No abstract

Heart failure with preserved ejection fraction (HFpEF) is a growing epidemiologic problem affecting more than half of the patients with heart failure (HF). HFpEF has a significant morbidity and mortality and so far no treatment has been clearly demonstrated to improve the outcomes in HFpEF, in contrast to the efficacy of treatment in heart failure with reduced ejection fraction (HFrEF).The failure of proven beneficial drugs in HFrEF to influence the outcome of patients with HFpEF could be related to the heterogeneity of the disease, its various phenotypes and multifactorial pathophysiology, incompletely elucidated yet. The diagnosis of HFpEF could be demanding or even inaccurate. Moreover, the therapeutic strategies were influenced by different cut-offs used to define preserved ejection fraction (EF). From this perspective, the current guidelines have classified HFpEF by an EF ≥ 50%, together with a distinct entity, heart failure with mid-range ejection fraction (HFmrEF), defined by an EF ranging from 41-49%.New therapies have been developed to interfere with the mediator pathways of HFpEF at the cellular and molecular level, including mineralocorticoid receptor antagonists, soluble guanylate cyclase stimulators, or angiotensin receptor-neprilysin inhibitors. A number of antidiabetic drugs, such as sodium/glucose cotransporter 2 inhibitors and dipeptidyl peptidase-4 inhibitors are promising options, being under research in large clinical trials. Until the results of ongoing trials shed light on these therapies, guidelines recommend empirical treatment for established HFpEF, and emphasize the crucial role of addressing cardiovascular comorbidities leading to HFpEF, in particular arterial hypertension.

Background. Oxidative stress (OS) and inflammation are major mechanisms involved in the progression of chronic heart failure (CHF (E/e' ≥ 13) had higher sUA (8.6 ± 2.3 vs. 7.3 ± 1.4, p=0.08) and NT-proBNP levels (643±430 vs. 2531±709, p=0.003) and lower EF (29.8 ± 3.9 % vs. 36.3 ± 4.4 %, p=0.001). p<0.001), MDA (r= 0.49, p= 0.001), MPO (r=0.34, p=0.001) and p= 0.003).Conclusion. In CHF, hyperuricemia is associated with disease severity. High sUA levels in CHF with normal renal function may reflect increased xanthine-oxidase activity linked with chronic inflammatory response.

Worsening chronic heart failure (HF) is responsible for recurrent hospitalization and increased mortality risk after discharge, irrespective to the ejection fraction. Symptoms and signs of pulmonary and systemic congestion are the most common cause for hospitalization of acute decompensated HF, as a consequence of increased cardiac filling pressures. The elevated cardiac filling pressures, also called hemodynamic congestion, may precede the occurrence of clinical congestion by days or weeks. Since HF patients often have comorbidities, dyspnoea, the main symptom of HF, may be also caused by respiratory or other illnesses. Recent studies underline the importance of the diagnosis and treatment of hemodynamic congestion before HF symptoms worsen, reducing hospitalization and improving prognosis. In this paper we review the role of integrated evaluation of biomarkers and imaging technics, i.e., echocardiography and pulmonary ultrasound, for the diagnosis, prognosis and treatment of congestion in HF patients.

696levels, associated with gas within the biliary tree (FIGURE 1A). Abdominal computed tomography (CT) confirmed the acute occlusive distention of the je junum and proximal ileum, as well as pneumobi lia. There was no presence of a gallstone in the air filled gallbladder, but a concentric intraluminal ring was present in the right iliac fossa, suggest ing a migrated gallstone in the bowel lumen, with a secondary ileoileal intussusception (FIGURE 1B -1E). The clinical diagnosis was acute intestinal obstruc tion probably due to gallstone ileus associated with secondary ileoileal intussusception, bilio enteric fistula, and pneumobilia.The emergent surgery revealed a jejunal ob struction by a gallstone of 2.5 cm in diameter, a spontaneous cholecystoduodenal fistula, and a secondary ileoileal intussusception due to gall stone displacement. The gallstone was extracted An 84 year old woman with a history of choleli thiasis was admitted for abdominal pain and per sisting vomiting, which had started more than a week earlier, as well as symptoms of acute small bowel obstruction, which she noted 3 days ear lier. On physical examination, she appeared dis tressed and dehydrated, while her abdomen was distended, diffusely painful, and soft, without re bound tenderness. A laboratory analysis revealed neutrophilic inflammation and mild cholestasis (increased conjugated bilirubin and serum alka line phosphatase levels). The levels of pancreat ic enzymes were normal, and other laboratory test results were unremarkable. Abdominal ul trasound revealed a shrunken gallbladder with the air inside, but without stones, and a nondi lated common bile duct. Plain abdominal X ray showed dilated small bowel loops with air fluid