology and mortality data were analysed.ResultsFollowing the findings of vegetations by echocardiography, the median survival time was 8.5 months. Staphylococcus aureus was the most common organism identified as causing endocarditis. The mitral and aortic valves were the most commonly involved sites of endocarditis. Patients with S. aureus endocarditis (SAE) had a significantly poorer survival when compared with patients without SAE (p=0.0217) over the 12-month period from diagnosis of endocarditis.ConclusionsOverall survival of patients with cancer and endocarditis is poor, with a worse outcome in patients with SAE.
Levels of intestinal toll-like receptor 4 (TLR4) impact inflammation in the neonatal gastrointestinal tract. While surfactant protein A (SP-A) is known to regulate TLR4 in the lung, it also reduces intestinal damage, TLR4 and inflammation in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. We hypothesized that SP-A-deficient (SP-A−/−) mice have increased ileal TLR4 and inflammatory cytokine levels compared to wild type mice, impacting intestinal physiology. We found that ileal TLR4 and proinflammatory cytokine levels were significantly higher in infant SP-A−/− mice compared to wild type mice. Gavage of neonatal SP-A−/− mice with purified SP-A reduced ileal TLR4 protein levels. SP-A reduced expression of TLR4 and proinflammatory cytokines in normal human intestinal epithelial cells (FHs74int), suggesting a direct effect. However, incubation of gastrointestinal cell lines with proteasome inhibitors did not abrogate the effect of SP-A on TLR4 protein levels, suggesting that proteasomal degradation is not involved. In a mouse model of experimental NEC, SP-A−/− mice were more susceptible to intestinal stress resembling NEC, while gavage with SP-A significantly decreased ileal damage, TLR4 and proinflammatory cytokine mRNA levels. Our data suggests that SP-A has an extrapulmonary role in the intestinal health of neonatal mice by modulating TLR4 and proinflammatory cytokines mRNA expression in intestinal epithelium.
Introduction: Although primarily a respiratory illness, COVID-19 frequently involves the cardiovascular system. Hypothesis: Accordingly, we assessed whether abnormal electrocardiographic findings, including cardiac dysrhythmias, ST/T wave changes, and QTc interval prolongation, predict adverse outcomes in patients with COVID-19. Methods: A multi-center retrospective study of hospitalized patients with COVID-19 was performed across 4 hospitals in Texas and 1 in New York. Initial and subsequent ECG findings among patients with uncomplicated disease course, patients with adverse clinical outcomes (need for vasopressors, mechanical ventilation or renal replacement therapy) and patients who died were analyzed. Univariable and multivariable Cox analyses were performed. Results: We identified 297 consecutive patients with COVID-19. Of these patients, 91% had available ECGs. Median heart rate on initial ECG was 92 bpm (IQR: 27), and median QTc interval was 442 msec (IQR: 40). Longer QTc interval on initial ECG was associated with adverse clinical outcomes (443 msec, IQR: 43) and death (457 msec, IQR: 52, vs 441.5 msec, IQR: 36; p=0.033). Cardiac dysrhythmias or ST/T wave changes were noted in subsequent ECGs of 46% of patients and were associated with adverse clinical outcomes (58%) or death (68% vs 33%; HR: 2.2, 95% CI: 1.3-3.6; p=0.002). Sixty-four patients (23%) developed a QTc interval >500msec during their hospitalization. In multivariable Cox analysis, history of coronary artery disease was independently associated with development of QTc>500msec (HR 2.1, 95% CI 1.0-4.4; p=0.047) while other baseline comorbidities were not. Patients with QTc>500msec were more commonly treated with azithromycin (91% vs 77%; p=0.048); no other differences in COVID-19 treatment were identified. In-hospital mortality among patients with QTc>500msec was 37% versus 13% among patients with shorter QTc intervals (HR: 2.6, 95% CI 1.5-4.5; p=0.001). Conclusions: Prolonged QTc interval on initial ECG of COVID-19 patients predicted adverse outcomes and death. Azithromycin was associated with development of QTc>500msec. Patients with a QTc interval >500msec had a 2.6 times higher risk for in-hospital mortality compared to patients with shorter QTc intervals.
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