Leiomyosarcoma of the inferior vena cava in a patient with Budd-Chiari syndrome.

A 65-year-old man with no history of cardiovascular disease was admitted because of abdominal pain, nausea and lower limb edema. At clinical examination he presented hepatomegaly, ascites and laboratory evidence of liver failure. The echocardiogram (Figure 1A) showed preserved biventricular function, but a large irregular mass was visible in the right atrium (arrow; Supplementary data, Movie 1 and 2). Computed tomography (Figure 1B) showed patchy contrast uptake and positron emission tomography (Figure 1C) showed pathological uptake of 18-fluoro-deoxyglucose in the mass (arrow), extending along the inferior vena cava (arrowheads), suggesting a neoplastic nature. At cardiovascular magnetic resonance (Figure 1D and E; Supplementary data, Movie 3 and 4) the mass involved the right atrium (arrow) and extended into the inferior vena cava (arrowheads); moreover, it presented irregular contours and signal characteristics typical of a neoplastic mass

State-of-the-Art of Transcatheter Left Atrial Appendage Occlusion

Left atrial appendage occlusion (LAAO) is an increasingly used alternative to oral anticoagulation in patients with atrial fibrillation, especially in patients with absolute/relative contraindications to these therapies. This review will cover three main aspects of the procedure. In the fist part of the manuscript, we focus on patient selection. We describe three main categories of patients with primary indication to LAAO, namely patients with previous or at a high risk of intracerebral bleeding, patients with a history of major gastrointestinal bleeding and patients with end-stage renal disease and absolute contraindication to novel oral anticoagulants. Some other potential indications are also described. In the second part of the manuscript, we review available devices, trying to highlight different aspects and potential specific advantages. The last section overviews different ways for pre-, intra- and postprocedural imaging, in order to improve procedural safety and efficacy and ameliorate patient outcome. The characteristics of available contemporary devices and the role of imaging in procedural planning, intraprocedural guidance and follow-up are described

The search for efficient diagnostic and prognostic biomarkers of heart failure

Several biomarkers have been tested for screening, diagnosis and prognosis purposes, as well as to guide treatment in heart failure, but only the assay of circulating B-type natriuretic peptides has widely recognized applications for clinical decision-making. Natriuretic peptides are sensitive in detecting the clinically overt or subclinical myocardial damage, but their plasma levels are increased following every generic insult to the cardiovascular system. Novel biomarkers are required to identify specific pathways of disease progression, such as diverse neurohormonal axes activation, inflammation and fibrogenesis, and to act as a tool for therapeutic tailoring. In this view, Gal-3 and ST-2 assays seem very promising, given their involvement in mechanisms of cardiac fibrosis and their prognostic value

Cardioprotection by remote ischemic conditioning: Mechanisms and clinical evidences

In remote ischemic conditioning (RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site (remote ischemic preconditioning), during the ischemic insult (remote ischemic perconditioning) or at the onset of reperfusion (remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy

Inflammatory activation during maximal physical effort predicts specific membrane damage of cardiomyocytes

Background: Elevated concentrations of cardiac troponin I (TnI) and heart-type fatty acid-binding protein (H-FABP) identify patients with chronic heart failure (CHF) and ongoing myocardial damage (OMD) who are at increased risk for future cardiac events. Chronic inflammation has been advocated to justify CHF progression, possibly related to the development of OMD. We hypothesized that maximal exercise test could be useful to sensitize the assessment of OMD and its possible correlation with inflammatory status. Methods: The serum concentrations of H-FABP, a sensitive marker of membrane damage of cardiomyocytes, TnI, marker of myofibrillar damage and TNFa, as marker of inflammation, were measured in 20 patients with CHF (mean EF 35%?9, NYHA I vs II 50% vs 50%, 50% with ischaemic CHF, 50% primitive, on optimal medical therapy) before, at peak exercise, 1 h and 4 h after a maximal cardiopulmonary stress test. Results: Physical effort caused a significant rise in H-FABP (3.5?1 ng/ml, 1 hour after effort vs. 2.9?0.9 ng/ml at basal condition, p=0.05) and TnI (10 patients had at basal condition TnI values above 0.04 ng/L, the cut-off considered as prognostic in literature, while 4 h after maximal exercise, 15 (75%) patients had values higher). No correlations were evident between basal nor exertional values of TnI and H-FABP. Basal TNFa did not predict OMD. Interestingly TNFa at peak exercise was the only predictor of H-FABP 1 h after stress (r=0.619 p<0.001), but not of TnI. Conclusions: Assessment of OMD following maximal exercise stress test could identify a subgroup of CHF patients with myocardial damage not evident in resting conditions. Inflammatory activation seems more associated with membrane rather than myofibrillar damage as indicated by H-FABP and TnI respectively

Renal denervation in resistant arterial hypertension: Effects on neurohormonal activation and cardiac natriuretic peptides

Renal denervation (RD) is an emerging treatment for resistant arterial hypertension (RAH). RAH is characterized by hyperactivity of catecholaminergic and renin–angiotensin–aldosterone systems (RAAS), with elevated arterial blood pressure and a higher prevalence of cardiovascular overload and remodeling. As renal innervation is involved in sympathetic and RAAS overactivation, RD has the potential to reduce blood pressure by influencing this pathophysiological network [1]. Indeed, RD has been shown to reduce renal norepinephrine spillover [2] and it seems to exert beneficial effects also on cardiac remodeling by reduction of cardiac hypertroph