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Six consecutive patients (3 men; mean age, 63 ± 14 years; age range, 38-81 years) with infrarenal abdominal aortic stenosis underwent unilateral or bilateral transradial approach for stenting of the aortic lesion. In 4 cases, isolated aortic stenting was performed through single transradial approach (in 2 cases with precise alignment to the proximal end of previously deployed iliac stents), whereas in the other 2 cases bilateral transradial approach was used for aortic stenting followed by bilateral stenting of the proximal iliac arteries. Either a "bare-on-the-wire" or a "support-catheter" technique was used, according to patient anatomy and technical requirements. The median follow-up was 14.3 months, at which time all patients had relief of symptoms without thromboembolic or bleeding complications. In this performance and safety evaluation, full transradial approach was effective and safe for treating infrarenal aortic stenosis that is isolated or associated with iliac disease.

Clopidogrel is an oral tyenopiridin with a central role in the management of acute coronary syndromes and after stent implantation. Despite the use of this drug, many patients continue to experience thrombotic events which are usually referred as "therapy failure". Actually, to date, only stent thrombosis is considered therapy failure: mainly, it could be due to patient genetic predisposition or drug interaction, in particular with proton pump inhibitors. Genetic mutations in the CYP2C19 cytochrome (involved in the metabolism of clopidogrel and many other drugs) may lead to a lower concentration of active metabolites of the drug. In the same way, proton pump inhibitors interaction with the cytochrome may reduce clopidogrel activation. To overcome the problem some authors have suggested to increase the dosage of the drug, to use other drugs, to genotype patients, and not to use proton pomp inhibitors in patients on double antiplatelet therapy. Recent studies have shown that the interaction between clopidogrel and proton pump inhibitors is far to be clinically relevant and that the variability between the different assay to determine patients response to the drug does not allow, to date, to rely on their use. Moreover, double clopidogrel dose is as effective as low one in preventing major cardiovascular events, with a significant reduction in stent thrombosis in spite of a modest increase in major bleeding. Aim of this review article was to update current knowledge on clopidogrel, particularly focusing on the problem of "resistance" and PPI interaction. Moreover, we will discuss current strategies to overcome the resistance.

Objective: The aim of this review is to examine the role of polymorphonuclear neutrophils (PMNs) in the evolution of atherosclerosis., Introduction: While the role of PMNs in the evolution of atherosclerosic process has failed until recently to attract much attention, a body of research carried out over the last decade has disclosed the unexpectedly complex behavior of these cells, unraveling an unexpected key role for PMNs in the onset and progression of atheroma., Methods: A PubMed database search was performed for studies providing evidences on the role of PMNs in the development and progression of atherosclerotic lesion., Results and Conclusions: Activated PMNs were shown to produce and release reactive oxygen species, inflammatory leukotrienes and proteolytic lysosomal enzymes, directly inducing vascular damage. Activated PMNs also secrete myeloperoxidase, involved in lipoprotein oxidation. PMNs have a finite lifespan and typically die through apoptosis, which thus represents a counter-regulatory mechanism limiting the toxic potential of these short-lived, terminally differentiated cells. Dysregulation of this process probably contributes to the pathogenesis and progression of several inflammatory diseases. Moreover, high circulating levels of PMN-platelet aggregates have been reported in patients with clinical atherosclerosis, and recent studies suggest that these aggregates may play a role in vascular response to injury. It has been suggested that this heterotypic interaction between platelets and leukocytes might represent a link between hemostasis/thrombosis and the inflammatory response.

Atherosclerosis is a complex process that begins with endothelial dysfunction, and continues with several inflammatory processes leading, eventually, to plaque rupture and formation of arterial thrombus. Increased platelet reactivity and classical coagulation pathways are not the only players of the whole thrombotic process: microparticles (MPs), irregularly shaped small vesicles released from the plasma membrane after cell activation, apoptosis, or exposure to shear stress have been demonstrated to be involved in such a process. MicroRNAs (MiRs), small-non-coding single-strand RNAs acting as post-transcriptional modulator of target gene expression are expressed in the large majority of eukaryotes. MiRs are implicated in several phenomena: control of metabolism, control of cell-differentiation, control of cell-proliferation and control of cell-apoptosis, therefore contributing to physiologic and pathogenic processes in hematologic, genetic, infective and cardiac diseases. Microparticles operate as a delivery system of MiRs, playing an active and important role in processes such as coagulation and thrombosis. These novel findings also suggest MPs and, in particular MIRs, as possible and promising therapeutic targets.

Heart failure is a growing global epidemic that involves in its pathophysiology a proinflammatory state. Since the first description of elevated cytokine levels in this setting, there has been increasing interest in understanding the role of these molecules in left-ventricular remodeling and function. Over the years, intense research on the 'cytokine theory' of heart failure has allowed evaluation of the role of inflammatory biomarkers not only as pathogenetic mediators, but also as potential tools in the diagnosis and risk stratification of heart failure patients. Whereas current evidence does not support the use of inflammatory biomarkers for the diagnosis of heart failure, the assessment of their levels and the connection between their changes and changes in clinical status and prognosis has been well validated. At present, the utility of anti-inflammatory therapies in heart failure is still debated, since trials of anti-inflammatory agents in this setting have pointed out controversial results. On the contrary, established treatments of heart failure, including β-blockers, renin-angiotensin system antagonists, and aldosterone-receptor blockers seem able to act by modulating cytokine expression, suggesting a new role for these molecules in guiding heart failure therapy. Therefore, the binomial topic of heart failure and inflammation still has a number of fields not completely explored: our aim is to update current knowledge and future perspectives.

Coronary artery disease is the leading cause of death in Europe and in the US and angina is the most common symptom associated with stable coronary artery disease. Despite receiving optimal antianginal therapy, based on agents such as beta-blockers, calcium channel antagonists and nitrates, many patients continue to experience angina. Furthermore, the administration of these drugs is limited by adverse effects such as bradycardia or hypotension. Ranolazine is a new antianginal agent, recently approved as add-on therapy in patients with stable angina. This review will focus on its mechanism of action, tolerability, highlighting the clinical benefit coming from its use.

Myeloperoxidase (MPO) is an enzyme stored in azurophilic granules of polymorphonuclear neutrophils and macrophages and released into extracellular fluid during inflammatory processes. Several studies have shown its involvement into oxidative stress and inflammation. Recently, MPO has been considered its role as a possible marker of plaque instability and a useful tool for the prognostic evaluation of patients with coronary artery disease. Aim of this review is to provide an overview of patophysiological, analytical and clinical characteristics of MPO and to summarize the evidence about its usefulness as diagnostic and prognostic marker in the setting of acute coronary syndrome.

Microparticles are circulating fragments derived from blebbing and shedding of cell membranes through several mechanisms that include activation, apoptosis and cell damage. In the past they were largely considered as unimportant cell "dust", but more refined detection techniques have revealed large variations in their relative proportion and concentration in numerous disease states. Importantly, these conditions include the most prevalent causes of death and disability in our societies, namely cardiovascular, neoplastic, and inflammatory diseases. Microparticles carry procoagulant, proapoptotic and neoangiogenetic materials in the blood stream, and can also be viewed as a technique cells may adopt to rapidly modify their phenotype, independently from genetic signals. In this review, we focus on the role of these very small ( 1 micron) particles, not only as mere markers of an underlying pathologic state, but also as primordial intercellular messengers and defense mechanism that every viable cell can exploit in distress conditions. In this view, we suggest that this old communication system could be the target of future high-tech interventions, with potential broad consequences.

Cardiac troponin is the marker of choice for the diagnosis of acute coronary syndrome. Its introduction in clinical practice consistently improved both sensibility and specificity as compared with other biomarkers, as creatin-chinase MB. However traditional troponin assays show some limits: the relatively long time elapsing between the onset of ischemia and the increase in serum concentration, and the difficulty in distinguishing ischemic from non ischemic damage. An earlier diagnosis could be obtained by adopting new high sensitivity troponin assays, with a coefficient of variation ≤10% at the 99° percentile of a reference healthy population, and capable of detecting circulating troponin in the most healty subjects. The difficulty in distinguishing ischemic from non ischemic harm can be overcome considering that only a rising and falling pattern can be attributed to ischemic harm. Further studies are needed to evaluate the prognostic role of low circulating troponin levels in healthy subjects and for properly fixing cut off values. Indeed biomarker increase has always to be considered in the specific clinical context.