bluuebunny/crossref_metadata_2025_split huggingface dataset:
CONSTRICTIVE PERICARDITIS DURING SARS-COV-2 INFECTION: A CASE REPORT
Authors: De Maio J , Caputi A , Martelli A , Campisano M , Ceresoli P , Bagni E 
Published: May 2024

Abstract
In our Department we witnessed numerous cases of pericarditis at the end of summer 2023, including that of a 44-year-old patient suffering from rheumatoid arthritis with breath-taking chest pain and fever. Objectively no rubbing, but mild-moderate pericardial effusion. On the EKG diffuse anomalies of ventricular repolarization; increased inflammation indices with negative troponin; positive Sars-Cov-2 PCR. During hospitalization, despite the improvement of clinical parameters, dyspnea persisted. On the control echocardiogram, disappearance of the pericardial effusion, but thickening of the pericardial sheets associated with a "notch" of the interventricular septum and an anomalous Doppler profile in the suprahepatic vein. These findings were subsequently confirmed by cardiac MRI, with diagnostic criteria for constrictive pericarditis. On the basis of these data, therapy with high doses of NSAIDs and colchicine was established. The patient is currently followed periodically by our clinics and feels well. In the literature, constrictive pericarditis is generally secondary to chronic conditions; in this case the contribution of Sars-Cov-2 infection and rheumatoid arthritis cannot be excluded.
ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY AND CARDIAC SARCOIDOSIS: THE GREY ZONE
Authors: Gualini E , Palazzini M , Giannattasio C , Garascia A , Ossola P , Gentile P , Ghidini S 
Published: May 2024

Abstract
Cardiac sarcoidosis (CS) is a rare multisystem disorder characterized by granulomatous infiltration of the myocardium, whose clinical manifestations can be extremely heterogeneus. We report the case of a 47–year–old man with a previous diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVD). In history he had a marked arrhythmic pattern with multiple episodes of sustained ventricular arrhythmias, biventricular disfunction (LVEF 37%, RVEF 32%) and extensive biventricular transmural late–gadolinium enhancement (greater than 50%) at cardiac RMN. At EKG epsilon wave mainly seen in precordial leads. In November 2022 he was implanted with bicameral defibrillator and in March 2023 he underwent ablation procedure for ventricular tachycardia with RF with endo–epicardial approach. In May 2023 he arrived at our Centre for acute decompensated heart failure. At restored hemodynamic stability, screening for the possible inclusion in transplant list was started. Right heart catheterization (RHC) showed low cardiac index with no pulmonary hypertension. Chest CT unexpectedly showed the presence of multiple micronodules with perilymphatic distribution with confluent appearance compatible with pulmonary sarcoidosis. In consideration of this result, the transplant program was temporarily postponed and investigations for possible cardiac involvement of an inflammatory nature were started. 18F–FDG PET–CT showed pulmonary, splenic, lymphonodal and especially cardiac uptake in the mid–distal segment of the lateral wall of the left ventricle and in the inferior–apical site suspicious for inflammatory pathology. Unfortunately, both lymphonodal and cardiac biopsies were inconclusive because of insufficient material. Nevertheless, the clinical scenario satisfied the Japanese criteria for possible CS; therefore, treatment with prednisone 1 mg/kg was started and a 18F–FDG PET–CT was planned after 3 months of steroid therapy. CS can disguise as a phenocopy of arrhythmogenic right ventricular cardiomyopathy because of several common characteristics, especially arrhythmic presentation. Due to these similarities, a careful overall evaluation of each patient with ARVD is mandatory as several transplant centers have reported cases of CS in explanted heart with a pretransplant misdiagnosis of ARVD or dilated cardiomiopathy. Performing a chest CT in all ARVD patients as part of transplant screening may be considered.
A RARE CASE OF TYPE A AORTIC DISSECTION PRESENTING AS ACUTE STROKE: A DIAGNOSTIC CHALLENGE
Authors: Saraullo S , Rizzuto M , Costantini D , Ruffo F , Corazzini A , Di Marco M , Renda G , Ricci F , Gallina S 
Published: May 2024

Abstract
A 60–year–old woman presented to the emergency department with acute left hemiplegia, not chest pains. Past medical history was significant for family history of aortic aneurysm, arterial hypertension. At brain–CT was reported hypodensity areas in posterior arm of the right internal capsule and in right tempero–polar lobe, confirmed on brain–MRI, and compatible with acute ischemic injury. Echocolor–dopper of epiaortic vessels documentated ulcerated plaque into the right common carotid artery (CCA). Selective catheterization found focal dissection obstructing the flow, treated with self–expanding stent. On echocardiography evalutation for suspiction of TAAD: dilatation of ascending aorta with flap oscillation, severe arotic regurgitation, pericardial effusion (Fig. 1). CT–Angiography was performed with evidence of type A dissection extending superiorly to the right CCA and inferiorly to the iliac bifurcation. For coma state, the patient was mechanically ventilated, and seriate CTs showed new ischemic lesions and hemorrhagic infarction of previous. Because of contraindication for cardiac surgery due neurological state, the patient was referred at medical therapy as bridge to hybrid aortic arc substitution at resolution of intracranial hemorrhages. In the next days there was progressive improvement neurological status with restoration of sensory and autonomic breathing with hemodynamic stability. Aortic dissection (AD) is defined as a disruption of the medial layer leading to the formation of two lumens separated by an intimomedial flap. AD is a critical diagnosis to make due to life–threatening outcomes and its non–specific presentation as in the case of our patient where the management of AD was delayed due to an unusual initial clinical presentation. Multimodality imaging approach has been fundamental for correct diagnosis and risk stratification. A limited number of studies have reported cases with stroke as the first symptom with concomitant TAAD. Concomitant intracerebral hemorrhage and TAAD is a very rare presentation and the optimal timing of surgery in these patients is unknown. In our opinion, patients who presents acute stroke should be carefully evaluated using multimodal imaging to exclude TAAD before administering reperfusion therapy. In addition, performing CAS before surgery for TAAD is challenging but might be a valid treatment option to maintain good brain perfusion and improve prognosis, but further investigations are needed.
SEVERE MITRAL REGURGITATION TREATED WITH TRANSCATHETER AORTIC VALVE IMPLANTATION IN MITRAL RING (TMVIR): A CASE REPORT
Authors: Vitale C , Giannini C , Costa G , Petronio A , De Carlo M 
Published: May 2024

Abstract

Introduction
The increasing prevalence of mitral regurgitation (MR), combined with a growing population of elderly patients at risk of being unsuitable for surgical options, has led to a greater interest in the use of less invasive treatments such as transcatheter heart valve (THV) implantation. This case involves the use of transcatheter aortic valve implantation in a patient with a previous mitral annuloplasty (TMViR).

Case Presentation
A 77–year–old woman had previously undergone mitral annuloplasty (Physio Ring II 32 mm, Medtronic), Neocord implantation and closure of the posterior commissure for severe MR due to anterior leaflet prolapse. She presented to our attention with worsening dyspnea (NYHA Class III) and a sudden weight gain. Transesophageal echocardiogram (TEE) revealed findings indicative of a previous mitral annuloplasty failure, with residual severe MR along with severe tricuspid regurgitation (TR). The case was discussed in the Heart Team and given the elevated surgical risk and the patient‘s anatomical unsuitability for edge–to–edge therapy, it was decided to perform a TMViR implantation. Under echocardiographic guidance and general anesthesia, right common right femoral vein access was obtained. After transseptal puncture, predilation of the interatrial septum was performed with balloon (Evercross 12 mm, Medtronic). Subsequent access to the left ventricle was achieved with a 6F PigTail catheter, and a stiff exchange guide (Safari S, Boston Scientific) was used to advance the 16Fr Delivery system. With the assistance of TEE, aortic valve implantation on the mitral ring was performed (Sapien 29 mm, Edwards Lifesciences) with rapid pacing via transvenous temporary PM placed in right ventricle (Spikeflow, Fiab). At the end of the procedure, two closure systems (Proglide, Abbott) were used for right femoral vein access. Post–implantation TEE showed a trivial paravalvular leak external to the annulus and a mean transvalvular gradient of 5 mmHg. The postoperative course proceeded without complications, facilitating the patient‘s discharge on the third postoperative day. Currently no further hospitalization in the last 6 months.

Conclusion
Despite surgical intervention remaining the gold standard in treating severe MR in patients who have undergone a previous annuloplasty, in patients at high surgical risk for a re–operation, who are not eligible for other percutaneous options, TMViR could be a safe and effective option for treatment.
ACUTE MYOCARDIAL INJURY IN A PATIENT WITH TYPE–1 NEUROFIBROMATOSIS: A CASE OF SUSPECTED PHEOCROMOCYTOMA–ASSOCIATED MYOCARDITIS
Authors: Cingolani M , Cannillo M , Suppo U , Almohani A , Renon F , Troiano F 
Published: May 2024

Abstract
A 54–year–old patient with an history of type–1 neurofibromatosis presented to the emergency department (ED) due to recurrent abdominal pain with diarrhea. Clinical examination didn’t show anything remarkable. She was mildly hypertensive, apyretic. During her staying in the ED, she complained about chest pain and an electrocardiogram (ECG) was performed. ECG showed sinus rhythm, normal heart rate, left ventricular (LV) hypertrophy with marked horizontal ST segment depression in the precordial leads and bimorphic ventricular ectopic beats with prevalent right bundle branch block superior axis morphology, likely from the medio–basal inferior LV. Troponin T (peak 958 ng/L, normal &lt;15 ng/L) and NTproBNP (peak 2357 ng/L, normal &lt;180 ng/L) were elevated, hemoglobin, creatinine and liver function were normal, C–reactive protein peaked at 120 mg/dL. Echocardiogram showed mildly reduced left ventricular ejection fraction (LVEF) with inferior and inferolateral hypokinesia and moderate mitral regurgitation (MR). She was admitted to cardiac intensive care unit with the suspected diagnosis of an acute coronary syndrome and was started on acetylsalicylic acid, metoprolol, furosemide and potassium canrenoate. Amiodarone was added due to frequent ventricular tachycardias. Due to the symptoms and the history of neurofibromatosis a whole body computed tomography (CT) was done. CT showed a 53 mm mass on the left adrenal gland with intense enhancement, suspected for a neoplastic origin (Figure 2). Plasmatic and urinary cathecolamines and metanephrines were increased. Positron–emission tomography (PET)/CT with 68Ga showed left adrenal uptake, compatible with a neuroendocrine tumor. Coronary arteriography showed normal coronary arteries. The patient underwent a cardiac magnetic resonance (CMR) study in the suspect of acute myocarditis. CMR showed normal biventricular function, an inferior basal hypokinesia with focal intramyocardial late gadolinium enhancement (LGE) suspected for a post–inflammatory origin and mild pericardial effusion. After pharmacological preparation a laparoscopic left adrenalectomy was performed, and histology confirmed the diagnosis of a composite pheocromocytoma. Three months after, the patient was asymptomatic, biochemistry showed normalization of both troponin T and endocrinological biomarkers, the echocardiogram showed preserved LVEF without areas of hypokinesia and mild MR. A follow–up CMR at six months from the acute injury has been scheduled.
PAPILLARY FIBROELASTOMA: AN UNUSUAL CAUSE OF TRANSIENT ISCHEMIC ATTACK
Authors: Lorenzini B , Palazzolo M , Carlà A , Occhiuzzi E , Sciarra L , Romano S 
Published: May 2024

Abstract
Papillary fibroelastomas (PFEs) are small, avascular benign tumors. Despite that, PFEs could lead to important clinical consequences such as transient ischemic attack and myocardial infarction. A 65–year–old female patient was admitted to our ER presenting a transient ischemic attack characterized by retrograde amnesia lasting about an hour. She had a history of systemic scleroderma and left breast cancer treated with local radiotherapy. In our hospital she underwent a neurological examination and a head CT which were negative for ongoing acute pathologies. An electrocardiogram was performed which showed sinus rhythm at 65 bpm. A transthoracic echocardiogram was also performed revealing a floating mass arising from left ventricular outflow tract between aortic and mitral valves. The transesophageal echocardiogram confirmed a solitary lesion approximately 2 centimeters long localized between A2 and A3 mitral valve scallops. The patient was therefore referred for surgery. During surgery the mass was found to arise from anterior mitral annulus and was resected. The histopathological examination of the mass confirmed the morphologic diagnosis of papillary fibroelastoma. Histologically PFEs are made up of a single layer of endocardial cells covering a matrix of collagen. The main risk factors for the development of PFEs are iatrogenic causes, such as radiotherapy, and autoimmune diseases such as systemic scleroderma. In 54% of cases PFEs are asymptomatic at the time of diagnosis. Since over 95% of PFEs present on the left side of the heart, systemic embolism is the most frequent presentation typically as transient ischemic attacks. Initial evaluation is accomplished with echocardiography. PFEs appear as echo–dense and pedunculated masses. Cardiac computed tomography and magnetic resonance imaging are second line modalities in PFEs evaluation. Definitive diagnosis of PFE requires pathological confirmation. Surgical resection remains the treatment of choice for all symptomatic patients. For symptomatic patients who are not surgical candidate, long term antiplatelets or anticoagulation therapy should be initiated. Asymptomatic patients should have surgical resection if the size of the tumor is &gt; 1 cm. PFEs are associated with significant morbidity and mortality. Echocardiography remains the most utilized diagnostic modality. Surgical treatment should always be considered. Antithrombotic therapy should be considered in non–surgical candidates.
UNUSUAL PATIENT IN CATH LAB: A CASE REPORT
Authors: Picardi G , Viceconte N 
Published: May 2024

Abstract

Background
Acute coronary syndromes occur in daily cardiologist’s practice. Atherosclerosis is doubtless the main etiology; however, it exists an alternative physiopathological mechanism: spontaneous coronary artery dissection (SCAD). Atherosclerosis and SCAD do not share the same risk factors: typical SCAD epidemiology comprehends young women often in pregnancy. SCAD is caused by sudden disruption of the coronary artery wall, resulting in separation of the inner intimal lining from the outer vessel wall.

Case Description
F.C. a 37–years–old, female, entered to the Emergency Department (ED) referring typical chest discomfort radiating to jaw and upper limbs lasting two hours. EKG presented ST segment elevation in V2–V4. Diagnosis of ACS–STEMI was performed. Urgent coronary angiography showed long dissection involving LDA. At first due to clinical relief, the physicians suggested to a conservative treatment and a watchful waiting. Soon the patient experimented malignant arrhythmias and percutaneous revascularization was necessary. True lumen engagement with guidewire was ensured by IVUS technique; Resolute Onyx 2.5 mmx34 mm was deployed in LDA mid tract, protecting the side brunch with further guidewire. Because of retrograde squeezing of intramural hematoma, a further Resolute Onyx 3 mmx8 mm was released proximally overlapped the first stent. Good result TIMI 3. After six months, the patient was asymptomatic and Coro CT confirmed the stents patency and absents of further dissections. Discussion: Randomized control trial about best treatment option in patient with SCAD are unavailable. Conservative therapy is often the first line, especially in dissections involving mid–distal tracts of main branch. The reason of this stands in a high percentage of spontaneous healing of dissections within 3–6 months, From data available in medical literature, PCI performed in atherosclerosis coronaropathy has better outcomes than PCI performed in SCAD. The latter is associated with a larger incidence in periprocedural complications. False lumen engagement with guidewire and intramural hematoma ‘squeezing’ after stent dilatation are the typical procedure complications.

Conclusions
Because of exiguous numbers, SCAD is a topic of large gap in evidence. Nowadays, lots of our knowledge about SCAD results from case reports or small meta–analysis. Indeed, the present case report offers it contribute to increase the state of art on this theme.
ANOTHER BRICK IN THE WALL: A STRANGE CASE OF A BIG HUG
Authors: Chiorazzo L , Gambioli V , Trambaiolo P , D‘Ambrosi A , Fina P , Miraldi F , Saade W , Granatelli A 
Published: May 2024

Abstract

Background
Left ventricular pseudoaneurysm (LVP) is a rare complication of myocardial infarction MI (less than 0,1% of all patients with MI) and develops when cardiac rupture is contained by adherent pericardium or scar tissue, thus contains no endocardium or myocardium, unlike a true left ventricular aneurysm (LVA).

Clinical Case
A 41–year–old man without remote cardiac history was admitted to the Emergency Department with chest pain that had started 7 days before after a referred ‘big hug’ from a friend. Results of the physical examination were unremarkable. Electrocardiogram: T waves negative in the inferior and lateral leads. Blood exams: normal troponins, C–reactive protein and D–dimer values. Chest computed tomography: no sign of pulmonary embolism. Transthoracic echocardiography (TE): ejection fraction 45%, voluminous aneurismal chamber communicating with the infero–posterior wall of the LV, stratified thrombus and mild mitral valve regurgitation. Coronary angiography: three vessel coronary artery disease. The last diagnosis was established by cardiac magnetic resonance imaging (MRI) which revealed a voluminous pseudoaneurysm of the inferior wall (56 mm x 50 mm with a 51 mm neck) and transmural late gadolinium enhancement (LGE) of the wall adjacent to the pseudoaneurysm with fibroadipose replacement and calcific metaplasia. The patient was transferred to the Cardiac Surgery Department. Intraoperatively the LVP was resected and the defect of the LV was repaired with a patch in bovine pericardium. In addition, coronary artery bypass grafting and mitral valve repair were performed.

Discussion
LVP develops when pericardium, in combination with thrombus and inflammation, surrounds a cardiac rupture. Inferior and posterolateral myocardial infarction (MI), due to occlusion of the Circumflex artery, are responsible for 82% of the LVP. LVP can be also found in the apical region due to anterior MI. In conclusion symptoms, signs, electrocardiographic abnormalities and radiographic findings seen in patients with LVP can be indistinguishable from those in patients with coronary disease alone. TE is the first non–invasive method for early diagnosis of LVA, but MRI is the gold standard for differential diagnosis between true aneurysm vs pseudoaneurysm. LGE of the pericardium is a new specific marker of pseudoaneurysm as opposed to true aneurysm.
EOSINOPHILIC MYOPERICARDITIS: A CASE SERIES
Authors: Laiso L , Bocchino P , Angelini F , Claudia R , Pidello S , Frea S , Gallone G , Gaetano Maria D 
Published: May 2024

Abstract

Background
Eosinophilic myocarditis is characterized by acute myocardial inflammation due to eosinophilic tissue infiltration.

Methods
Diagnosis was based on laboratory tests, Echo and CMR; EMB was performed in uncertain cases. Treatment was performed according to the etiology of EM. All patients underwent regular follow–up at our Center.

Results
This study includes 9 patients (89% Caucasian, 78% women, mean age 48.2±13.6 years), admitted in our Center from February 2021 to November 2023. 66.67% cases occurred in the setting of eosinophilic granulomatosis with polyangiitis, 11% was secondary to B–cell lymphoblastic leukemia, and 22% were labelled as idiopathic EM. All patients presented with high eosinophil count (6133±4893/mcL), elevated CRP (57±66 mg/L) and hs–troponin I (3610±5166 ng/L) levels, and 67% cases NT–proBNP (10751±4038 ng/L) was elevated. 67% patients presented with dyspnea, 56% with chest pain, and 56% with fever. On ECG, sinus tachycardia, low QRS voltages and ST segment depression with negative T–waves were common. Thickening of the myocardial walls with reduction of GLS was seen in all cases; in 44% cases, the EF was below 50%; 56% cases had mild pericardial effusion. 1 patient had intraventricular thrombi at CMR, another one had bilateral pulmonary embolism. On CMR, all patients had areas of hypokinesia, myocardial edema, and myo–pericardial late gadolinium enhancement. EMB was performed in 5 cases, confirming the presence of intramyocardial eosinophilic infiltrates. 7 patients required CICU, and 1 needed inotrope (dobutamine) use. The patient with ALL was treated with combined chemotherapy. The other EM cases were treated with immunosuppressive therapy consisting of corticosteroids and either cyclophosphamide or rituximab or mepolizumab. All patients received cardioprotective therapy with BBs and ACE–inhibitors; in patients with pericardial involvement, colchicine was administered. All patients showed rapid clinical improvement following immunosuppressive therapy initiation, with prompt reduction of circulating eosinophils and hs–troponin I values and normalization of the ejection fraction. On CMR imaging, edema disappeared at follow–up, with LGE replacement in one case. All patients were alive and in good conditions at the last follow–up.

Conclusions
EM is an underdiagnosed life–threatening disease. A careful assessment of the etiology, as prompt therapy, is mandatory to achieve clinical amelioration and good mid–term prognosis.