The Constricted Heart: A 31-Year-Old Man with a Case of Constrictive Tuberculous Pericarditis.

BACKGROUND Constrictive pericarditis occurs due to chronic pericardial inflammation and adherence of the cardiac pericardial layer. Etiologies include toxins, infection, cardiac surgery, and idiopathic causes. Outside the United States, the most common cause of constrictive pericarditis is tuberculosis (TB). Constrictive pericarditis is the most severe complication of tuberculous pericardial disease. CASE REPORT A 31-year-old man who recently immigrated to the United States presented with a 2-week history of constitutional symptoms, dyspnea, and pleuritic chest pain. Physical examination was pertinent for bilateral lower extremity pitting edema, decreased bilateral breath sounds, and jugular venous distension. Transthoracic echocardiogram revealed a left ventricular ejection fraction of 45%, pericardial thickening, and an exaggerated septal bounce. Right heart catheterization showed discordant and concordant right ventricular pressure tracings. Cardiac magnetic resonance imaging revealed bilateral pleural effusions and circumferential pericardial thickening. Thoracocentesis was significant for an exudative effusion, with elevated adenosine deaminase levels. Subsequent QuantiFERON-TB Gold testing was positive, and he underwent elective pericardiectomy. Pericardial histopathology revealed necrotizing caseating granulomas. He was discharged on a 6-month course of rifampicin, isoniazid, pyrazinamide, and ethambutol therapy, with close multidisciplinary care team outpatient follow-up. CONCLUSIONS This case highlights the importance of a high index of clinical suspicion for tuberculous pericarditis in patients presenting with constitutional and heart failure symptoms and a relevant travel history, to ensure prompt diagnosis and treatment. This case also reflects the importance of coordination of care between cardiology, infectious disease, pathology, and cardiothoracic surgery teams in the management of tuberculous constrictive pericarditis.

Constrictive pericarditis in a patient with fiberglass lung disease: a case report.

BACKGROUND: Fiberglass has a larger aerodynamic diameter and is less likely to be inhaled into the lungs. Further, it will be cleared even if it is mechanically broken into smaller pieces and inhaled into the lungs. Fiberglass lung disease has been well documented if long term exposure but was thought reversible and would not cause severe diseases. The diagnosis of fiberglass lung disease depends on exposure history and histopathological findings. However, the exact occupational exposure history is often difficult to identify because mixed substance exposure often occurs and fiberglass disease is not as well-known as asbestosis. CASE PRESENTATION: A 66-year-old man had unexplained transudative pericardial effusion requiring pleural pericardial window operation twice at another medical center where asbestosis was told because of his self-reported long-term asbestosis exposure and the histopathological finding of a ferruginous body in his lung. Constrictive pericarditis developed two years later and resulted in congestive heart failure. Radical pericardiectomy combined with lung biopsy was performed following chest computed tomography imaging and the transudative nature of pericardial effusion not compatible with asbestosis. However, the histopathologic findings of his lung and pericardium at our hospital only showed chronic fibrosis without any asbestosis body. The patient's lung was found to be extremely fragile during a lung biopsy; histopathologic specimens were reviewed, and various fragments of fiberglass were found in the lung and pericardium. The patient's occupational exposure was carefully reevaluated, and he restated that he was only exposed to asbestosis for 1-2 years but was heavily exposed to fiberglass for more than 40 years. This misleading exposure history was mainly because he was only familiar with the dangers of asbestos. Since most fiberglass lung diseases are reversible and the symptoms of heart failure resolve soon after surgery, only observation was needed. Ten months after radical pericardiectomy, his symptoms, pleural effusion, and impaired pulmonary function eventually resolved. CONCLUSION: Fiberglass could cause inflammation of the pericardium, resulting in pericardial effusion and constrictive pericarditis, which could be severe and require radical pericardiectomy. Exact exposure history and histopathological examinations are the key to diagnosis.

Calcific pericarditis strangling the heart, an answer to unexplained heart failurediagnostic modalities.

Pericardial calcification is often found incidentally from imaging studies and may be a clue to constrictive pericarditis. Constrictive pericarditis often mimics other causes of heart failure, pulmonary, or liver disease, making it hard to diagnose. Tuberculosis is the most common infectious aetiology of Constrictive Pericarditis. Living in developing countries, such as Indonesia, should warn us of the possibility of tuberculous constrictive pericarditis as a differential diagnosis of unexplained heart failure. The presented case came with complaints of shortness of breath, especially on exertion for five years, which worsened in the last 6 months. The past history of pulmonary Tuberculosis with the Cardiac CT findings confirmed the diagnosis of Constrictive Pericarditis.

COVID-related constrictive pericarditis requiring pericardiectomy: a case report.

BACKGROUND: The COVID-19 pandemic was primarily considered a respiratory malady in the early phases of the outbreak. However, as more patients suffer from this illness, a myriad of symptoms emerge in organ systems separate from the lungs. Among those patients with cardiac involvement, myocarditis, pericarditis, myocardial infarction, and arrhythmia were among the most common manifestations. Pericarditis with pericardial effusion requiring medical or interventional treatments has been previously reported in the acute setting. Notably, chronic pericarditis with pericardial thickening resulting in constriction requiring sternotomy and pericardiectomy has not been published to date. CASE PRESENTATION: A patient with COVID-19-associated constrictive pericarditis three years after viral infection requiring pericardiectomy was reported. The COVID-19 infection originally manifested as anosmia and ageusia. Subsequently, the patient developed dyspnea, fatigue, right-sided chest pressure, bilateral leg edema, and abdominal fullness. Following recurrent right pleural effusions and a negative autoimmune work-up, the patient was referred for cardiothoracic surgery for pericardiectomy when radiographic imaging and hemodynamic assessment were consistent with constrictive pericarditis. Upon median sternotomy, the patient's pericardium was measured to be 8 mm thick. Descriptions of the clinical, diagnostic, and therapeutic features are provided. Within the first week after the operation, the patient's dyspnea resolved; one month later, leg edema and abdominal bloating were relieved. CONCLUSIONS: Although an association between COVID-19 and cardiac complications has been established, this case adds another element of virus severity and chronic manifestations. The need for sternotomy and pericardiectomy to treat COVID-19-related constrictive pericarditis is believed to be the first reported diagnosis.

Rare severe constrictive pericarditis complication in Erdheim-Chester disease: A case report and literature review.

Erdheim-Chester disease (ECD) is a rare, non-Langerhans cell histiocytosis with diverse clinical features. It is characterized by systemic histiocyte infiltration of the bone, skin, central nervous system, lung, kidney, and cardiovascular system. Pericardial involvement is frequently revealed through either pericardial effusion or pericardial thickening in patients with ECD. Although most patients remain asymptomatic, progressive pericarditis, effusion, or cardiac tamponade may occur. Herein, we report a rare and unusual presentation of ECD in a 51-year-old man who experienced severe constrictive pericarditis. The patient presented with uncontrolled fluid retention and heart failure. After the diagnosis of ECD, interferon alpha treatment was administered. The patient recovered dramatically with decreased pleural and pericardial effusion, as well as improvements in the echocardiographic signs of constrictive pericarditis. Despite several therapeutic options described in the literature for managing ECD-related pericardial disease, a standard treatment has not been established. This report highlights the importance of early treatment based on accurate diagnosis of an unusual ECD complication.

Successful Visceral and Parietal Pericardiectomy for Refractory Effusive-Constrictive Pericarditis: A Challenging Case Report.

BACKGROUND Effusive-constrictive pericarditis (ECP) is an uncommon clinical syndrome characterized by the coexistence of pericardial effusion and constriction involving the visceral pericardium. This differs from constrictive pericarditis, which presents with thickening of the pericardium without effusions. Specific diagnostic criteria of ECP include the failure of right atrial pressure to decrease by 50% or reach a new level below 10 mmHg after normalization of intrapericardial pressure. CASE REPORT We present the case of a 32-year-old obese man with multiple comorbidities who initially presented with flu-like symptoms and pleural effusion with development of constrictive-like symptoms. Despite undergoing numerous pericardiocentesis and appropriate medical management, the patient's condition failed to improve, leading to the likely diagnosis of effusive-constrictive pericarditis. Cultures of pericardial fluid revealed E. -faecium, which required multiple antimicrobial therapy. Despite infection, the exact etiology of ECP remained unknown and likely idiopathic. Common causes of ECP include idiopathic, tuberculosis, cardiac surgery complications, radiation, or neoplasia. Ultimately, the patient underwent a pericardiectomy involving the visceral and parietal pericardium, resulting in hemodynamic stability and resolution of symptoms. CONCLUSIONS This case highlights the challenges in diagnosing and managing ECP, emphasizing the importance of considering surgical intervention in refractory cases. ECP initially presents as a pericardial effusion, often addressed through pericardiocentesis; however, in a small subset of patients, sustained symptoms and altered hemodynamics persist following pericardiocentesis, necessitating further evaluation and management. The success of pericardiectomy in our patient highlights the potential efficacy of surgical intervention in improving outcomes for patients with ECP.

Pericardial Disease in Cardiac Amyloidosis: A Comprehensive Review.

In patients with cardiac amyloidosis, pericardial involvement is common, with up to half of patients presenting with pericardial effusions. The pathophysiological mechanisms of pericardial pathology in cardiac amyloidosis include chronic elevations in right-sided filling pressures, myocardial and pericardial inflammation due to cytotoxic effects of amyloid deposits, and renal involvement with subsequent uremia and hypoalbuminemia. The pericardial effusions are typically small; however, several cases of life-threatening cardiac tamponade with hemorrhagic effusions have been described as a presenting clinical scenario. Constrictive pericarditis can also occur due to amyloidosis and its identification presents a clinical challenge in patients with cardiac amyloidosis who concurrently manifest signs of restrictive cardiomyopathy. Multimodality imaging, including echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, is useful in the evaluation and management of this patient population. The recognition of pericardial effusion is important in the risk stratification of patients with cardiac amyloidosis as its presence confers a poor prognosis. However, specific treatment aimed at the effusions themselves is seldom indicated. Cardiac tamponade and constrictive pericarditis may necessitate pericardiocentesis and pericardiectomy, respectively.

Diagnostic procedure for localized constrictive pericarditis leading to bilateral pleural effusion: two case reports.

Constrictive pericarditis is a rare disease. Localized constrictive pericarditis leading to bilateral pleural effusion is more difficult to recognize, and the diagnostic procedure can be ambiguous. Here, we report two patients diagnosed with localized constrictive pericarditis who presented with bilateral pleural effusion. A thorough work-up showed that the pleural effusion was nonspecific, as was the pathology of the pleura. One patient had a history of pericardial effusion 2 years ago, and the other had undergone surgery for an anterior mediastinum teratoma. Pericardial scarring was found on their chest CT scans. The patients underwent pericardiectomy, and localized pericardial thickening was excised. The bilateral pleural effusion was effectively cured, and the patients showed satisfactory recovery on follow-up. Physicians should be aware of localized pericarditis leading to bilateral pleural effusion, and pericardiectomy is an effective diagnostic and therapeutic procedure.

Surgical treatment of constrictive pericarditis at a single center: 10 years of experience.

BACKGROUND: Constrictive pericarditis (CP) is a pericardial disease characterized by the pericardium becoming calcified or fibrotic as a result of chronic inflammation, which impairs diastolic filling by compressing the cardiac chambers. Pericardiectomy is a promising surgical option for treating CP. In this study, we reviewed over 10 years of preoperative, perioperative, and short-term postoperative follow-ups of patients who underwent pericardiectomy for constrictive pericarditis at our clinic. METHODS: Between January 2012 and May 2022, 44 patients were diagnosed with constrictive pericarditis. Twenty-six patients underwent pericardiectomy for CP. Median sternotomy is the surgical approach of choice because it provides easy access for complete pericardiectomy. RESULTS: The patient median age was 56 (min: 32, max: 71), and 22 out of 26 patients (84.6%) were male. Twenty-one patients (80.8%) complained of dyspnea, which was the most common reason for admission. Twenty-four patients (92.3%) were scheduled for elective surgery. Cardiopulmonary bypass (CPB) was used during the procedure in six patients (23%). The duration of intensive care stay was two days (min: 1, max: 11), and the total hospitalization was six days (min: 4, max: 21). No in-hospital mortality was observed. CONCLUSION: The median sternotomy approach provides a critical advantage in terms of performing a complete pericardiectomy. Although CP is a chronic condition, early diagnosis and planning of pericardiectomy before irreversible deterioration of cardiac function leads to a notable reduction in mortality and morbidity.

Cardiac tamponade.

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive-constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive-constrictive pericarditis.

The Evolving Etiologic and Epidemiologic Portrait of Pericardial Disease.

Pericardial disease includes a variety of conditions, including inflammatory pericarditis, pericardial effusions, constrictive pericarditis, pericardial cysts, and primary and secondary pericardial neoplasms. The true incidence of this varied condition is not well established, and the causes vary greatly across the world. This review aims to describe the changing pattern of epidemiology of pericardial disease and to provide an overview of causative etiologies. Idiopathic pericarditis (assumed most often to be viral) remains the most common etiology for pericardial disease globally, with tuberculous pericarditis being most common in developing countries. Other important etiologies include fungal, autoimmune, autoinflammatory, neoplastic (both benign and malignant), immunotherapy-related, radiation therapy-induced, metabolic, postcardiac injury, postoperative, and postprocedural causes. Improved understanding of the immune pathophysiological pathways has led to identification and reclassification of some idiopathic pericarditis cases into autoinflammatory etiologies, including immunoglobulin G (IgG)4-related pericarditis, tumour necrosis factor receptor-associated periodic syndrome (TRAPS), and familial Mediterranean fever in the current era. Contemporary advances in percutaneous cardiac interventions and the recent COVID-19 pandemic have also resulted in changes in the epidemiology of pericardial diseases. Further research is needed to improve our understanding of the etiologies of pericarditis, using the assistance of contemporary advanced imaging techniques and laboratory testing. Careful consideration of the range of potential causes and local epidemiologic patterns of causality are important for the optimization of diagnostic and therapeutic approaches.

Sclerotherapy of oesophageal varices may induce chronic constrictive pericarditis in children.

Constrictive pericarditis is rare in children and can be difficult to diagnose. It has been described in adults after sclerotherapy of oesophageal varices but not in children. We report two cases of chronic constrictive pericarditis after sclerotherapy of oesophageal varices in children with portal cavernoma. Constrictive pericarditis should be considered as a cause of refractory ascites.

Safety Signal between Azacitidine and Pericarditis.

BACKGROUND: Drug-induced pericarditis is an important cause of pericarditis and if unnoticed and unmanaged can lead to constrictive pericarditis, pericardial effusion, and cardiac tamponade. OBJECTIVE: The objective of this analysis was to determine if a significant signal exists between azacitidine use and pericarditis. METHODS: A pharmacovigilance analysis was performed using the FDA Adverse Event Database. RESULTS: 48 reports of azacitidine-induced pericarditis with azacitidine as the suspect drug were identified. The most common indications for azacitidine use in the adverse event reports were myelodysplastic syndrome (48%) and acute myelogenous leukemia (27%). Physicians reported 44% of the azacitidine-induced pericarditis reports, while other health professional reported 52% of the reports. The disproportionality analysis showed a proportional reporting ratio of 5.0, χ2 of 149.8, reporting odds ratio of 5.0, and IC025 of 1.8. Literature review found 3 case reports of azacitidine-induced pericarditis. CONCLUSION: The signal between azacitidine and pericarditis was found to be statistically significant. Clinicians should be aware of the possible risk of pericarditis when prescribing azacitidine. If there is suspicion for azacitidine-induced pericarditis, clinicians should consider discontinuation of azacitidine to improve patient's symptoms and reduce the likelihood of the development of constrictive pericarditis, pericardial effusion, and cardiac tamponade.

Left Ventricular Angiogram in Constrictive Pericarditis.

A 14-year-old boy presented with dyspnea on exertion and easy fatiguability for 1 year. He also had an episode of pedal edema 6 months prior, which resolved with diuretics. He had a history of tuberculosis treated with a 6-month course of antitubercular therapy. After a series of tests and analyses, it was evident that longitudinal contraction of the left ventricle was preserved, whereas the circumferential contraction was severely impaired. Pericardial calcification also could be seen encircling the left and right ventricles. Pericardial calcification is evident in around 25% of cases of constrictive pericarditis and predominantly seen in those with tubercular and pyogenic etiology. The subepicardial myocardial fibers are responsible for radial shortening and subendocardial fibers are responsible for longitudinal shortening. In constrictive pericarditis, the involvement of the subepicardial fibers leads to reduction in the circumferential shortening. The patient was referred for pericardiectomy.

Right Heart Failure With Recurrent Pericardial Effusion Mimicking Effusive-Constrictive Pericarditis Several Years After Renal Transplantation.

Pericardial disease is a rare complication after renal transplantation. We present a patient who developed high-output cardiac failure from a large arteriovenous (AV) fistula with recurrent pericardial effusion resulting in a constrictive hemodynamic pattern that was revealed during cardiac catheterization. Pericardiectomy was considered for recurrent effusive pericarditis, but per cardiac surgery recommendations, closure of the AV fistula dramatically cured the patient's heart failure, and no recurrence of pericardial effusion was seen during follow-up almost a year later.

Non-pulmonary Disseminated Tuberculosis Complicated by Constrictive Pericarditis and Cutaneous Gumma.

A 23-year-old previously healthy male presented to the hospital with symptoms of heart failure. He was diagnosed with pericarditis and found to have a reduced left ventricular ejection fraction of 25%. He was noted to have mediastinal lymphadenopathy. Pulmonary and abdominal sampling were non-diagnostic for infection, autoimmune disease, or malignancy. A QuantiFERON Gold returned positive. After a thorough travel history and detailed exam, the patient was diagnosed with disseminated tuberculosis after the discovery of a cutaneous gumma that was found to have acid-fast bacilli present on biopsy with Fite's stain. 18F-FDG PET CT and cardiac MRI were pursued given that pericardial and myocardial biopsy could not be safely performed due to the patient's hemodynamics. 18F-FDG PET CT and cardiac MRI did not demonstrate any myocardial pathology responsible for the left ventricular ejection fraction. This case highlights that pulmonary involvement is not necessary for disseminated TB, Fite's stain may be used to identify M. tuberculosis, and that cardiac MRI and 18F-FDG PET CT may be useful to delineate myocardial involvement in high-risk situations.

Degos disease complicated by constrictive pericarditis in remote phase: a case report.

BACKGROUND: Degos disease, also known as malignant atrophic papulosis, is characterised by cutaneous manifestations due to chronic thrombo-obliterative vasculopathy. There have been reports of the rare late-onset Degos disease complicated by constrictive pericarditis (CP). This study reports a case of CP caused by Degos disease that developed 20 years after diagnosis. CASE PRESENTATION: A 62-year-old woman who had been taking aspirin for 20 years for Degos disease was hospitalised for worsening of heart failure. The patient was diagnosed with CP and underwent pericardiectomy. Pathological findings suggested the involvement of Degos disease. The postoperative course was uneventful, and her heart failure and Degos disease did not worsen. CONCLUSIONS: The study findings suggests that Degos disease can cause long-term CP. Aspirin effectively inhibited the progression of Degos disease, and surgical treatment was necessary when heart failure due to CP was refractory to treatment.

Ultrasonic Wave Pericardiectomy for IgG4-Related Constrictive Pericarditis.

An 80-year-old woman presented with rare immunoglobulin G4 (IgG4)-related constrictive pericarditis. She underwent pericardiectomy, pericardiotomy, and crosshatching incision of the epicardium using an ultrasonic wave scalpel suitable for the feature of IgG4-related disease. Thereafter, her cardiac function improved remarkably. Additional corticosteroid therapy contributed to maintaining her healthy condition. Definitive diagnosis was based on novel organ-specific criteria. Herein, we highlight that the most important point in the pathological diagnosis of IgG4-related constrictive pericarditis is to determine the presence of IgG4-positive plasma cell infiltration and storiform fibrosis or obstructive phlebitis specific to chronic inflammation.