Viral Pericarditis Research Articles

Cardiac tamponade caused by acute coxsackievirus\xa0infection related pericarditis complicated by aortic stenosis in a hemodialysis patient: a case report

BackgroundPericardial effusion is observed in the majority of viral pericarditis cases; however, viral pericarditis accompanied by a large effusion resulting in cardiac tamponade is rare.Case presentationHere, we report the case of a 75-year-old hemodialysis patient with acute viral pericarditis complicated by aortic stenosis. The patient was referred with a diagnosis of aortic stenosis and pericardial effusion. The pericardial effusion had increased during the preoperative examinations, and the inflammatory reaction had progressed. We decided to abort the surgical intervention and start oral administration of anti-inflammatory agents. We subsequently performed a pericardiocentesis. High antibody titers to coxsackievirus were noted in the pericardial effusion. Since no recurrence of the pericardial effusion was observed, the patient underwent an aortic valve replacement 2 months later. The pericardium completely adhered to the heart. Pathological examination of the pericardium showed fibrous pericarditis without active inflammation.ConclusionsHere, we successfully treated a hemodialysis case with severe aortic stenosis complicated by cardiac tamponade and worsened by acute viral pericarditis. We waited for the pericarditis to resolve after administering anti-inflammatory agents and performed pericardial drainage before carrying out aortic valve replacement. The perioperative course of our case was unique and suggestive.

Cystic mediastinal mass

Case presentationA 32-year-old woman with no other medical history presented with 1-month history of fever, weight loss and dyspnoea. On examination she had elevated jugular venous pressure and tachycardia. Her...

Ten questions about constrictive pericarditis

Constrictive pericarditis is one of the most feared complications of patients with pericarditis, especially if recurrent. The common perception is that the higher the number of recurrences, the higher the risk of constriction. However, the risk of constriction is related to the etiology and not to the number of recurrences. Constriction has never been reported as a complication of idiopathic recurrent pericarditis, while the risk is low (<1%) after a first attack of idiopathic or viral pericarditis, intermediate for immune-mediated etiologies (2-5%, e.g. systemic inflammatory diseases, post-pericardiotomy syndromes) and cancer, and high especially for bacterial etiologies (20.30%, e.g. tuberculosis, purulent pericarditis). Constriction may be reversible in the setting of pericarditis and about 7-10% of patients with acute pericarditis may have transient constriction during the acute phase of inflammation, due to increased pericardial stiffness. Empiric anti-inflammatory therapy may prevent pericardiectomy in one half of cases.The clinical diagnosis is not easy but feasible with prompt recognition of the clinical symptoms and signs that may mimic heart failure and chronic hepatic disease (e.g. jugular vein distention, peripheral edema, ascites), the echocardiographic signs (e.g. septal bounce, respiratory variations of transmitral and tricuspid flows, annulus reversus, inferior vena cava plethora), and other imaging features (e.g. pericardial thickening in about 80% of cases, pericardial calcifications).In this paper, we will try to give an answer to common clinical doubts for assessing the risk of constriction, making the diagnosis, and addressing the therapy of these patients also underlying the possible outcomes.

A Case of Impending Cardiac Tamponade Caused by Effusive Constrictive Pericarditis

Pericarditis is the most common pericardial disease worldwide, and can be recurrent in one third of the patients with viral and idiopathic pericarditis [1]. The diagnosis of pericarditis should be based on clinical criteria, history, clinical findings, electrocardiographic (ECG) changes and evidence of a pericardial effusion [2]. Elevation of the inflammatory markers and evidence of pericardial inflammation by an imaging technique such as contrast enhancement on the pericardium-CT scan or pericardial edema and pericardial late gadolinium enhancement on cardiac magnetic resonance imaging (MRI) are additional supportive criteria in the diagnosis [1].

Tuberculous and Infectious Pericarditis

Viral pericarditis is the most common cause of acute pericarditis and it is typically responsive to aspirin or nonsteroidal anti-inflammatory drugs. Tuberculous pericarditis is common in immunocompromised patients or in immunocompetent patients in endemic areas. The diagnosis of tuberculous pericarditis usually requires a multidisciplinary approach, and presumptive treatment should be started for people with suspected infections living in endemic areas. Antituberculous treatment along with corticosteroid therapy can reduce complications from constrictive pericarditis. Purulent pericarditis is fatal if untreated. Bacterial and fungal cultures from pericardial fluid and blood are essential to determine the best treatment.

Protocolo diagnóstico y tratamiento de las afectaciones pericárdicas de etiología infecciosa

TypesInfectious pericarditis encompasses three different aetiologies: viral, purulent and tuberculous. DiagnosisDiagnosis of each of these three entities requires specific study which should be protocolised. Viral pericarditis requires integral testing of the pericardial fluid or tissue which includes histological, cytological, immunohistological and molecular study. In the case of purulent pericarditis, diagnosis is based on findings of pericardial fluid of purulent appearance with a predominance of leukocytes and microbiological analysis. Finally, tuberculous pericarditis requires the tubercle bacillus to be demonstrated in the pericardial fluid or tissue. TreatmentTreatment will be specific to the aetiology.

Case Report of Pathognomonic Findings of Severe Colchicine Effect in the Esophagus, a Rarely Reported Site of Colchicine Effect

Colchicine, a medication commonly used to treat gout, interferes with the cell cycle and can injure rapidly reproducing cells, including proliferative cells in gastrointestinal mucosa, primarily in the small bowl. Esophageal injury is rarely reported, and when reported is typically mild. A case is reported of severe injury to esophageal mucosa secondary to colchicine. A 47-year-old male with a medical history of systemic lupus erythematosus, intermittently treated with corticosteroids for 2 years, recently treated with azithromycin therapy for upper respiratory infection and hydroxychloroquine for polyarthritis, presented with dyspnea and severe substernal chest pain, exacerbated by deep inspiration, and ameliorated by leaning forward. Physical examination revealed an afebrile man with stable vital signs and no friction rub. Laboratory tests revealed Hb=12.6 g/dl, creatinine=1.33 mg/dl, CRP=3.4 mg/dl, ESR=51 mm/hr, D-Dimer=1140 ng/ml, and troponin level was within normal limits. EKG revealed PR segment depression and upwardly concave ST elevation, findings suggestive of pericarditis. Echocardiogram revealed no pericardial effusion. CT angiogram of chest was negative for pulmonary embolus, but showed prominent distal esophagus wall. Patient was admitted for acute pericarditis, likely viral versus lupus pericarditis. Patient treated with prednisone 50 mg/ day and colchicine 0.6 mg twice daily with significant symptomatic improvement. Esophagogastroduodenoscopy revealed LA grade C reflux esophagitis and nonbleeding small gastric ulcers. He was treated with an oral proton pump inhibitor and discharged home. Pathological examination of esophageal biopsies revealed mild chronic gastritis at the gastroesophageal junction, with cytotoxic colchicine effect, but no intestinal metaplasia, dysplasia, or H. pylori infection. Colchicine prevents tubulin protein polymerization, prevents mitotic spindle formation and causes mitotic arrest during metaphase. The pathognomonic histopathologic finding is ring mitoses accompanied by increased glandular cell apoptosis and epithelial pseudostratification. Small bowel is the most severely affected site in the GI tract by colchicine, but in the present case the esophagus was significantly affected, a highly uncommon finding. Colchicine toxicity typically manifests soon after therapy initiation; in the current case endoscopic biopsies were performed one day after receiving 3 doses of colchicine therapy. The irregular arrangement of nuclei, increase in mitotic figures, and hyperchromatism of nuclei are pathognomonic of colchicine, but this finding can occasionally mimic dysplasia. Nontoxic doses of colchicine do not cause mucosal changes, except in areas with increased cell proliferation, such as a hyperplastic polyp, where nontoxic levels of colchicine can cause mitotic arrest and ring figures, and mimic a sessile serrated adenoma. These pathologic findings should be assessed in conjunction with clinical presentation to avoid missing the diagnosis of colchicine toxicity.Figure: Esophagogastroduodenoscopy showing deep linear erosions in distal esophagus. The lesions are unlikely from Mallory-Wiess tear in the absence of antecedent vomiting.Figure: Medium power photomicrograph of esophageal squamous mucosa showing brisk mitotic activity involving almost the entire thickness of the epithelium. Right inset shows high power view of characteristic ring mitosis associated with colchicine effect.Figure: Medium power photomicrograph of gastric cardial epithelium at gastroesophageal junction showing brisk mitotic activity in columnar epithelial cells. Right inset shows a high power view of numerous mitotic figures.

Recurrent Idiopathic Pleural Effusions: Do Consider Constricitve Pericarditis as a Cause

SESSION TITLE: Fellow Case Report Slide: Disorders of the Pleura SESSION TYPE: Affiliate Case Report Slide PRESENTED ON: Sunday, October 23, 2016 at 03:15 PM - 04:15 PM INTRODUCTION: We present a case of a healthy man presenting with recurrent dyspnea and no noted improvement after thoracentesis which led to further work up revealing constrictive pericarditis. CASE PRESENTATION: A 59 year old Caucasian male presents to hospital with recurrent dyspnea. He had initially presented with complaints of dyspnea and chest tightness after he had an episode of upper respiratory tract infection a week ago. When he had presented to the hospital he was noted to be in atrial fibrillation along with a left sided pleural effusion. Effusion was drained, he did not notice any improvement in his breathing so dyspnea was attributed to underlying conduction abnormalities and ablation was scheduled for following week. Echocardiogram revealed dys-synchronous ventricular septal motion probably secondary to conduction abnormality, mild left ventricular systolic dysfunction of 50%,small pericardial effusion.Pleural studies revealed pH 7.46, white blood cell count of 1070/mm3 with 38%neutrophils, 24%lymphocytes, 36%monocytes,red blood cells of 32000/mm3, protein 3 g/dl,lactate dehydrogenase(LDH) of 107 U/L(serum protein 7.6 g/dl,LDH 181 U/L). Pleural fluid cytology and cultures were negative. Trans-esophageal Echocardiogram on day of scheduled ablation revealed no irregular rhythm, increasing pericardial effusion and recurrent pleural effusion with continued symptoms.Physical exam was relevant for elevated JVD , distant heart sounds, regular rhythm, pericardial rub, decreased air entry on left lung base. Repeat thoracentesis was exudative. Further work up with cardiac catheterization revealed near equalization of diastolic pressures and findings suggestive of constriction. Patient underwent pericardiectomy with signs of immediate hemodynamic improvement. Surgical pathology revealed pericardium with dense fibrosis and organizing thrombus consistent with constrictive pericarditis. Left pleural biopsy was performed and no pathologic alteration was noted. DISCUSSION: We suspect viral pericarditis leading to pleural effusion as the most likely cause of his constrictive pericarditis. The treatment of constrictive pericarditis is surgical resection of the pericardium. CONCLUSIONS: Pleural effusions transudative or exudative are often associated with constrictive pericarditis. A high index of suspicion is needed in the diagnosis to avoid delay. Right heart catheterization is gold standard. Reference #1: A 43-Year-Old Man With a Large Recurrent Right-Sided Pleural Effusion Chest. 2000;117(4):1191-1194. DISCLOSURE: The following authors have nothing to disclose: Susheela Hadigal, Almotasembellah Aljaafareh, Divya Patel No Product/Research Disclosure Information

Pericardial Effusion due to Primary Malignant Pericardial Mesothelioma: A Common Finding but an Uncommon Cause.

This case report describes a 37-year-old female who was admitted to our Emergency Department because of shortness of breath. On physical examination, she had dyspnea and tachycardia and blood pressure was 80/50 mmHg with a pulsus paradoxus of 22 mmHg. Neck veins were distended, heart sounds were distant, and dullness was found on both lung bases. Her chest X-ray revealed bilateral pleural effusion and cardiomegaly. On both computed tomography and echocardiography the heart was of normal size and a large pericardial effusion was noted. The echocardiogram showed signs of impending tamponade, so the patient underwent an emergent pericardiocentesis. No infectious etiology was found and she was assumed to have viral pericarditis and was treated accordingly. However, when the pericardial effusion recurred and empirical therapy for tuberculosis failed, a pericardial window was performed. A typical staining pattern for mesothelioma was found on her pericardial biopsy specimen. Since no other mesodermal tissue was affected, a diagnosis of primary malignant pericardial mesothelioma was made. Chemotherapy was not effective and she passed away a year after the diagnosis was made. This case highlights the difficulties in diagnosing this uncommon disease in patients that present with the common finding of pericardial effusion.

Cardiac tamponade – unusual clinical manifestation of undiagnosed malignant neoplasm

Cardiac tamponade may be the first or predominant symptom of some pathologies but its etiology is not uncommonly unknown on admission to hospital. The purpose of this study was to evaluate the predominant causes of cardiac tamponade in previously healthy patients treated emergently in a single cardiac surgical center. The study involved 81 patients with the mean age of 58.1±16.0 years who underwent emergent subxyphoid pericardiotomy due to cardiac tamponade. Pericardial effusion was analyzed macro- and microscopically. Examinations done in the cardiac surgical department revealed pericarditis secondary to infection (n=17) or autoimmunologic processes (n=2) and malignancy in 18 patients (predominantly of the lungs (n=11)). Pericardial effusion obtained from patients with viral and autoimmunologic-induced pericarditis was straw-color and odorless while with bacterial infections dark yellow, iridescent and usually malodorous. Additional workup in the regional hospitals enabled to reveal malignant tumors in 29 patients, leukemia or lymphoma in 5 subjects. In all but one of the neoplastic cases, pericardial fluid was turbid and dark red or plummy. In 10 patients etiology of tamponade remained unknown. In conclusion, cardiac tamponade in previously healthy patients may be occasionally the predominant symptom of cancer, especially of the lungs. Macroscopic intraoperative appearance of pericardial fluid may be helpful in identification of causative condition of cardiac tamponade.

Evaluation and Treatment of Pericarditis: A Systematic Review.

Pericarditis is the most common form of pericardial disease and a relatively common cause of chest pain. To summarize published evidence on the causes, diagnosis, therapy, prevention, and prognosis of pericarditis. A literature search of BioMedCentral, Google Scholar, MEDLINE, Scopus, and the Cochrane Database of Systematic Reviews was performed for human studies without language restriction from January 1, 1990, to August 31, 2015. After literature review and selection of meta-analyses, randomized clinical trials, and large observational studies, 30 studies (5 meta-analyses, 10 randomized clinical trials, and 16 cohort studies) with 7569 adult patients were selected for inclusion. The etiology of pericarditis may be infectious (eg, viral and bacterial) or noninfectious (eg, systemic inflammatory diseases, cancer, and post-cardiac injury syndromes). Tuberculosis is a major cause of pericarditis in developing countries but accounts for less than 5% of cases in developed countries, where idiopathic, presumed viral causes are responsible for 80% to 90% of cases. The diagnosis is based on clinical criteria including chest pain, a pericardial rub, electrocardiographic changes, and pericardial effusion. Certain features at presentation (temperature >38°C [>100.4°F], subacute course, large effusion or tamponade, and failure of nonsteroidal anti-inflammatory drug [NSAID] treatment) indicate a poorer prognosis and identify patients requiring hospital admission. The most common treatment for idiopathic and viral pericarditis in North America and Europe is NSAID therapy. Adjunctive colchicine can ameliorate the initial episode and is associated with approximately 50% lower recurrence rates. Corticosteroids are a second-line therapy for those who do not respond, are intolerant, or have contraindications to NSAIDs and colchicine. Recurrences may occur in 30% of patients without preventive therapy. Pericarditis is the most common form of pericardial disease worldwide and may recur in as many as one-third of patients who present with idiopathic or viral pericarditis. Appropriate triage and treatment with NSAIDs may reduce readmission rates for pericarditis. Treatment with colchicine can reduce recurrence rates.

Pharmacotherapeutic considerations for using colchicine to treat idiopathic pericarditis in the USA.

The clinical significance of colchicine in the treatment of acute idiopathic (viral) pericarditis (IP) was only elucidated less than a decade ago. Multiple trials have shown the benefit of colchicine in decreasing the rate of recurrence, primarily in the European population. However, the colchicine formulation used in these trials is not available in Western countries such as the USA. In the USA, two formulations are available: the 0.6mg capsule and the 0.6mg tablet. As a result, higher doses than administered in the European trials must be utilized to treat IP. However, the use of these dosage forms has never been studied in the treatment of IP. Pharmacokinetic and pharmacodynamic knowledge of colchicine germane to clinicians such as drug disposition and drug-drug or drug-disease interactions have not been extensively reviewed in recent years. Furthermore, the safety of colchicine in the treatment of IP has not been extensively studied, and literature regarding adverse drug events originates from data in patients treated for familial Mediterranean fever and gout. This review will help the clinician understand pharmacotherapeutic considerations and thereby optimize therapy and ensure patient safety when using colchicine to treat IP.

Arrhythmias in viral myocarditis and pericarditis.

Acute viral myocarditis and acute pericarditis are self-limiting conditions that run a benign course and that may not involve symptoms that lead to medical assessment. However, ventricular arrhythmia is frequent in viral myocarditis. Myocarditis is thought to account for a large proportion of sudden cardiac deaths in young people without prior structural heart disease. Identification of acute myocarditis either with or without pericarditis is therefore important. However, therapeutic interventions are limited and nonspecific. Identifying those at greatest risk of a life-threatening arrhythmia is critical to reducing the mortality. This review summarizes current understanding of this challenging area in which many questions remain.

Pharmacotherapy update of acute idiopathic pericarditis.

Idiopathic (viral) pericarditis is the most common form of pericardial disease in the Western world. Despite the combination of colchicine and nonsteroidal antiinflammatory drugs (NSAIDs) plus aspirin (ASA), considered first-line therapy, the incidence of recurrent pericarditis is ~20-30%. In addition, secondary recurrence without optimal first-line therapy is ~50%. This is due to the many clinical challenges, such as inappropriate NSAID/ASA duration of therapy, the use of corticosteroid therapy, contraindications or intolerances to therapy, adverse effects, and issues related to adherence. This review describes contemporary pharmacotherapeutic management of idiopathic (viral) pericarditis, with a particular emphasis on the role of colchicine. Emerging therapies and management strategies, such as high-sensitivity C-reactive protein-guided therapy and novel immunotherapies, are also reviewed. Ultimately, understanding appropriate treatment will assist the clinician in helping decrease the risk of recurrent, incessant, and refractory pericarditis.

Predictors of post pericardiotomy low cardiac output syndrome in patients with pericardial effusion.

Introduction: Pathological involvement of pericardium by any disease that resulting in effusion may require decompression and pericardiectomy. The current article describes rare patients with effusion who after pericadiectomy and transient hemodynamic improvement rapidly developed progressive heart failure and subsequent multi organ failure. Methods: During periods of five years, 423 patients in our hospital underwent pericardiotomy for decompression of effusion. The clinical characteristics of those patient with postoperative low cardiac output (B group) (14 cases) recorded and compared with other patients without this postoperative complication (A group) by test and X2. Significant variables in invariables (P≤0.1) entered in logistic regression analysis and odd ratio of these significant variables obtained. Results: Idiopathic pericardial effusion, malignancy, renal failure, connective tissue disease, viral pericarditis was found in 125 patients (27%), 105 patients (25.4%), 65 patients (15.6%), 50 (17.1%) and 10 (2.4%) of patients subsequently. The factors that predict post-operative death in logistic regression analysis were malignancy, radiotherapy, constrictive pericarditis inotropic drug using IABP using, pre-operative EF and pericardial calcification. Conclusion: Certain preoperative variables such as malignancy, radiotherapy, low EF, calcified pericardium and connective tissue disease are associated with POLCOS and post-operative risk of death. This paradoxical response to pericardial decompression may be more frequent than currently appreciated. Its cause may relate to the sudden removal of the chronic external ventricular support from the effusion or thicken pericardium resulting in ventricular dilatation and failure or intra operative myocardial injury due to pericardiectomy of calcified pericardium, radiation and cardiomyopathy.

Idiopathic pericarditis and pericardial effusion in children: contemporary epidemiology and management.

BackgroundMulticenter studies on idiopathic or viral pericarditis and pericardial effusion (PPE) have not been reported in children. Colchicine use for PPE in adults is supported. We explored epidemiology and management for inpatient hospitalizations for PPE in US children and risk factors for readmission.Methods and ResultsWe analyzed patients in the Pediatric Health Information System database for (1) a code for PPE; (2) absence of codes for underlying systemic disease (eg, neoplastic, cardiac, rheumatologic, renal); (3) age ≥30 days and <21 years; and (4) discharge between January 1, 2007, and December 31, 2012, from 38 hospitals contributing complete data for each year of the study period. Among 11 364 hospitalizations with PPE codes during the study period, 543 (4.8%) met entry criteria for idiopathic or viral PPE. Significantly more boys were noted, especially among adolescents. No temporal trends were noted. Median age was 14.5 years (interquartile range 7.3 to 16.6 years); 78 patients (14.4%) underwent pericardiocentesis, 13 (2.4%) underwent pericardiotomy, and 11 (2.0%) underwent pericardiectomy; 157 (28.9%) had an intensive care unit stay, including 2.0% with tamponade. Median hospitalization was 3 days (interquartile range 2 to 4 days). Medications used at initial admission were nonsteroidal anti‐inflammatory drugs (71.3%), corticosteroids (22.7%), aspirin (7.0%), and colchicine (3.9%). Readmissions within 1 year of initial admission occurred in 46 of 447 patients (10.3%), mostly in the first 3 months. No independent predictors of readmission were noted, but our statistical power was limited. Practice variation was noted in medical management and pericardiocentesis.ConclusionsOur report provides the first large multicenter description of idiopathic or viral PPE in children. Idiopathic or viral PPE is most common in male adolescents and is treated infrequently with colchicine.

Descending Necrotizing Mediastinitis With Diffuse ST Elevation Mimicking Pericarditis: a Case Report

BackgroundDescending necrotizing mediastinitis (DNM) is a potentially fatal disease that requires aggressive treatment, including mediastinal exploration. The inflammation associated with DNM may involve the heart, which produces acute changes in the electrocardiogram (ECG). As a result, the ECG may mimic pericarditis, causing some diagnostic confusion. ObjectivesThe objectives of this case report are to describe a case of DNM presenting electrocardiographically with pericarditis, and to discuss how to differentiate between benign viral pericarditis and DNM, and the management of these two diseases. Case ReportWe present the case of a previously healthy 50-year-old man who presented to the Emergency Department for chest pain and presumed pericarditis. The patient presented with ST elevation on multiple leads on ECG, tenderness in the neck, widened mediastinum on the chest radiograph, and nonspecific laboratory test results. Echocardiography revealed normal ventricle function and the presence of mild pericardial effusion. The emergency physician performed contrast-enhanced neck computed tomography (CT) to rule out deep-neck infection. The CT scan showed marginal rim-enhancing abscesses in the retropharyngeal, bilateral submandibular, and anterior visceral spaces with extension into the thoracic cavity. Contrast-enhanced chest CT was performed consecutively. The final diagnosis was deep-neck infection with DNM. The patient underwent mediastinoscopy-assisted drainage and neck fasciotomy twice and received 7 weeks of therapy with intravenous meropenem. ConclusionThe present case highlights the importance of considering a mediastinal cause for acute ECG changes.

Why Do Doctors Make Mistakes? A Study of the Role of Salient Distracting Clinical Features

Diagnostic errors have been attributed to faulty reasoning and cognitive biases, but minimizing errors requires understanding the mechanisms underlying biases. The authors investigated whether salient distracting features (SDFs)-case findings that tend to grab physicians' attention because they are strongly associated with a particular disease, but are indeed unrelated to the problem-misdirect diagnostic reasoning, causing errors. In a 2012 study conducted at Erasmus Medical Centre, Rotterdam, 72 internal medicine residents diagnosed 12 clinical cases (6 simple, 6 complex) in three different formats: without a SDF, with a SDF in the beginning, and with a SDF at the end. In a within-subjects design, each participant solved 2 simple cases and 2 complex cases in each format. Proportions of correct diagnoses in each case type were compared by performing repeated-measures analysis of variance (ANOVA). There was a significant main effect of SDFs and a significant interaction effect between SDFs and case complexity. The presence of SDFs in the beginning of complex cases caused errors decreasing the proportion of correct diagnoses in comparison both with cases without SDFs (0.18, 95% CI, 0.13-0.23 versus 0.43, 95% CI, 0.35-0.51; P < .001) or with SDFs at the end (0.18, 95% CI, 0.13-0.23 versus 0.36, 95% CI, 0.29-0.43; P < .001). SDFs did not affect performance when presented near the end of cases. SDFs early in a case are apparently an important source of diagnostic errors. Physicians should be aware of the need to overcome their influence.

Abstract 18735: Worsening Right Ventricular Structural Mechanics in Constrictive Pericarditis; Pericardiectomy Didn’t Fix the Problem!

Introduction: Constrictive pericarditis (CP) is the result of scarring and consequent loss of the normal elasticity of the pericardial sac. Pericardiectomy is the definitive treatment for most cases of constriction. However it is believed structural changes in the right ventricle (RV) may result in tricuspid regurgitation (TR) after total pericardiectomy in patients with CP. Case report This is the case of a 55-year-old man who had a history of viral pericarditis, HTN and heart failure. He was evaluated for progressive pedal edema and ascites, found to have CP with equalization of RV and LV diastolic pressures and respiratory discordance of systolic pressures, consistent with CP on right heart catheterization. He underwent pericardiectomy and was found to have extensive pericardial adhesions and severe calcifications. Seven weeks later, he presented with complaints of fluid overload and was noted to have newly decreased RV systolic function accompanied by increase in RV volume with tricuspid annular dilation and 2-3+TR (Table and Figure). Diuretics were reinitiated and he is followed for potential tricuspid valve surgery. Discussion TR may develop post pericardiectomy in patients with CP. This is commonly noted with persistent RV failure symptoms post operatively. It may be caused by RV dilation and worsening TR, which results in increased RV strain, signifying poor status of longitudinal RV function. Tricuspid regurgitation is explained by RV and tricuspid annular dilatation. It is important to have a detailed evaluation perioperatively in patients with CP undergoing pericardiectomy.

Pericarditis aguda

Acute pericarditis is an acute inflammation of the pericardium and the most common pathology of this membrane. 80–90 % of cases of acute pericarditis are idiopathic or viral, while the remaining cases are specific etiologic forms. Its main clinical manifestations are: chest pain, pericardial friction rub and fever. For diagnosis at least 2 of the following 4 criteria should be present: characteristic chest pain; pericardial friction rub; suggestive electrocardiographic changes and new or worsening pericardial effusion. Electrocardiogram is an important diagnostic tool, and classically evolves in a sequence of four stages. Echocardiography is recommended in patients with hemodynamic compromise. Differential diagnosis with diseases that cause chest pain must be made. Acute pericarditis complications are: pericardial effusion without tamponade, cardiac tamponade, constrictive pericarditis and recurrence. Acute myopericarditis is frequent. In 70–90 % of patients, viral or idiopathic acute pericarditis has benign and self-limiting course and without serious complications. Most patients respond to treatment with nonsteroidal antiinflammatory agents. Colchicine is indicated to prevent recurrent episodes of pericarditis. Usually corticosteroids should be avoided.