Gender and Ethnic Disparities of Acute Kidney Injury in COVID-19 Infected Patients: A Literature Review

Coronavirus disease 2019(COVID-19) has become a public health emergency of concern worldwide. COVID-19 is a new infectious disease arising from Coronavirus 2 (SARS-CoV-2). It has a strong transmission capacity and can cause severe and even fatal respiratory diseases. It can also affect other organs such as the heart, kidneys and digestive tract. Clinical evidence indicates that kidney injury is a common complication of COVID-19, and acute kidney injury (AKI) may even occur in severely ill patients. Data from China and the United States showed that male sex, Black race, the elderly, chronic kidney disease, diabetes, hypertension, cardiovascular disease, and higher body mass index are associated with COVID-19‐induced AKI. In this review, we found gender and ethnic differences in the occurrence and development of AKI in patients with COVID-19 through literature search and analysis. By summarizing the mechanism of gender and ethnic differences in AKI among patients with COVID-19, we found that male and Black race have more progress to COVID-19-induced AKI than their counterparts.

Homocysteine Plasmatic Concentration in Brain-Injured Neurocritical Care Patients: Systematic Review of Clinical Evidence

Background: Hyperhomocysteinemia (HHcy) is considered as an independent risk factor for several diseases, such as cardiovascular, neurological and autoimmune conditions. Atherothrombotic events, as a result of endothelial dysfunction and increased inflammation, are the main mechanisms involved in vascular damage. This review article reports clinical evidence on the relationship between the concentration of plasmatic homocysteine (Hcy) and acute brain injury (ABI) in neurocritical care patients. Materials and methods: a systematic search of articles in the PubMed and EMBASE databases was conducted, of which only complete studies, published in English in peer-reviewed journals, were included. Results: A total of 33 articles, which can be divided into the following 3 subchapters, are present: homocysteine and acute ischemic stroke (AIS); homocysteine and traumatic brain injury (TBI); homocysteine and intracranial hemorrhage (ICH)/subarachnoid hemorrhage (SAH). This confirms that HHcy is an independent risk factor for ABI and a marker of poor prognosis in the case of stroke, ICH, SAH and TBI. Conclusions: Several studies elucidate that Hcy levels influence the patient’s prognosis in ABI and, in some cases, the risk of recurrence. Hcy appears as biochemical marker that can be used by neuro-intensivists as an indicator for risk stratification. Moreover, a nutraceutical approach, including folic acid, the vitamins B6 and B12, reduces the risk of thrombosis, cardiovascular and neurological dysfunction in patients with severe HHcy that were admitted for neurocritical care.

Prognostic Value of T1 Mapping and Feature Tracking by Cardiac Magnetic Resonance in Patients With Signs and Symptoms Suspecting Heart Failure and No Clinical Evidence of Coronary Artery Disease

Background The ability of left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) by cardiac magnetic resonance for risk stratification in suspected heart failure is limited. We aimed to evaluate the incremental prognostic value of cardiac magnetic resonance‐assessed extracellular volume fraction (ECV) and global longitudinal strain (GLS) in patients with signs and symptoms suspecting heart failure and no clinical evidence of coronary artery disease. Methods and Results A total of 474 consecutive patients (57±21 years of age, 56% men) with heart failure‐related symptoms and absence of coronary artery disease underwent cardiac magnetic resonance. After median follow‐up of 18 months, 59 (12%) experienced the outcome of all‐cause death or heart failure hospitalization (DeathCHF). In univariate analysis, cardiac magnetic resonance‐assessed LVEF, LGE, GLS, and ECV were all significantly associated with DeathCHF. Adjusted for a multivariable baseline model including age, sex, LVEF and LGE, ECV, and GLS separately maintained a significant association with DeathCHF (ECV, hazard ratio [HR], 1.44 per 1 SD increase; 95% CI 1.13–1.84; P =0.003, and GLS, HR, 1.78 per 1 SD increase; 95% CI, 1.06–2.96; P =0.028 respectively). Adding both GLS and ECV to the baseline model significantly improved model discrimination (C statistic from 0.749 to 0.782, P =0.017) and risk reclassification (integrated discrimination improvement 0.046 [0.015–0.076], P =0.003; continuous net reclassification improvement 0.378 [0.065–0.752], P <0.001) for DeathCHF, beyond LVEF and LGE. Conclusions In patients with signs and symptoms suspecting heart failure and no clinical evidence of coronary artery disease, joint assessment of GLS and ECV provides incremental prognostic value for DeathCHF, independent of LVEF and LGE.

Anesthesia and Developing Brains: Unanswered Questions and Proposed Paths Forward

Anesthetic agents disrupt neurodevelopment in animal models, but evidence in humans is mixed. The morphologic and behavioral changes observed across many species predicted that deficits should be seen in humans, but identifying a phenotype of injury in children has been challenging. It is increasingly clear that in children, a brief or single early anesthetic exposure is not associated with deficits in a range of neurodevelopmental outcomes including broad measures of intelligence. Deficits in other domains including behavior, however, are more consistently reported in humans and also reflect findings from nonhuman primates. The possibility that behavioral deficits are a phenotype, as well as the entire concept of anesthetic neurotoxicity in children, remains a source of intense debate. The purpose of this report is to describe consensus and disagreement among experts, summarize preclinical and clinical evidence, suggest pathways for future clinical research, and compare studies of anesthetic agents to other suspected neurotoxins.

Impact of Cancer Cachexia on Cardiac and Skeletal Muscle: Role of Exercise Training

Cachexia is a multifactorial syndrome that presents with, among other characteristics, progressive loss of muscle mass and anti-cardiac remodeling effect that may lead to heart failure. This condition affects about 80% of patients with advanced cancer and contributes to worsening patients’ tolerance to anticancer treatments and to their premature death. Its pathogenesis involves an imbalance in metabolic homeostasis, with increased catabolism and inflammatory cytokines levels, leading to proteolysis and lipolysis, with insufficient food intake. A multimodal approach is indicated for patients with cachexia, with the aim of reducing the speed of muscle wasting and improving their quality of life, which may include nutritional, physical, pharmacologic, and psychological support. This review aims to outline the mechanisms of muscle loss, as well as to evaluate the current clinical evidence of the use of physical exercise in patients with cachexia.

Circulating MicroRNAs for Diagnosis of Acute Pulmonary Embolism: Still a Long Way to Go

Venous thromboembolism (VTE) represents the third most frequent cause of acute cardiovascular syndrome. Among VTE, acute pulmonary embolism (APE) is the most life-threatening complication. Due to the low specificity of symptoms clinical diagnosis of APE may be sometimes very difficult. Accordingly, the latest European guidelines only suggest clinical prediction tests for diagnosis of APE, eventually associated with D-dimer, a biomarker burdened by a very low specificity. A growing body of evidence is highlighting the role of miRNAs in hemostasis and thrombosis. Due to their partial inheritance and susceptibility to the environmental factors, miRNAs are increasingly described as active modifiers of the classical Virchow’s triad. Clinical evidence on deep venous thrombosis reported specific miRNA signatures associated to thrombosis development, organization, recanalization, and resolution. Conversely, data of miRNA profiling as a predictor/diagnostic marker of APE are still preliminary. Here, we have summarized clinical evidence on the potential role of miRNA in diagnosis of APE. Despite some intriguing insight, miRNA assay is still far from any potential clinical application. Especially, the small sample size of cohorts likely represents the major limitation of published studies, so that extensive analysis of miRNA profiles with a machine learning approach are warranted in the next future. In addition, the cost-benefit ratio of miRNA assay still has a negative impact on their clinical application and routinely test.

Inflammation and the Link to Vascular Brain Health: Timing Is Brain

Inflammation and its myriad pathways are now recognized to play both causal and consequential roles in vascular brain health. From acting as a trigger for vascular brain injury, as evidenced by the coronavirus disease 2019 (COVID-19) pandemic, to steadily increasing the risk for chronic cerebrovascular disease, distinct inflammatory cascades play differential roles in varying states of cerebrovascular injury. New evidence is regularly emerging that characterizes the role of specific inflammatory pathways in these varying states including those at risk for stroke and chronic cerebrovascular injury as well as during the acute, subacute, and repair phases of stroke. Here, we aim to highlight recent basic science and clinical evidence for many distinct inflammatory cascades active in these varying states of cerebrovascular injury. The role of cerebrovascular infections, spotlighted by the severe acute respiratory syndrome coronavirus 2 pandemic, and its association with increased stroke risk is also reviewed. Rather than converging on a shared mechanism, these emerging studies implicate varied and distinct inflammatory processes in vascular brain injury and repair. Recognition of the phasic nature of inflammatory cascades on varying states of cerebrovascular disease is likely essential to the development and implementation of an anti-inflammatory strategy in the prevention, treatment, and repair of vascular brain injury. Although advances in revascularization have taught us that time is brain, targeting inflammation for the treatment of cerebrovascular disease will undoubtedly show us that timing is brain.