Introduction Myocardial infiltration by primary cardiac neoplasm is a rare condition and the pathological spectrum includes more widespread benign cell types, providing exceptional diagnostic and therapeutic challenges. Refractory heart failure, pericardial effusion and arrhythmias due to infiltrative mass are the most common clinical manifestations. Multimodality imaging, with echocardiography, computed tomography and magnetic resonance imaging, is essential to determine the characteristics of a cardiac tumor. Clinical case: A 35-year-old man without cardiovascular risk factors presented with two months of shortness of breath and weight loss. A previous history of acute myeloid leukemia undergoing allogenic bone marrow transplant was reported. Transthoracic echocardiography revealed an apical thrombus in left ventricle with inferior and septal hypokinesia conditioning mildly reduced ejection fraction, circumferential pericardial effusion without cardiac tamponade and abnormal right ventricular thickening (Figure 1). The cardiac magnetic resonance imaging confirmed diffuse thickening of the right ventricular free wall (maximum diameter 30 mm), suspected for myocardial infiltration, extending to the right atrium and left ventricle with an ischemic pattern of the inferior wall (Figure 2). No coronary artery disease was found by coronary angiography, but the right coronary artery was incorporated by the pathological tissue in chest computed tomography scan. Cardiac positron emission tomography demonstrated the presence of neoplastic tissue with increased metabolic activity, whose similar characteristics were also evident in the ascending aorta and aortic arch. Being the percutaneous endomyocardial biopsy inconclusive, a pericardiectomy was performed through a median sternotomy incision, showing widespread cardiac neoplastic infiltration. Histopathological analysis, done on samples taken by surgical myocardial biopsy, revealed tissue involvement by a rare and aggressive cardiac anaplastic large T-cell non-Hodgkin lymphoma (ALK -, Ki-67 90%). Few days after surgery, the patient developed a refractory cardiogenic shock and unluckily died before establishing an adequate therapy. Conclusion Primary cardiac lymphoma is very infrequent and the non-specificity of the symptoms makes the diagnosis extremely challenging and often limited to autopsy findings. Our case highlights the importance of an appropriate diagnostic algorithm that can allow an early diagnosis and an adequate therapy of this otherwise fatal pathology. In this condition surgical removal of the tumor in not indicated, being chemotherapy the only effective treatment. However, because of rarity, data are lacking to produce definitive regarding guidelines.

Introduction Dilated cardiomyopathy (DCM) is a condition whose etiologies may be various. DCM with ventricular disfunction is a frequent complication of chemotherapy. Peripartum cardiomyopathy is characterized by a reduced ejection fraction (EF), presenting toward the end of pregnancy or in the first months after delivery. Lipodystrophy may be associated to dilated and hypertrophic cardiomyopathy. Material and Methods A 28-years-old pregnant woman in her late 33rd week was admitted with acute heart failure complicated by pulmonary edema. The patient had history of acute lymphoblastic leukemia during childhood treated with chemo and radiotherapy, followed by hematopoietic stem cell transplantation (HSCT). Afterwards she developed partial acquired lipodystrophy, causing diabetes mellitus, insulin resistance, dyslipidemia, leptin deficiency and steatohepatitis. A mild left ventricular disfunction had been reported before HSCT, with complete recovery at follow up. After admission, the scenary rapidly deteriorated towards cardiogenic shock, so a caesarean section was performed. Transthoracic echocardiography revealed diffuse hypokinesia conditioning severe left ventricular (LV) dysfunction (EF 24%), moderate mitral and tricuspidal valve regurgitation and left to right shunt in possible atrial septal defect. A cycle of levosimendan was administrated, with subsequent improvement in LV function (EF 32%). Cardiac magnetic resonance (CMRI) showed hypokinetic DCM with no pathological findings in T1, T2, STIR sequences nor LGE. In parallel, empty sella in possible Sheehan Syndrome was hypothesized. A diagnosis of peripartum cardiomyopathy on the basis of a chemotherapy-induced cardiomyopathy in a good compensation status was made, with no evidence of lipodystrophy-related cardiac involvement. After recovery the patient was discharged with optimal cardiological therapy and a wearable cardioverter defibrillator. During follow up, the patient improved ventricular function (EF 40%) without any registered arrhythmia. She will be evaluated for heart transplantation. Conclusions Pregnancy in patients with cardiac disease can be life-threatening for mother and fetus, a multidisciplinary approach and a correct timing are crucial to achieve the best possible result. Left ventricular disfunction can be related to many etiologies, and instrumental tests such as echocardiogram and CMRI are crucial to evaluate the cause of the disfunction. Close follow up in patients who underwent chemo/radiotherapy or are affected by metabolic diseases may avoid long-term cardiac complications.

Aims Post-cardiac injury syndrome (PCIS) is an inflammatory state involving pericardium, epicardium, and myocardium causing a clinical picture in which epicardial and pericardial symptoms are prevalent. It appears mediated by autoimmune mechanisms and may appear as late post myocardial infarction pericarditis (Dressler’s Syndrome) or as a post traumatic pericarditis in the case of spontaneous thoracic trauma or iatrogenic pericarditis. Apart from the acute setting, pericardial effusion can be a manifestation of PCIS after interventional procedures. Methods and results A 57 years old hypertensive woman suffering from recurrent atrial fibrillation episodes underwent a technically difficult radio-frequency catheter ablation because of complex pulmonary veins anatomy and wide scar in the left atrial wall. During the procedure she developed cardiac tamponade and 410 ml of blood were drained by pericardiocentesis and re-infused without recurrent pericardial effusion during further in-hospital stay. She was discharged on apixaban 5 mg b.i.d. with Hb value of 10.2 g/dl. Two weeks later the patient was hospitalized for worsening cough, atypical chest pain, dyspnoea and modest orthopnea. C-reactive protein levels were 8.7 mg/dl, Hb was 9.9 g/dl and platelet count 484 000/ml; blood cultures were negative. An urgent thoracic CT scan showed bilateral pleural effusion and ubiquitous pericardial effusion (2.5–3 cm), without signs of active bleeding from the cardiac chambers into the pericardium. After stopping apixaban, the patient was given colchicine (1 mg/die). A total of 1200 ml of hematic pericardial fluid was drained from the pericardium over a 5-day period. Autoimmune blood tests were negative, as well as antibodies to pericardiotropic viruses. Pericardial fluid was negative for quantiferon and direct BK. On day 9, the drain was removed and steroidal treatment was started (prednisone 25 mg/die with scheduled tapering). Further echocardiographic exams were stable without pericardial effusion; a chest X-ray scan (at day 16) showed reversal of the water bottle shaped heart and of the pleural effusion. Conclusions Early myocardial infarct-associated pericarditis and Dressler’s syndrome account for about 20% of cases of PCIS accompanied by symptoms of epicardial and pericardial origin. PCIS is quite common after cardiac surgery, but it may be also observed even after iatrogenic trauma occurring during cardiac interventions: PCI, pacemaker lead insertion, radiofrequency ablation and Swan–Ganz catheterization. Blood entering the pericardium is thought to play a pivotal etiological role in iatrogenic PCIS, with consequent huge inflammatory reaction in the mesothelial tissue resulting in clinical manifestations of pericarditis. In animal models of PCIS, systemic release of cardiac antigens and self-antigen specific responses has been hypothesized. In our case cardiac tamponade complicating the ablation procedure probably initiated the epicardial and pericardial inflammatory response. Even if based on few data, the patient was treated with colchicine first, avoiding aspirin because of the hemorrhagic pericardial fluid; glucocorticoids were then started when symptoms and signs of PCIS slowly resolved despite colchicine treatment. The pericardial fluid was hemorrhagic (Hb 5.9 g/dl) and treatment with apixaban, in the context of an inflammatory mesothelial response, could have caused this peculiar, hemorrhagic, pericardial reaction.

Aims The diagnosis of acute coronary syndrome with persistent ST segment elevation, although apparently simple to detect by electrocardiographic abnormalities, can sometimes be insidious due to a difficult differential diagnosis with aortic dissection. Performing a coronary angiography in case of aortic dissection can be potentially life-threatening so, when suspected, this diagnosis needs to be rule out. Furthermore, coronary vasculitis is a rare but devastating complication of giant cell arteritis. Methods and results We describe a case of 62-year-old man hospitalized for acute coronary syndrome with persistent ST segment elevation involving the inferior wall. Ha was a heavy smoker with familiar history of cardiovascular disease and recent suspicion of Horton arteritis with aortic involvement under investigation, no previous cardiological events. Presenting symptoms are chest pain, sweating, bradycardia, and hypotension. In the emergency department, due to the history of suspected arteritis, chest CT scan was performed in order to rule out the hypothesis of aortic dissection before proceeding to coronarography. No signs of aortic rupture but the presence of thickening of the aorta from the arch to the carrefour was found. The coronary angiography showed critical stenosis in the medial tract of the circumflex artery and thrombotic subocclusion in the middle segment of the right coronary (culprit lesion—Figure 1) that was treated with PCI using drug-eluting stent. The echocardiogram showed mild left ventricular disfunction (EF 53%) due to posterolateral hypokinesia, no other pathological findings. Blood tests revealed anaemia, elevated platelets, and an increase of inflammation markers. Peak Hs-troponin was 18 000 ng/L (n.v. < 0.02 ng/ml). After 2 days we performed elective revascularization of the circumflex artery using a drug-eluting stent. Considering the medical history, we performed temporal artery biopsy and a total body PET scan that showed accumulation of radioactive tracer from the aortic arch to the sub-renal abdominal aorta, with a thickened wall. After that empirical corticosteroid therapy was started and some days later the result of the temporal artery biopsy confirmed the diagnosis of Horton arteritis. The patient was discharged to a rehabilitation structure in good general condition with cardioactive and corticosteroid therapy after 9 days of hospitalization. Conclusions Horton arteritis usually involves the external carotid artery and its branches, but sometimes inflammation of the aorta occurs in a subgroup of patients and rarely can involve the coronary arteries. An acute coronary syndrome in patients with Horton arteritis can be very insidious because aortic dissection can be the hidden cause, so chest CT scan must be performed before coronary angiography to avoid acute complication associated with an elevated mortality. Furthermore, being the vasculitic inflammation the trigger of the coronary involvement immunosuppressive therapy could be helpful to prevent subsequent acute coronary events.

Aims Left ventricular free wall rupture is one of the mechanical complications of myocardial infarction with an incidence of 2–4%. Sometimes the myocardial rupture hasn’t an immediate fatal evolution, nor is easy to be diagnosed because it is contained by the pericardium and thrombus formation, leading to pseudoaneurysm of the left ventricle. Pseudoaneurysms need a prompt surgical correction for their high risk of rupture both in the acute phase and later. Methods and results A 57 years old, smoker, woman with no previous cardiological history was admitted to our cardiological department for acute coronary syndrome with persistent ST segment elevation involving the postero-lateral wall (door to balloon time about 10 h, Killip class I and peak hs-TnI value was 27.67 ng/ml n.v. ˂0.02 ng/ml). The echocardiography showed mild left ventricular disfunction (LV EF 45%), postero lateral akinesia and moderate mitral regurgitation; ubiquitous pericardial effusion (1 cm) was present, particularly along the anterior left ventricular wall, with irregular echo-dense aspect. She underwent urgent coronarography that showed a critical stenosis of the distal third of the left circumflex and a thrombotic occlusion of the first marginal branch. The distal circumflex was treated with angioplasty and stent implantation but we couldn’t obtain the reperfusion of the marginal branch. Post procedural echocardiogram was unchanged and no free wall rupture was detected. 7 days after the admission, the patient showed persistent elevation of white blood count and CRP and developed fever, promptly empirically treated with a cephalosporin (blood cultures collected before were negative). After two new episode of fever with persisting biochemical flogistic parameters, a rheumatologic cause of the pericardial effusion was considered in the presence of positive antinuclear antibodies suggesting the diagnosis of Systemic Lupus Erythematosus. Steroidal therapy was prescribed which caused clinical improvement without complete resolution of the pericardial effusion. On day 20 of hospital stay a new echocardiographic evaluation showed a discontinuation of the postero lateral myocardial wall (Figure 1), about 1 cm in width, widely communicating with the left ventricular cavity and suggestive for a left postero-lateral ventricular pseudoaneurysm. The patient underwent surgical intervention and it was possible to expose a big clot occluding the pseudoaneurysmatic cavity communicating with the left ventricular chamber through an inlet about 1 cm in diameter, that was repaired with a bovine pericardial patch (Bard Sauvage technique). After surgery the patient was supported with an IABP and inotropes and was discharged to a rehabilitation structure on day 29 of hospital stay. Four months after the hospital discharge the patient died for a recently diagnosed pancreatic cancer. Conclusions Pseudoaneurisms are life-threatening complications of myocardial infarction that sometimes are hardly diagnosed. When correctly recognized surgical correction can lead to a good prognosis.