Ischemic stroke remains the second leading cause of death and among the major causes of morbidity worldwide. Therapeutic options are currently limited to early reperfusion strategies, while pharmacological neuroprotective strategies despite showing promising results in the experimental setting constantly failed to enter the clinical arena. Inflammation plays an important role in the pathophysiology of ischemic stroke and mediators of inflammation have been longtime investigated as possible prognostic marker and therapeutic target for stroke patients. Here, we summarized available evidence on the role of cytokines, soluble adhesion molecules and adipokines in the pathophysiology, prognosis and therapy of ischemic stroke.
Metabolic syndrome (MetS) accounts for different metabolic disorders including impaired fasting glucose (IFG), high blood pressure (BP), abdominal obesity, high triglycerides (TGs) and low high-density lipoprotein cholesterol (HDL-C). 1 From being a condition typically associated with Western lifestyle and habits, the incidence
Obesity epidemic reached the dimensions of a real global health crisis with more than one billion people worldwide living with obesity. Multiple obesity-related mechanisms cause structural, functional, humoral, and hemodynamic alterations with cardiovascular (CV) deleterious effects. A correct assessment of the cardiovascular risk in people with obesity is critical for reducing mortality and preserving quality of life. The correct identification of the obesity status remains difficult as recent evidence suggest that different phenotypes of obesity exist, each one associated with different degrees of CV risk. Diagnosis of obesity cannot depend only on anthropometric parameters but should include a precise assessment of the metabolic status. Recently, the World Heart Federation and World Obesity Federation provided an action plan for management of obesity-related CV risk and mortality, stressing for the instauration of comprehensive structured programs encompassing multidisciplinary teams. In this review we aim at providing an updated summary regarding the different obesity phenotypes, their specific effects on CV risk and differences in clinical management.
The amount of physical activity (PA) people practice everyday has been reducing in the last decades. Sedentary subjects tend to have an impaired lipid plasma profile with a higher risk of atherosclerosis and related cardio- and cerebrovascular events. Regular PA helps in both primary and secondary cardiovascular prevention because of its beneficial effect on the whole metabolism. Several studies reported lower levels of plasma lipids in trained subjects, but the precise mechanisms by which PA modulates lipoproteins remain only partially described. Thereupon, proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serin protease whose main function is to reduce the amount of low-density lipoprotein cholesterol (LDL-C) receptors, with the direct consequence of reducing LDL-C uptake by the liver and increasing its circulating pool. Accordingly, recently developed PCSK9 inhibitors improved cardiovascular prevention and are increasingly used to reach LDL-C goals in patients at high CV risk. Whether PA can modulate the levels of PCSK9 remains partially explored. Recent studies suggest PA as a negative modulator of such a deleterious CV mediator. Yet the level of evidence is limited. The aim of this review is to summarize the recent reports concerning the regulatory role of PA on PCSK9 plasma levels, highlighting the beneficial role of regular exercise on the prevention of atherosclerosis and overall CV health.
Unmet needs challenge clinical management of sepsis especially concerning patient profiling, enhancing recovery, and long-term sequelae. Here, we preliminarily focused on sclerostin (SOST) as a candidate biomarker to encompass such a broad range of clinical needs related to sepsis. Seventy-three septic patients were enrolled at internal medicine wards between January 2017 and December 2019 in this pilot study. Clinical examination and blood sample analyses were collected at enrollment and after 7 and 14 days. SOST levels were assessed on serum by ELISA. Thirty-day mortality was set as primary outcome. In-hospital and long-term mortality (2.5 years of median follow-up) were assessed as secondary outcomes. Patients were frail, elderly, and heterogeneous in terms of comorbidity burden. SOST levels were associated with age, cardiovascular comorbidities, and time to early death (30 days). When regression models were built, SOST displayed a high predictive value toward 30-day mortality (OR 13.459 with 95% CI 1.226–148.017) with ever better performance than validated scoring scales for critical ill patients. Such a predictive value of SOST was further confirmed for in-hospital (HR 10.089 with 95% CI 1.375–74.013) and long-term mortality (HR 5.061 with 95% CI 1.379–18.570). SOST levels generally decreased over 7 to 14 days after enrollment (p for trend < 0.001). The degree of this variation further predicted long-term mortality (HR for Δ SOST T0–day 14: 1.006 with 95% CI 1.001–1.011). Our results suggest a role for SOST in both short- and long-time prediction of worse outcome in septic elderly admitted to internal medicine wards.
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