Abstract Background pericardial diseases during pregnancy are rare. The most common are hydropericardium – typically in the third trimester, with spontaneous resolution – and pericarditis. Echocardiogram is the imaging method of first choice for diagnosis. Clinical case a 38–year–old woman, at gestational week 24, came to the Emergency Department due to anxiety, shortness of breath, cough, gastroesophageal reflux, inappetence, and sialorrhea, all of which started with the pregnancy and worsened overtime. She underwent cardiological evaluation because of troponin discovered via blood test. The evaluation highlighted mild pericardial effusion. Hence, she was admitted to the Cardiology Department, where a progressive increase of effusion – from mild to severe (in particular in front of apical and posterior segments) without hemodynamic impact – was noted. Corticosteroid therapy was started without clinical improvement and the patient displayed orthopnea, diaphoresis, and oliguria. Through an echographic re–evaluation an hypervascular mass was identified in parasternal view. After a multidisciplinary discussion, a CT scan of thorax and abdomen with contrast (MRI was impracticable due to orthopnea) was carried out with evidence of a mediastinal solid lesion (11,5 x 7 mm) compressing superior vena cava, trachea and principal bronchial branches suggestive of lymphoproliferative disease. A pericardiocentesis was perfomed with evacuation of 400 ml of bloody fluid. The worsening of blood gas test required a tracheal intubation. Therefore, an emergency Cesarean section was executed, and a surgical biopsy of mass was taken with detection of diffuse large B–cell non–Hodgkin‘s lymphoma. Hgh doses of corticosteroids and chemotherapeutic drugs were administered and the patient was extubated after two days. After four therapeutic cycles, a PET–CT scan confirmed remission of the disease. Conclusion pregnancy is not a predisposing condition for pericardial diseases. Although pericardial involvement is benign in most cases, the use of corticosteroid therapy after the 20th week of gestation is indicated in suspected pericarditis to avoid fetal complications from NSAIDs. If there is no response, the use of advanced imaging methods (even potentially dangerous to the fetus) should not be procrastinated.

A 66–year–old woman presented to medical attention for low back pain, weight loss and evening fever for about 2 weeks, with concomitant mood deflection. Blood cultures were positive for Streptococcus mutans. Lumbar spondylodiscitis was found on spinal MRI and splenic infarction on abdominal ultrasound. The echocardiogram revealed the presence of vegetations on the aortic valve, which was severely regurgitant, and on the tricuspid valve, which was moderately regurgitant, in a setting of preserved biventricular dimensions and function. The patient was diagnosed with infective endocarditis, complicated by systemic embolization. The hospital stay was complicated, despite the appropriate antibiotic therapy, with acute pulmonary edema and cardiogenic shock, with a sudden worsening of the left ventricular function which became severely reduced, in the presence of an "apical ballooning" appearance. Anterior T–wave inversion with prolongation of the QT interval was documented on the electrocardiogram. Coronary lesions were excluded by coronary CT scan. According to the InterTAK criteria, the patient achieved a score of 80, suggestive of a high probability of Takotsubo syndrome. In the following days, thanks to continuous infusion of diuretics and inotropic support, a hemodynamic compensation was obtained; there was a progressive recovery of the left ventricular function and of the apical wall motion abnormalities, with suspension of the inotropic support and reduction of the dosage of the diuretic. We concluded for Takotsubo syndrome in the setting of acute infective endocarditis. The patient, with a stabilized clinical picture, finally underwent cardiac surgery to replace the aortic and tricuspid valves without complications. Takotsubo syndrome (TS) is a condition characterized by a transient impairment of left ventricular function and kinetics, typically triggered by physical or emotional stress. In the literature only four cases of concomitant endocarditis and TS are reported, in which other triggers are recognizable (recent surgery, cerebral involvement with embolization or meningitis). In our case, there are no other apparent triggers other than endocarditis. Endocarditis could therefore represent in itself a new trigger for TS or even manifest, from the beginning, with a TS.

Abstract Background Prosthetic valve endocarditis (PVE) occurs in 1–6% of patients with valve prostheses. The most common agent of late PVE are S. aureus and Streptococci. Spondylodiscitis may precede the onset of endocarditis or may be the first clinical manifestation. Coronary embolization is a rare but possible complication of endocarditis. Case report: A 61 years–old man was admitted to the Emergency Department for low back pain, fever and chest pain. Four years before he underwent mitral valve bioprosthesis implantation and hybrid myocardial revascularization (percutaneous on right coronary artery). During observation cardiac arrest from ventricular fibrillation occurred, treated with single shock and evidence of anterolateral myocardial infarction at ECG. An urgent coronarography revealed chronic occlusion of CABG on LAD and acute occlusion, of possible embolic origin, involving LAD mid tract, first diagonal branch and intermediate branch. Thromboaspiration and subsequent PTCA was performed. For hemodynamic instability inotropic and vasopressor supports were started. A transthoracic echocardiogram showed severe left ventricular dysfunction (EF 25%) and 3.5x1mm endocardial vegetation on the mitral bioprosthesis without significant bioprosthesis dysfunction (confirmed by transesophageal echocardiogram). Blood cultures resulted positive for Streptococcus gordonii and antibiotic therapy based on the antibiogram was begun. Cardiac surgery was ruled out due to prohibitive surgical risk despite high probability of embolization. Because of the history of back pain spinal MRI was performed with evidence of cervial and lumbosacral spondylodiscitis. Neurosurgical indications were ruled out. Levosimendan infusion allowed weaning of vasopressor and inotropic therapy, however without improvement of left ventricular ejection fraction. Daily echocardiographic follow–up showed disappearance of the vegetation. Antibiotic targeted therapy was continued for 5 months, given the persistence of spondylodiscitis, in anticipation of intracardiac defibrillator (ICD) implantation in primary prevention. Conclusion PVE is a severe clinical condition associated with high morbidity and mortality. Antibiotic therapy is recommended for at least 6 weeks in PVE, in this case prolonged up to 5 months given the need to implant an ICD. Regarding the treatment of embolic infarction thromboaspiration is recommended as the initial strategy and, if successful, may be the only interventional option.

We describe the case of a 42–year–old man who presented to the emergency department suffering from asthenia, dyspnea and tachycardia. The patient had been diagnosed, two years earlier, with acute myeloid leukemia (AML), treated with two lines of chemotherapy and allogeneic bone marrow transplantation from a family donor. Atrial fibrillation with rapid ventricular response was documented at the ECG. The echocardiogram showed moderate left ventricular dysfunction in the presence of dishomogeneous thickening of left and right ventricular wall and a severe circumferential pericardial effusion causing cardiac tamponade, with the need of urgent pericardiocentesis. AML relapse was documented at the laboratory tests. The suspected cardiac involvement was investigated with cardiac MRI which documented thickening and diffuse late gadolinium enhancement at the level of the left and right ventricular wall, the interatrial septum and the atria walls. The pericardium and the epicardial fat were also thickened and endowed with contrast enhancement. A lymphocyte assay was performed on pericardial fluid and showed the presence of a blast population (approximately 27% of white blood cells) with variable expression of myeloid antigens. The clinical, radiological and finally immunophenotypic picture therefore concluded with relapse of acute myeloid leukemia with myocardial and pericardial infiltration. Acute myeloid leukemia usually presents with symptoms related to bone marrow failure. Clinically significant cardiac involvement is rare but should be considered when cardiorespiratory symptoms occur. Cardiac manifestations include coronary artery disease, heart failure, conduction disturbances, myocarditis, pericarditis, and pericardial effusion. Understanding the underlying pathophysiology and recognizing potential cardiac manifestations could help in the early diagnosis, evaluation, and treatment of these patients. Echocardiography or cardiac MRI could reveal morphological, structural and signal abnormalities of the cardiac structures and therefore should raise the suspicion of a possible myocardial infiltration by leukemia cells, both in patients with a positive history of leukemia and in those in whom cardiac involvement could represent the first manifestation of a hematological pathology.

Abstract Background Cardiac arrest is the third cause of death in Europe. It is a medical emergency characterized by high mortality and morbidity. Myocardial infarction is the leading cause of cardiac arrest. Data collection through national and international registries is essential to advance knowledge and improve diagnostic and therapeutic practices. Purpose: we assess the epidemiological impact of OHCA within a territory of approximately 300.000 inhabitants and follow patients’ intrahospital clinical pathway with the aim to identify possible predictors of survival and neurological outcome. Methods an electronic database is used to collect and share data across the Emergency Medical Services (EMS) and reference Cardiologists. Respectively, the EMS collects out–of–hospital patient data, whereas Cardiologists collect all information about intrahospital progress. Results during an observation period of two years, 100 patients with OHCA were enrolled. The majority were male and the average age was 65 years old. The first rhythm identified was shockable in 41% of the cases. Witnesses performed cardiopulmonary resuscitation and used automatic external defibrillator respectively in 57% and 10% of the cases. Only 34% of the victims obtained ROSC and were admitted into the cardiac intensive care unit and half of them died before discharge. Within this group, cardiac arrest was caused by myocardial infarction in 46% of the cases. Of these, culprit lesion was located in the left anterior descending artery in 46,2 % of the cases. It appears that a blood pH value below 7,04 – measured at the arrival in Emergency Department – is a poor prognostic predictor of ROSC, with a 79% sensitivity and 86% specificity (AUC 0,81, 95% CI 0,644 – 0,977). On the other hand, a plasma level of lactic acid expresses multiorgan damage secondary to cardiac arrest and therefore represents a predictor of survival and neurological outcomes, but not ROSC. Conclusion during the two years of observation, the incidence of OHCA turned out to be slightly lower compared to the data available in the literature. Mortality remains extremely high: only 12% of the population survives, of which 16% with poor neurological outcome. Blood gas analysis, if correctly interpreted, could be an optimal tool to target therapeutic choices for cardiac arrest victims. Further studies with a higher sample size will be needed to validate this data.

Abstract Background Calcific aortic valve disease (CAVD) is the western world’s leading degenerative valve disease affecting nearly 2% of the general population. Considered for a long time as the result of a passive process, nowadays CAVD is referred as an active process mediated by different cell types and involving several molecular mediators and cellular pathways. Aim of the Study The aim of this study was to investigate the role played by renal function during the progression of CAVD. Materials and Methods – We enrolled 116 patients affected by CAVD from the Cardiology departments of the Treviso Hospital and the High Specialization Rehabilitative Hospital of Motta di Livenza (TV). For each patient at the time of the recruitment a clinical visit was carried out that included the collection of anamnestic, anthropometric and echocardiographic data. Blood samples were collected from each subject at the recruitment to measure the following biochemical parameters: creatinine, lipidic profile, phospho–calcium metabolism. The GFR was estimated by using the CKD–EPI 2009 equation. To investigate the predictive role of renal function in the progression of CAVD, only patients (n = 49) with at least two transthoracic echocardiograms (TTE) were selected for the prospective analysis. These patients were followed for an average of 18.9 ± 11 months. The rate of progression of valvular disease was assessed in terms of difference in indexed valve area per month (ΔAVA/month). Results We observed that fast progressors had a significant reduction of eGFR at baseline as compared to slow progressors (60.62 ± 18.83 ml/min/1.73m2 vs. 77.22 ± 11.46 ml/min/1.73m2, p = 0.001). An increased risk of rapid progression of valvulopathy was found in patients with eGFR < 60 ml/min/1.73m2 (RR = 2.64, IC95%=1.50–4.60, p = 0.001) compared to subjects with normal renal function. A close to significance correlation was also found between values of circulating Pi and ΔAVA/month (r = –0.252, p = 0.084). Conclusions The present study showed that reduction of renal function, and in particular the presence of CKD (eGFR values <60 ml/min/1.73m2), is significantly associated with an increased risk of rapid progression of calcified aortic valvulopathy; this risk is further increased by the concomitant presence of increased levels of phosphatemia. Overall, these data indicate the potential predictive role of eGFR on the risk of accelerated calcific valvulopathy in non–dialysed patients.

A 53-year-old male with negative medical history and absence of cardiovascular risk factors was found positive for SARS-CoV2 infection on 9 December 2020. During the quarantine, on 12 December 2020, he suffered a sudden onset of oppressive chest pain with dyspnoea. The ECG performed by Emergency Medical Service showed inferior ST-elevation myocardial infarction. The emergency coronary angiography showed long endoluminal thrombosis due to a complicated atherosclerotic plaque in the third tract of the right coronary artery (confirmed by IVUS). Thrombus aspiration and implantation of a medicated stent were performed with an excellent final result (Fig. 1). Tirofiban intravenous bolus was administrated followed by Prasugrel loading. The ECG after the procedure showed marked sinus tachycardia (over 130 bpm) with persistence of ST-elevation in the inferior leads. The following day the molecular swab for SARS-CoV2 was negative but the patient remained sweaty, dyspnoic with desaturation despite high flow oxygen, tachycardic and with low systolic pressure. On cardiac ultrasound, the right ventricle was dilated and strongly dysfunctional. Pulmonary pressure was 40mmHg with dilated and fixed inferior vena cava. D-dimer was 17071 ng/mL. A Chest Computer Tomography confirmed the diagnostic suspicion of pulmonary embolism by documenting gross cardio-embolic defects affecting the right and left main pulmonary artery that extend to the peripheral branches assigned to all lobes (Fig. 2). The chest CT also showed typical aspects of SARS-CoV2 related pneumonia and a small area of infarcted lung parenchyma (Fig. 3). The patient was therefore treated with anticoagulant therapy with full dose of low molecular weight heparin and antibiotic therapy. The subsequent hospitalization proceeded on a regular basis, with a progressive reduction of the oxygen and progressive recovery of the biventricular pump function. The patient also underwent a venous ultrasound of the lower limbs which documented thrombosis of the right sural vein and a transoesophageal echocardiography which excluded the presence of patent foramen ovale. At discharge, anticoagulant therapy with Apixaban 5mg x 2 and single anti-aggregation therapy with Prasugrel 10 mg for 12 months was set. (Table Presented).