Primitive neuroectodermal tumor of the pericardium: a case report and literature review

Background The primitive neuroectodermal tumors (PNETs) are a family of highly malignant tumors with a multidirectional differential potential. The tumors are characterized by aggressive small round tumor cells that originate from the spinal cord of the central and sympathetic nervous systems. Cases involving the pericardium are extremely rare. Herein, we present a case of peripheral primitive neuroectodermal tumor (pPNET) that originated in the pericardium. Case presentation A 23-year-old woman presented with cough and progressive dyspnea for 1 month, followed by eyelid and facial edema for 10 days, without any apparent cause. Significantly elevated tumor markers were detected in her blood. A cardiac ultrasound revealed a 74 mm × 61 mm spherical mass that was attached to the left pericardium, as well as massive pericardial effusion. Positron emission tomography-CT (PET-CT) showed focal hypermetabolism in the left pericardium. Via histopathology and immunohistochemistry, the spherical mass was identified as PNETS. The patient was successfully treated with a combination of surgical resection via thoracotomy and postoperative chemotherapy, and she was disease-free for 7 years at follow-up. Unfortunately, at 7 years after the treatment, the patient’s pPNET recurred. Positron emission tomography-MRI (PET-MRI) and 64-slice coronary CTA revealed that the aorta and multiple coronary arteries were involved. Subsequently, the patient refused a heart transplant and voluntarily left the hospital. Conclusions This paper reports on a rare and recurrent case of PNET in the parietal pericardium. With respect to the different biologic characteristics and prognoses of pPNETs (compared to other known pericardium tumors), it is essential to consider this entity as a differential diagnosis in pericardium tumors.

Left Ventricular Pseudoaneurysm as a Complication of Myocardial Infarction; A Case Series and Review of the Literature

Introduction: Pseudoaneurysm may occur as a rare complication of myocardial infarction (MI) when a hemorrhagic process is covered by adherence of the visceral or parietal pericardium or of both, preventing the formation of cardiac tamponade. Pseudoaneurysm is prone to rupture because they are not easy to diagnose. Case presentation: Here, we report three cases of left ventricular pseudo-aneurysm (LVP) that all were related to MI. Two patients were managed conservatively, one of them was lost to follow-up, and the other one expired one month later. One patient underwent surgery, but he expired during post-operation period. Conclusions: High mortality rate of LVP emphasizes the importance of looking for it in cardiac evaluation of patients with history of MI. Due to available non-invasive modalities, the ability to differentiate LVP from other cardiac pathologies is improving. Still, the most recommended management of LVP is early surgery.

NO Synthase but not NO, HNO or H2O2 Mediates Endothelium-Dependent Relaxation of Resistance Arteries from Patients with Resistant Cardiovascular Disease

Background and Purpose: Superoxide anions can reduce the bioavailability and actions of endothelium-derived NO. In human resistance-sized arteries, endothelium-dependent vasodilatation can be mediated by H2O2 instead of NO. We tested the hypotheses that in resistance arteries from patients with resistant cardiovascular disease (CVD), endothelium-dependent vasodilatation uses mechanisms that are either insensitive to oxidative stress or involve a reactive oxygen species. Experimental Approach: Small arteries were isolated from biopsies of the parietal pericardium of patients undergoing elective cardiothoracic surgery and were studied by immunohistochemical and organ chamber techniques. Key Results: NO-synthases 1, 2 and 3, superoxide dismutase 1 and catalase proteins were observed in the microvascular wall. Relaxing responses to bradykinin were endothelium dependent. During submaximal depolarization-induced contraction, these relaxations were inhibited by inhibitors of NO-synthases (NOS) and soluble guanylyl cyclase (sGC) but not by scavengers of NO or HNO, inhibitors of cyclooxygenases, neuronal NO-synthase, superoxide dismutase or catalase, or by exogenous catalase. During contraction stimulated by endothelin-1, these relaxations were not reduced by any of these interventions except DETCA which caused a small reduction. Conclusion and Implications: In resistance arteries from patients with resistant CVD, endothelium-dependent relaxations seem not to be mediated by NO, HNO or H2O2 although NOS and sGC can be involved. These vasodilator responses proceed during excessive oxidative stress.

Idiopathic Effusive Constrictive Pericarditis Accompanying Multiple Complications: A Case Report

IntroductionEffusive constrictive pericarditis (ECP) is a unique clinical syndrome that is characterized by the coexistence of pericardial effusion and constrictive pericardium. The etiology of ECP usually contains tuberculosis, idiopathic, and neoplastic causes. The early diagnosis, treatment strategy and prognostic predictor of ECP still remain a big problem nowadays due to the sophisticated clinical situations. Case PresentationWe here report a rare case of idiopathic ECP with thickened adherent visceral pericardium and normal parietal pericardium, accompanying multiple complications mainly comprising severe tricuspid regurgitation, hypoproteinemia, and proximal deep venous thrombosis. The patient was referred for radical pericardiectomy successfully, but the long-term prognosis may be unfavorable. DiscussionThis case aims to provide some clinical experience of such situation in which the clinician should weight the benefits and the risks to a particular patient.

A Rare Constrictive Pericarditis with Complete Separation between the Visceral and Parietal Pericardium: A Case Report

Background: Pericarditis is the most common form of pericardial disease, while constrictive pericarditis is challenging in diagnosis and is easily overlooked. Case report: A 30-year-old female presented with abdominal distension and mild lower extremity edema for 3 months. The patient was initially suspected of having cirrhosis caused by Wilson Disease. Following liver biopsy and multiple investigation, thickened, calcified pericardium was detected by echocardiography and chest computed tomography. The patient was finally diagnosed with chronic constrictive pericarditis and received pericardiectomy. Intraoperatively, we found that the heart was entirely constricted by the thickened and calcified visceral pericardium, which was completely separated from the parietal pericardium. The patient received successful pericardiectomy and had relief of symptoms after surgery. Conclusion: Patients with constrictive pericarditis may present with symptoms similar to that of chronic liver diseases, which makes it difficult and complicated for diagnosis. This case highlights the importance of comprehensive preoperative evaluation and maintaining clinical suspicion of pericarditis in patients with features of elevated systemic venous pressure. In addition, constrictive pericarditis with complete separation between visceral and parietal pericardium has seldom been reported.

Excision of visceral pericardium for chronic effusive constrictive pericarditis

Chronic effusive-constrictive pericarditis was successfully treated by removal of the visceral pericardium in a 15-year-old Thai female. The constrictive visceral pericardium was barely detected by noninvasive studies. This case highlights the importance of removal of the visceral pericardium in this condition. If only the parietal pericardium is removed, the patient will not improve clinically.

Diseases of the Pericardium, Cardiac Tumors, and Cardiac Trauma

The pericardium consists of an outer fibrous layer and an inner serous layer. The serous layer covers the surface of the heart and the proximal portion of the large vessels (visceral pericardium), folds back on itself, and lines the fibrous layer (parietal pericardium). Normal pericardial thickness is less than or equal to 2 mm. The space between the visceral and the parietal layer forms the pericardial cavity, which normally contains 10 to 50 mL of fluid. The pericardium lubricates and reduces friction, serves as a barrier against infection, maintains the heart in a relatively stable position within the thoracic cavity, and prevents acute distention of the cardiac chambers. None of these functions, however, is essential for life, and the pericardium may, in fact, be absent at birth. This review contains 16 figures, 1 table, and 50 references. Key Words: Pericardium, parietal pericardium, visceral pericardium

Diseases of the Pericardium, Cardiac Tumors, and Cardiac Trauma

The pericardium consists of an outer fibrous layer and an inner serous layer. The serous layer covers the surface of the heart and the proximal portion of the large vessels (visceral pericardium), folds back on itself, and lines the fibrous layer (parietal pericardium). Normal pericardial thickness is less than or equal to 2 mm. The space between the visceral and the parietal layer forms the pericardial cavity, which normally contains 10 to 50 mL of fluid. The pericardium lubricates and reduces friction, serves as a barrier against infection, maintains the heart in a relatively stable position within the thoracic cavity, and prevents acute distention of the cardiac chambers. None of these functions, however, is essential for life, and the pericardium may, in fact, be absent at birth. This review contains 16 figures, 1 table, and 50 references. Key Words: Pericardium, parietal pericardium, visceral pericardium

Fibrinous pleuropneumonia caused by Pasteurella multocida associated with bovine lymphoma

ABSTRACT: In this work, we describe an unusual case of fibrinous pleuropneumonia caused by Pasteurella multocida associated with generalized lymphadenomegaly in a bovine. The animal had a one-month history of generalized superficial lymphadenomegaly that progressed to anorexia and submandibular oedema, resulting in spontaneous death. At necropsy, the parenchyma of the lymph nodes and multiple organs was obliterated by a dense proliferation of round neoplastic cells (lymphoma). Additionally, the neoplasm presented multifocal areas of haemorrhage and necrosis, characteristic of lymphoma. The parietal and visceral pleura and parietal pericardium were enlarged and covered diffusely with large amounts of a yellowish fibrillary material. The lungs were mildly enlarged, non-collapsed, and firm and exhibited interlobular septae that were thickened with a gelatinous material. Histopathological examination showed that the parietal and visceral pleura were enlarged due to a diffuse and severe inflammatory infiltrate composed of degenerate neutrophils associated with severe fibrin deposition, characteristic of fibrinous pleuropneumonia. Pleura and parietal pericardium fragments were cultivated in aerobic and microaerobic microbiological conditions. Round greyish colonies of gram-negative coccobacilli that were shiny and non-haemolytic were observed in sheep blood agar. The biochemical profile was indicative of Pasteurella spp. Molecular identification was performed by partial 16S rRNA amplification following sequencing. Pasteurella multocida was confirmed as the primary bacterium associated with the bovine fibrinous pleuropneumonia. We are able to infer that the lymphoma caused immunodepression, which increased the animal’s susceptibility to atypical infectious microorganisms such as pathogenic P. multocida.

Ectopia cordis: a case report and review of literature

The Ectopia cordis is a rare congenital condition. It is characterized by the abnormal position of the heart outside the thoracic cavity, associated with defects in the parietal pericardium, diaphragm, sternum, and, in most cases, cardiac malformations. The reported prevalence is 5.5 to 7.9 per million live births. The designation Ectopia cordis was first proposed by Abott in 1998, although cases of patients with similar defects had been reported in past. Only 267 cases have been reported as of 2001, most (95%) associated with other cardiac abnormalities. A 10 hour old, normal, vaginally delivered, full-term male neonate, weighing 2020 grams was brought with an externally visible, beating heart over the lower chest wall. The antenatal period was uneventful, though no ultrasonography was done. The beating heart was covered with a membrane with greenish purulent matter over it, most probably, due to pseudomonas/proteus infection. Rest of the anterior abdominal wall was intact. Ectopia cordis is produced by segmental defects in mesodermal development in the third week of intrauterine life, and/or amniotic band syndrome that causes simultaneous cerebral and Thoraco-abdominal malformations. The existence of Ectopia cordis with severe congenital heart disease may be confirmed in the prenatal period by vaginal echocardiography at 10-12 weeks of gestation or by abdominal echocardiography by 20-22 weeks. Surgery is the only hope of survival, for such patients, although the overall success rate is very poor. In recent years, surgery has been attempted in one or two phases with variable results that depend, mainly on the type of associated heart disease.