Atherosclerosis represents the most common pathological substrate of coronary heart disease (CHD), and the characterization of the disease as a chronic low-grade inflammatory condition is now largely accepted. A number of mediators of inflammation have been widely studied, both as surrogate biomarkers and as causal agents, in the pathophysiological network of atherogenesis and plaque vulnerability. The epidemiological observation that biomarkers of inflammation are associated with clinical cardiovascular risk supports the theory that targeted anti-inflammatory treatment appears to be a promising strategy in reducing residual cardiovascular risk on the background of traditional medical therapy. A large number of randomized controlled trials have shown that drugs commonly used in cardiovascular disease (CVD), such as statins, may be effective in the primary and secondary prevention of cardiovascular events through an anti-inflammatory effect. Moreover, several anti-inflammatory drugs are being tested for their potential to reduce residual cardiovascular risk on the background of validated medical therapy for atherosclerotic disease. In this paper, we review relevant evidence with regard to the relationship between inflammation and CVD, from pathogenesis to therapeutic strategies.

Beyond its role in hemostasis, von Willebrand factor (VWF) is an emerging mediator of vascular inflammation. Recent studies highlight the involvement of VWF and its regulator, ADAMTS13, in mechanisms that underlie vascular inflammation and immunothrombosis, like leukocyte rolling, adhesion, and extravasation; vascular permeability; ischemia/reperfusion injury; complements activation; and NETosis. The VWF/ADAMTS13 axis is implicated in the pathogenesis of atherosclerosis, promoting plaque formation and inflammation through macrophage and neutrophil recruitment in inflamed lesions. Moreover, VWF and ADAMTS13 have been recently proposed as prognostic biomarkers in cardiovascular, metabolic, and inflammatory diseases, such as diabetes, stroke, myocardial infarction, and sepsis. All these features make VWF an attractive therapeutic target in thromboinflammation. Several lines of research have recently investigated “tailor-made” inhibitors of VWF. Results from animal models and clinical studies support the potent anti-inflammatory and antithrombotic effect of VWF antagonism, providing reassuring data on its safety profile. This review describes the role of VWF in vascular inflammation “from bench to bedside” and provides an updated overview of the drugs that can directly interfere with the VWF/ADAMTS13 axis.

A reduction in hospital admissions for acute coronary syndromes (ACS) has been observed globally in the aftermath of the pneumonia outbreak caused by coronavirus disease 2019 . 1 Despite emergence of anecdotal reports, formal evaluation of variation in percutaneous coronary intervention (PCI) rates during the COVID-19 outbreak has not yet been reported. Italy is one of the countries most heavily affected by the COVID-19 pandemic with 168,941 confirmed cases and 22,170 deaths as of April 5, 2020.We investigated the association between the outbreak of COVID-19 and PCI rates for ACS in the Campania region, which with 5.8 million residents represents about 10% of the Italian population. Data were obtained from 20 out of 21 PCI centers over an 8-week period, including 4-week before and 4-week after the COVID-19 outbreak corresponding with the first reported case declared by the Civil Protection Department on February 27, 2020. Incidence rates and their ratios were calculated using Poisson regression analysis and interactions for gender and age were estimated by adding the interaction term to the regression models. 2 Population denominators, which were used as offset, were obtained from the Italian census. The ratio change in PCI rates for the entire 8-week interval was estimated by adding a linear term to the Poisson regression. The study was approved by the Ethics Committee of the University of Naples Federico II (Naples, Italy).From January 30, 2020 to March 26, 2020, a total of 1,831 PCIs were performed in the Campania region; of them 738 (40.31%) were elective PCI (not included), 604 (32.99%) PCI for non-ST-segment elevation acute ACS (NSTE-ACS), and 489 (26.71%) PCI for ST-segment elevation myocardial infarction (STEMI). Mean age was 65.7 years (standard deviation 12), and 804/1,093 PCIs (73.56%) were performed in men. There were no differences in mean age

Left ventricular (LV) global longitudinal strain (GLS) has established itself in the last decade as a reliable, more objective method for the evaluation of LV systolic function, able to detect subtle abnormalities in LV contraction even in the presence of preserved ejection fraction (EF). However, recent studies have demonstrated that GLS, similar to LV EF, has important load dependency. Non-invasive myocardial work (MW) quantification has emerged in the last years as an alternative tool for myocardial function assessment. This new method, incorporating measurement of strain and LV pressure, has shown to overcome GLS and LV EF limitations and provide a loading-independent evaluation of myocardial performance. The presence of a commercially available echocardiographic software for the non-invasive MW calculation has allowed the application of this new method in different settings. This review sought to provide an overview on the current knowledge of non-invasive MW estimation, showing its potential applications and possible added value in clinical practice.