Nonalcoholic fatty liver disease (NAFLD) is the commonest chronic liver disease and affects a considerable proportion of the general population. NAFLD is independently associated with increased risk for cardiovascular events, particularly coronary heart disease. Importantly, even though NAFLD is more prevalent in patients with major cardiovascular risk factors (e.g., type 2 diabetes mellitus, obesity and hypertension), the association between NAFLD and cardiovascular disease appears to be independent of these risk factors. However, NAFLD also appears to increase the risk for ischemic stroke, a leading cause of mortality and long-term disability worldwide. It also appears that nonalcoholic steatohepatitis is more strongly related to the risk of ischemic stroke than isolated hepatic steatosis. Moreover, emerging data suggest that patients with NAFLD experience more severe ischemic stroke and have more unfavorable prognosis after an acute ischemic stroke in terms of functional dependency and short- and long-term mortality. These associations have major public health implications, since ischemic stroke is the second leading cause of death worldwide and an important cause of long-term disability. The aim of the present review is to summarize the current knowledge regarding the relationship between NAFLD and ischemic stroke incidence, severity and outcome. Given these associations, it might be useful to evaluate patients with acute ischemic stroke for the presence of NAFLD and to manage those with NAFLD more aggressively.

In the last decades, the role of inflammation in the pathogenesis of atherosclerosis has been the topic of intense research. Several markers of inflammation have shown predictive value for first and recurrent coronary events in patients without and with established Coronary Heart Disease (CHD). Among these markers, lipoprotein- associated phospholipase A2 (Lp-PLA2) has recently received considerable attention. In the present review, the potential role of Lp-PLA2 as a marker of CHD risk and as a therapeutic target is discussed. Elevated Lp- PLA2 mass and activity appears to be associated with increased risk for CHD, both in the general population and in patients with established CHD. However, it is unclear whether the measurement of Lp-PLA2 improves risk discrimination when incorporated in models that include traditional cardiovascular risk factors. Moreover, the lack of effect on CHD events of darapladib, a potent, selective Lp-PLA2 inhibitor, in two large, randomized, placebo-controlled trials and the mostly negative findings of genetic association studies suggest that Lp-PLA2 is unlikely to represent a causal factor in atherogenesis. Therefore, it is doubtful whether Lp-PLA2 will constitute a therapeutic target for the prevention of CHD.

: In the past decade, the Transradial Approach (TRA) has constantly gained ground among interventional cardiologists. TRA's anatomical advantages, in addition to patients' acceptance and financial benefits, due to rapid patient mobilization and shorter hospital stay, made it the default approach in most catheterization laboratories. Access-site complications of TRA are rare, and usually of little clinical impact, thus they are often overlooked and underdiagnosed. Radial Artery Occlusion (RAO) is the most common, followed by radial artery spasm, perforation, hemorrhagic complications, pseudoaneurysm, arterio-venous fistula and even rarer complications, such as nerve injury, sterile granuloma, eversion endarterectomy or skin necrosis. Most of them are conservatively treated, but rarely, surgical treatment may be needed and late diagnosis may lead to life-threatening situations, such as hand ischemia or compartment syndrome and tissue loss. Additionally, some complications may eventually lead to TRA failure and switch to a different approach. On the other hand, it is the opinion of the authors that non-occlusive radial artery injury, commonly included in TRA's complications in the literature, should be regarded more as an anticipated functional and anatomical cascade, following radial artery puncture and sheath insertion.

Vascular calcification represents the deposition of calcium phosphate salts in the tunica media of the vascular wall. It occurs during aging but is accelerated and pronounced in patients with diabetes mellitus, chronic kidney disease (CKD) and established cardiovascular disease. Due to the loss of elasticity of the vessel wall, vascular calcification might result in left ventricular hypertrophy and compromise coronary perfusion. Accordingly, several studies showed that vascular calcification is associated with increased risk for cardiovascular morbidity and mortality. Accumulating data suggest that microRNAs (miRs) play an important role in vascular calcification. A variety of miRs have been implicated in the development of vascular calcification, whereas others appear to play a protective role. Accordingly, miRs might represent promising targets for the prevention of vascular calcification and its adverse cardiovascular sequelae. However, given the complexity of regulation of this process and the multitude of miRs involved, more research is needed to identify the optimal candidate miRs for targeting.

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