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.

Our findings indicate that epicardial fat reflects carotid artery stiffness in hypertension-induced organ damage.

Our study demonstrated that obesity, in absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both right and left ventricle. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.

We evaluated the relationship between renal resistive index (RRI) of the intrarenal vasculature and cardiovascular (CV) organ damage such as left ventricular hypertrophy (LVH), diastolic dysfunction and carotid atherosclerosis in a large sample of hypertensive patients. 566 hypertensive patients underwent echocardiography with conventional Doppler and Doppler tissue imaging (DTI), carotid and renal ultrasonography. In addition, lipids profile, creatinine in serum, and urinary albumin concentrations were determined. The patients were divided according to their RRI values in 2 groups: o70 and X70. Subjects with high RRI were older, had higher systolic and pulse pressure (PP) and more years of hypertension, compared to those with low RRI (Po0.0001). Patients with the higher RRI showed an increased left ventricular mass index (LVMI) and carotid intima-media thickness (IMT) with a higher prevalence of LVH, carotid plaques and microalbuminuria (Po0.001). There were differences in overall diastolic parameters, in particular when evaluated by DTI (Po0.001). A positive correlation was found between RRI and age, PP, carotid IMT, LVMI, SBP and a negative correlation was found with DTI diastolic parameters (Po0.001). Age, PP, carotid IMT and LVMI were independently related to RRI. While, RRI was independently related to IMT and IVRT. RRI, especially the higher values, are positively correlated with target organ damage in hypertensive patients, indicating that renal vascular resistance is related to morphologic and hemodynamic alteration of the CV system. The evaluation of RRI could predict the presence of early CV damage and provide an accurate estimate of overall risk.

No abstract

No abstract

No abstract