The prevalence of PSCI is high after minor ischemic stroke. In particular, attention and working memory and executive function are most commonly impaired. Although the risk factors for PSCI are numerous, shorter total sleep time and degree of hypoxia at night warrant further attention.

Background Inflammation is involved in the pathogenesis and progression of coronary artery diseases (CADs), including acute coronary syndrome. The neutrophil-to-lymphocyte ratio (NLR) has been identified as a novel marker of the pro-inflammatory state. We aimed to evaluate the predictive efficacy of the NLR for the prognosis of patients with new-onset ACS. Methods We retrospectively included consecutive patients with new-onset ACS treated with emergency coronary angiography. NLR was measured at baseline and analyzed by tertiles. The severity of coronary lesions was evaluated by the Gensini score. Correlations of NLR with the severity of CAD and the incidence of major adverse cardiovascular diseases (MACEs) during follow-up were determined. Results Overall, 737 patients were included. The NLR was positively correlated with the severity of coronary lesions as assessed by Gensini score (P < 0.05). During the follow-up period (mean, 43.49 ± 23.97 months), 65 MACEs occurred. No significant association was detected between baseline NLR and the risk of MACEs during follow-up by either Kaplan–Meier or Cox regression analysis. Multivariable logistic regression analysis showed that a higher NLR was independently associated with coronary lesion severity as measured by the Gensini score (1st tertile vs. 3rd tertile hazard ratio [HR]: 0.527, P < 0.001, and 2nd tertile vs. 3rd tertile HR: 0.474, P = 0.025). Conclusions The NLR may be associated with coronary disease severity at baseline but is not associated with adverse outcomes in patients with new-onset ACS. Ethics Approval Number 2019XE0208

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Recent evidence indicates that a large proportion of deaths from coronavirus disease 2019 (COVID-19) can be attributed to cardiovascular disease, including acute myocardial infarction, arrhythmias and heart failure. Indeed, severe infection increases the risk of heart failure among patients with COVID-19. In most patients, heart failure arises from complex interactions between pre-existing conditions, cardiac injury, renin-angiotensin system activation, and the effects of systemic inflammation on the cardiovascular system. In this review, we summarize current knowledge regarding pathogen-driven heart failure occurring during treatment for COVID-19, the potential effects of commonly used cardiovascular and anti-infective drugs in these patients, and possible directions for establishing a theoretical basis for clinical treatment.