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A 25-years old white female was admitted to our emergency department presenting with dyspnea, fever, cough and nausea. Her medical background included a small ventricular septal defect (VSD) (congenital) with a left to right shunt, micropolicistic ovary syndrome, Sars Cov 2 infection on January 2022, history of cutaneous infection after sternal piercing in the last three years. Patient showed onset of fever, headache and nausea since 20 days and had a history of ampicillin and cephalosporin usage for 15 days for comunitary pneumonia. Upon arrival in the emergency room, physical examination revealed temperature 38°C, crackles on down right lung fields, regular but tachycardic rhythm, 3/6 holosystolic murmur in the third left intercostal space, also skin redness around the piercing zone. Laboratory test showed increasing of WB (white blood cells), C-reactive protein (CPR) and procalcitonin. Because of worsening of respiratory conditions, CT chest was performed, showing tree in bud sign, with pulmonary pattern suggestive of staphylococcal “emboligenous-like” infectious state. According to patient's clinical history and CT results, she was referred to transthoracic echocardiogram (TTE) demonstrating the presence, on the right side of the small VSD, of a isoechoic large mass (20x 13 mm) with irregular margins attached to the right ventricular wall near the ostium of the VSD, compatible with vegetation; septal tricuspid valve leaflet involvement could not be ruled out. Methicillin-susceptible Staphylococcus aureus (MSSA) was detected six times from blood cultures; therapy with oxacillin 2 gr every 4 hours combined with daptomycin 750 mg daily was started. Cardiac MRI performed after few days, documented the infective involvement of the ventricular and atrial side of the septal leaflet with moderate tricuspid regurgitation (TR). Congenital heart disease (especially Tetralogy of Fallot, bicuspid aortic valve, aortic coarctation, ventricular septal defect) is a lifelong risk factor for infective endocarditis (IE). Size of VSD is generally not correlated with IE that is directly correlated with turbulent flow; tricuspid valve involvement is mostly seen in VSD, often complicated by pulmonary embolism. In this predisposing situation, skin infection of the piercing zone could have caused transient bacteremia which led to the formation of vegetations in the highest turbulence flow zone.

A 65-year-old female was admitted to our hospital for sudden onset of typical chest pain at rest lasting few minutes. Her medical background included systemic hypertension, type 2 diabetes, dyslipidaemia, and mild obesity. Upon arrival in the emergency room, the electrocardiogram didn’t reveal signs of acute myocardial ischaemia and serial cardiac troponin T measurements were persistently negative. A transthoracic echocardiogram (TTE) was performed, showing mild ventricular hypertrophy, no regional wall motion abnormalities, and a preserved left ventricular ejection fraction. A highly echogenic tubular structure, located slightly on the atrial side of the atrioventricular groove was noted in multiple apical views. Its tubular shape was suggestive of a vascular structure, but its location was atypical for a normal vessel; indeed its persistence in more than an echocardiographic plane excluded an artefact. According to patient’s clinical history and her high cardiovascular risk profile she was referred for coronary angiography, demonstrating no critical stenosis but an anomalous aortic origin of a coronary artery (AAOCA) from the inappropriate sinus of Valsalva: the left main coronary artery (LMCA) arose from the right coronary cusp and then took a caudal posterior loop running posterior to the aortic root. In light of these findings we could associate the tubular structure seen at TTE to the retroaortic course of LMCA, a finding recently described as retroaortic anomalous coronary (RAC) sign. Among AAOCA, the retroaortic course of the LMCA is an uncommon diagnosis in adults, and its association with a single coronary origin is extremely rare. Although it has been usually considered a benign clinical entity, it is associated with an increased risk in morbidity and mortality during valve surgery. The presence of RAC sign at TTE was demonstrated to be highly suggestive of an anomalous coronary artery (specificity 93.9%) and strongly associated with retroaortic LMCA course at computed tomography angiography. 234 Figure B

Background Pulmonary hypertension (PH) patients show, during exercise, an excessive increase in ventilation (V E ) compared to carbon dioxide output (VCO 2 ), determining a high V E /VCO 2 slope. There are several possible causes, including an elevated dead space ventilation (V D ), V E /perfusion (Q) mismatch and/or an enhanced peripheral or central chemoreceptor activity. We evaluated the causes of exercise hyperventilation in PH patients. Methods Eighteen group I and IV PH patients underwent cardiopulmonary exercise test with blood gas analysis at every minute. V E , alveolar ventilation (V A ) and V D vs. VCO 2 relationship were calculated. Resting chemoreceptor sensitivity was analyzed through hypoxia/hypercapnia tests. Results PeakVO 2 and V E /VCO 2 slopes were 1.06±0.24l/min and 39.1±9.0, respectively. Throughout the exercise, 30% of V E was due to V D . V E /VCO 2 slope significantly correlated with V D /VCO 2 slope (r=0.82, p A /VCO 2 slope (r=0.3, p=ns). Peak exercise end-tidal CO 2 (PetCO 2 ) correlated with V D /VCO 2 slope (r=−0.79, p E /VCO 2 slope (r=−0.91, p 2 were elevated without arterial hypoxemia suggesting a high V E /Q mismatch. Chemoreceptor peripheral response to hypoxia and central CO 2 response were both enhanced being peripheral responses to hypoxia and hypercapnia 0.416±0.402 (normal ref values=0.285±0.221) l/min/O 2 Sat and 0.076±0.047 (0.066±0.430) l/min/mmHg, respectively; central hypercapnic chemosensitivity was 4.475±3.99 (2.352±0.936) l/min/mmHg. Conclusions Increased DS, V E /Q mismatch and chemorecptor response are among the main mechanisms involved in exercise hyperventilation in PH. ClinicalTrial.gov NCT02892981

AIMS Mineralocorticoid receptor antagonists (MRAs) have been demonstrated to improve outcomes in reduced ejection fraction heart failure (HFrEF) patients. However, MRAs added to conventional treatment may lead to worsening of renal function and hyperkalaemia. We investigated, in a population-based analysis, the long-term effects of MRA treatment in HFrEF patients. METHODS AND RESULTS We analysed data of 6046 patients included in the Metabolic Exercise Cardiac Kidney Index score dataset. Analysis was performed in patients treated (n = 3163) and not treated (n = 2883) with MRA. The study endpoint was a composite of cardiovascular death, urgent heart transplantation, or left ventricular assist device implantation. Ten years' survival was analysed through Kaplan-Meier, compared by log-rank test and propensity score matching. At 10 years' follow-up, the MRA-untreated group had a significantly lower number of events than the MRA-treated group (P

Aims The cardio-renal syndrome plays a critical role in acute heart failure (HF). Levosimendan, an inodilator drug, has a positive but controversial effect on kidney. Our aim was to evaluate its effects on both renal and systemic haemodynamic parameters as well as on renal function, explaining the possible mechanisms involved. Methods and results Patients with acute decompensated HF, moderate renal impairment, wedge pressure >20 mmHg and EF

In normal coronary arteries, several different mechanisms of blood flow regulation exist, acting at different levels of the coronary tree: endothelial, nervous, myogenic and metabolic regulation. In addition, physiologic blood flow regulation is also dependent on the activity of several coronary ion channels, including ATP-dependent K+ channels, voltage-gated K+ channels and others. In this context, ion channels contribute by matching demands for homeostatic maintenance. They play a primary role in rapid response of both endothelium and vascular smooth muscle cells of larger and smaller arterial vessels of the coronary bed, leading to coronary vasodilation. Consequently, an alteration in ion channel function or expression could be directly involved in coronary vasomotion dysfunction.

Background Poor diuretic response in acute heart failure is related to poor clinical outcome. The underlying mechanisms and pathophysiology behind diuretic resistance are incompletely understood. We evaluated a combined approach using clinical characteristics and biomarkers to predict diuretic response in acute heart failure (AHF). Methods and results We investigated explanatory and predictive models for diuretic response—weight loss at day 4 per 40 mg of furosemide—in 974 patients with AHF included in the PROTECT trial. Biomarkers, addressing multiple pathophysiological pathways, were determined at baseline and after 24 h. An explanatory baseline biomarker model of a poor diuretic response included low potassium, chloride, hemoglobin, myeloperoxidase, and high blood urea nitrogen, albumin, triglycerides, ST2 and neutrophil gelatinase-associated lipocalin (r2 = 0.086). Diuretic response after 24 h (early diuretic response) was a strong predictor of diuretic response (β = 0.467, P

Heart failure is a major public health problem because of its high prevalence and impact on mortality, morbidity, quality of life, and social costs. The aim of this analysis was to estimate the effects of the novel inodilator levosimendan versus standard inotropic therapy (ST) of dobutamine in acute heart failure. A study population of 292 patients with acute heart failure was derived from an observational registry of patients referred to our department. Of these, 147 patients received iv levosimendan (0.05-0.1 μg·kg·min for 24 hours), and 145 patients were treated with ST. Duration of hospitalization, survival at 1 month, and the rehospitalization rate during the year after the index hospitalization were evaluated. Cost-effectiveness analysis was performed. The mean length of hospitalization was 12.08 and 13.57 days in the levosimendan and ST groups, respectively (P < 0.05). Rehospitalization rates were lower in the levosimendan group at 6 months (1.44% vs. 2.3%; P < 0.05) and 12 months (7.6% vs. 14.3%; P < 0.05). Mortality rate at 1 month was 2.1% versus 6.9% in the levosimendan and ST groups, respectively (P < 0.05). The per-capita cost of treatment with levosimendan was €78.86 higher than that with ST during the first hospitalization but €280.22 lower when the rehospitalization rate was considered.

Background: Deregulation of microRNAs (miRNAs) may be involved in the pathogenesis of heart failure (HF) and renal disease. Our aim is to describe miRNA levels related to early worsening renal function in acute HF patients.Method and results: We studied the association between 12 circulating miRNAs and Worsening Renal Function (WRF; defined as an increase in the serum creatinine level of 0.3 mg per deciliter or more from admission to day 3), absolute change in creatinine and Neutrophil Gelatinase Associated Lipocalin (NGAL) from admission to day 3 in 98 patients hospitalized for acute HF.At baseline, circulating levels of all miRNAs were lower in patients with WRF, with statistically significant decreased levels of miR-199a-3p, miR-423-3p, and miR-let-7i-5p (p-value Conclusions: Our results show that the levels of circulating miRNAs at hospital admission for acute HF were consistently lower in patients who developed worsening of renal function. MiR-199a-3p was the best predictor of WRF in these patients. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

Introduction: Numerous reports suggest, among HIV+ patients (pts), an increased rate of acute coronary syndrome and cardiac death. Several data suggest that endothelial dysfunction is a major mechanisms in the development of coronary atherosclerosis in non-HIV infected patients. Hypothesis: The aim of our study is to assess coronary microvascular function using Doppler-flow wire in HIV+ patients in therapy with HAART. Methods: Thirteen HIV-infected patients were enrolled from the Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and Geriatric Sciences of the “Sapienza” University of Rome (Italy). The main inclusion criteria were: Framingham risk score Diagnostic coronary angiography was performed via percutaneous radial approach. Microvascular function was assessed by measuring coronary flow velocity reserve (CFR). Intracoronary functional tests were performed to evaluate both endothelium-dependent microvascular function [via intracoronary (IC) infusion of acetylcholine (2.5[[Unable to Display Character: –]]10 μg)] and non-endothelium-dependent microvascular function [via IC infusion of adenosine (5 μg) ]. Results: All the patients presented a Framingham risk score Conclusion: Microvascular function is not compromised in HIV + pts who presented coronary atherosclerotic plaque. Microvascular dysfunction, involved in pathophysiology of coronary artery disease in general population, seems to be not implicated in coronary atherosclerosis in HIV + pts. These data suggest a peculiar pathophysiological mechanisms for HIV related atherosclerosis.

Background: According to guidelines, implantable cardioverter defibrillator (ICD) is recommended in prevention of sudden cardiac death (SCD) in heart failure (HF) patients (pts). Guidelines have several limitations because ICD indication is based mainly on left ventricular ejection fraction (EF). Recent data showed that, independently from EF, 123-iodine metaiodobenzylguanidine imaging (123-I MIBG) could help to identify HF pts at high risk of SCD [heart/ mediastinum (H/M) ratio ≤1.6 and a summed score (SS) > 26], who may benefit of ICD. Aim: Our aim is to assess, in a real world registry, the role of 123-I MIBG for the prediction of ventricular tachyarrhythmia (VT) causing appropriate ICD therapy in HF pts. Methods: We consecutively enrolled 97 patients admitted to our hospital with diagnosis of HF, left ventricular ejection fraction (LVEF) ≤35% and indication to ICD. All patients underwent MIBG imaging. The patients were classified into two groups: Group 1 with H/M≤1.6 , SS> 26; Group2 with H/M>1.6, SS Results: 65 pts were included in group 1 and 32 pts in group 2. All baseline characteristics were similar in 2 groups apart from the etiology (table 1). In group 1, H/M ratio was 1.37±0.3 vs 1.8 ± 0.2 in group 2 (p=0.0002); SS was 37.5± 9.7 vs 16 ±6 in group 2 (p = 0.0001). At 1 year follow-up VTs causing appropriate ICD therapy in group 1 were 13.4% vs 1.28% in group 2(p=0.02); overall cardiac events were in group 1 16.4 % vs 1.92% in group 2 (p=0.02). Conclusion: Our results suggest that 123 I-MIBG can identify patients at increased risk for arrhythmic death and can be useful in the decision-making of ICD implantation independently from ejection fraction.