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Significance There is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population.

To investigate the effects of severity of long-standing congestive heart failure (CHF) on pulmonary function, we studied 53 (47 men) consecutive patients, all heart transplant candidates. Their mean (+/- SD) age and ejection fraction were 47 +/- 12 years and 23 +/- 7%, respectively. All patients underwent spirometry, lung volume, diffusion capacity (DLCO), maximum inspiratory (PImax) and expiratory pressure (PEmax) measurement. Maximum cardiopulmonary exercise test on a treadmill was also performed to determine maximum oxygen consumption (VO2max). On the basis of VO2max, the patients were then divided into those with a VO2max > 14 ml min-1 kg-1 (group 1, n = 30) and those with a VO2max < or = 14 ml min-1 kg-1 (group 2, n = 23). In comparison with group 1, group 2 patients had lower FEV1/FVC (70 +/- 8% vs 75 +/- 7%, P = 0.008), lower FEF25-75 (46 +/- 21 vs 70 +/- 26%pred, P < 0.001), lower TLC (76 +/- 15 vs 85 +/- 13%pred, P = 0.02) and lower PImax (68 +/- 20 vs 87 +/- 22 cmH2O, P = 0.003), but comparable DLCO (84 +/- 15 vs 88 +/- 20%pred, P = N.S.), and PEmax (99 +/- 25 vs 96 +/- 22 cmH2O, P = N.S.). In conclusion, our data suggest that respiratory abnormalities, such as restrictive defects, airway obstruction, and inspiratory muscle weakness, are more pronounced in patients with severe CHF than in those with mild-to-moderate disease. Further studies are required to investigate the extent to which these abnormalities contribute to dyspnoea during daily activities in patients with heart failure.

Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients (BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilatorinduced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.

Objective-To compare pulmonary function and respiratory muscle strength in patients with ischaemic and idiopathic dilated cardiomyopathy, well matched for indices of heart failure. Methods-The study involved 30 patients with ischaemic cardiomyopathy and 30 with idiopathic dilated cardiomyopathy. The groups were well matched for age, weight, and clinical severity of cardiac dysfunction as assessed by ejection fraction and the New York Heart Association functional class. There were more smokers in the ischaemic group (p < 0.05), but indices of pulmonary function were comparable. Conclusions-For a given degree of cardiac dysfunction, the respiratory muscles are weaker in patients with idiopathic dilated cardiomyopathy than in those with ischaemic cardiomyopathy. (Heart 1999;81:618-620) Results-Mean

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Preoperative low-dose amiodarone therapy does not seem to be related to significant postoperative lung toxicity, but it is associated with various cardiac complications and an increased need for more intense inotropic support after cardiac operations. These findings may be related to the drug's depressant effect on the myocardium.

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