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.

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.

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.

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.

Post-cardiac injury syndrome after surgical repair of atrial septal defect: Reporting a rare occurrence.

A 16-year-old male with past medical history of congenital atrial septal defect surgical repair, presented with recurrent pericarditis secondary to post-cardiotomy injury syndrome (PCIS), After failing medical therapy, he ultimately underwent pericardiectomy for symptom resolution, PCIS is underdiagnosed in children and should be considered in patients with recurrent chest, pain.

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.

Constrictive Pericarditis: An Incidental Finding.

How to cite this article: Chandrakala, Khan H, Purushotham N. Constrictive Pericarditis: An Incidental Finding. J Assoc Physicians India 2023;71(11):85-86.

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.

Clinical genetic testing in four highly suspected pediatric restrictive cardiomyopathy cases.

BACKGROUND: Restrictive cardiomyopathy (RCM) presents a high risk for sudden cardiac death in pediatric patients. Constrictive pericarditis (CP) exhibits a similar clinical presentation to RCM and requires differential diagnosis. While mutations of genes that encode sarcomeric and cytoskeletal proteins may lead to RCM, infection, rather than gene mutation, is the main cause of CP. Genetic testing may be helpful in the clinical diagnosis of RCM. METHODS: In this case series study, we screened for TNNI3, TNNT2, and DES gene mutations that are known to be etiologically linked to RCM in four pediatric patients with suspected RCM. RESULTS: We identified one novel heterozygous mutation, c.517C>T (substitution, position 517 C → T) (amino acid conversion, p.Leu173Phe), and two already known heterozygous mutations, c.508C>T (substitution, position 508, C → T) (amino acid conversion, p.Arg170Trp) and c.575G>A (substitution, position 575, G → A) (amino acid conversion, p.Arg192His), in the TNNI3 gene in three of the four patients. CONCLUSION: Our findings support the notion that genetic testing may be helpful in the clinical diagnosis of RCM.

Immunoglobulin G4-related constrictive pericarditis and the importance of a thorough workup: a case report.

BACKGROUND: Constrictive pericarditis remains a problematic diagnosis and a thorough investigation is critical. Among possible aetiologies, immunoglobulin-G4 (IgG4)-related pericardial disease is an unusual cause of pericardial constriction. We report a challenging diagnostic case of pericardial constriction due to IgG4-related disease. CASE PRESENTATION: A 68-year old male with a history of inferior myocardial infarction with right ventricle (RV) involvement was thrice-hospitalized due to marked ascites and peripheral oedema. Systemic congestion was initially attributed to RV dysfunction due to previous infarction. Yet, at the final admission, a re-assessment echocardiogram followed by cardiac computed tomography, magnetic resonance and right heart catheterization raised a possible diagnosis of constrictive pericarditis with a finding of abnormal pulmonary venous return. Patient therefore underwent pericardiectomy and surgical correction of pulmonary venous return. Pericardium histology revealed an IgG4-related pericardial constriction. Patient was later discharged on corticosteroids with marked symptomatic improvement. CONCLUSION: IgG4-related disease remains a rare cause of pericardium constriction while also presenting a challenging diagnosis in everyday clinical practice. This case exemplifies the difficulties faced by clinicians when reviewing a possible case of constrictive pericarditis, while highlighting the importance of a multimodality assessment.

Multimodality Imaging of Constrictive Pericarditis: Pathophysiology and New Concepts.

PURPOSE OF REVIEW: The unique pathophysiological changes of constrictive pericarditis (CP) can now be identified with better imaging modalities, thereby helping in its early diagnosis. Through this review, we outline the pathophysiology of CP and its translation into symptomology and various imaging findings which then are used for both diagnosis and guiding treatment options for CP. RECENT FINDINGS: Multimodality imaging has provided us with the capability to recognize early stages of the disease and identify patients with a potential for reversibility and can be treated with medical management. Additionally, peri-procedural planning and prediction of post-operative complications has been made possible with the use of advanced imaging techniques. Advanced imaging has the potential to play a greater role in identification of patients with reversible disease process and provide peri-procedural risk stratification, thereby improving outcomes for patients with CP.

Pericardial Manifestations of Thyroid Diseases.

PURPOSE OF REVIEW: Thyroid disorders, especially hypothyroidism, are known to be associated with pericardial diseases. The aim of this paper is to review the current knowledge of the pericardial manifestations of hypothyroidism and hyperthyroidism. RECENT FINDINGS: Many reports have described associations between dysthyroidism, which encompasses hypothyroidism and hyperthyroidism, and several pericardial diseases, including acute pericarditis, constrictive pericarditis, pericardial effusion, and tamponade. The diagnosis of dysthyroidism-induced pericardial diseases consists of a combination of thyroid blood levels that fall outside of the normal range and the exclusion of other causes. Treatment of the thyroid disorder is key, along with treatment of the pericardial disease as recommended by the guidelines. Early recognition of the thyroid disorder is key in patients with pericardial diseases, since treating the underlying cause should assist resolution of the pericardial issues and ideally prevent recurrence and possible future complications of suboptimally treated pericarditis or pericardial effusions.

Idiopathic Pericardial Ossification Causing Chronic Constrictive Pericarditis.

BACKGROUND: Chronic constrictive pericarditis (CCP) is usually caused by the fibroinflammatory reaction of the visceral and parietal pericardium that encase the heart. The cause of CCP is various including tuberculosis, trauma, prior surgery, radiation, and malignancy. MATERIAL AND METHODS: We examined the pericardiectomy specimen of a case of CCP in a 17-year-old boy. RESULTS: The histopathology of the pericardium revealed pericardial ossification bony remodeling and hematopoiesis within the intertrabecular marrow spaces. No granulomatous or neoplastic etiology was identified. CONCLUSION: Idiopathic pericardial ossification can cause CCP in pediatric patients.

Multimodality imaging of constrictive pericarditis in H syndrome.

This is the first report of constrictive pericarditis (CP) in a 16-year-old boy with H syndrome with pericardial involvement predominantly over the right ventricle with favorable response to anti-inflammatory treatment. H syndrome, first reported in 2008, is a new auto-inflammatory syndrome with multiorgan involvement due to mutation in the SLC29A3 gene. We described the echocardiographic characteristics of asymmetric pericardial involvement and presented the cardiac computed tomography angiographic and magnetic resonance imaging findings. We reviewed the echocardiographic signs of CP, introduced tricuspid E/A respiratory alternans as a novel echocardiographic sign of right ventricular dominant CP, and explained the underlying mechanism.

Preoperative Pericardial Effusion is Associated with Low Cardiac Output Syndrome After Pericardiectomy for Constrictive Pericarditis.

BACKGROUND: Low cardiac output syndrome is the main cause of death after pericardiectomy. METHODS: Patients who underwent pericardiectomy for constrictive pericarditis from January 2009 to October 2020 at our hospital were included in the study. Histopathologic studies of pericardium tissue from every patient were performed. All survivors were followed up. RESULTS: Ninety-two consecutive patients underdoing pericardiectomy were included in the study. The incidence of postoperative low cardiac output syndrome was 10.7% (10/92). There were five operative deaths. Mortality and incidence of LCOS in the group with pericardial effusion were significantly higher than those in the group without pericardial effusion. Tuberculosis of the pericardium (60/92, 65.2%) was the most common histopathologic finding in this study. Both univariate and multivariate analyses showed that preoperative pericardial effusion is associated with increased rate of low cardiac output syndrome. Eighty-five survivors were in NYHA class I (85/87, 97.7%), and two were in class II (2/87, 2.3%) at the latest follow up. CONCLUSIONS: Preoperative pericardial effusion is associated with low cardiac output syndrome after pericardiectomy. Tuberculosis of the pericardium was the most common histopathologic finding in this study. For constrictive pericarditis caused by tuberculous bacteria, systematic antituberculosis drugs should be given. Preoperative pericardial effusion is associated with increased rate of low cardiac output syndrome. Perfect preoperative preparation is very important to reduce the incidence of postoperative low cardiac output syndrome and mortality. It is very important to use a large dose of diuretics with cardiotonic or vasopressor in a short time after the operation.

Assessment of Pericardial Disease with Cardiovascular MRI.

Disorders of the pericardium are common and can result in significant morbidity and mortality. Advances in multimodality imaging have enhanced our ability to diagnose and stage pericardial disease and improve our understanding of the pathophysiology of the disease. Cardiovascular MRI (CMR) can be used to define pericardial anatomy, identify the presence and extent of active pericardial inflammation, and assess the hemodynamic consequences of pericardial disease. In this way, CMR can guide the judicial use of antiinflammatory and immune modulatory medications and help with timing of pericardiectomy. CMR can also be used to diagnose congenital disorders of the pericardium. Furthermore, CMR can be used to define pericardial masses and understand their malignant potential.

Diagnosis and Management of Tuberculous Pericarditis: What Is New?

PURPOSE OF REVIEW: This review provides an update on the immunopathogenesis of tuberculous pericarditis (TBP), investigations to confirm tuberculous etiology, the limitations of anti-tuberculous therapy (ATT), and recent efficacy trials. RECENT FINDINGS: A profibrotic immune response characterizes TBP, with low levels of AcSDKP, high levels of γ-interferon and IL-10 in the pericardium, and high levels of TGF-ß and IL-10 in the blood. These findings may have implications for future therapeutic targets. Despite advances in nucleic acid amplification approaches, these tests remain disappointing for TBP. Trials of corticosteroids and colchicine have had mixed results, with no impact on mortality, evidence of a reduction in rates of constrictive pericarditis and potential harm in those with advanced HIV. Small studies suggest that ATT penetrates the pericardium poorly. Given that there is a close association between high bacillary burden and mortality, a rethink about the optimal drug doses and duration may be required. The high mortality and morbidity from TBP despite use of anti-tuberculous drugs call for researches targeting host-directed immunological determinants of treatment outcome. There is also a need for the identification of steps in clinical management where interventions are needed to improve outcomes.

Pericarditis in Systemic Rheumatologic Diseases.

PURPOSE OF REVIEW: We review the epidemiology, pathophysiology, and management of pericarditis most commonly complicating autoimmune and autoinflammatory conditions. RECENT FINDINGS: Typically, pericarditis occurs in the context of a systemic flare of the underlying disease but infrequently, it is the presenting manifestation requiring a high index of suspicion to unravel the indolent cause. Pericardial involvement in rheumatic diseases encompasses a clinical spectrum to include acute, recurrent and incessant pericarditis, constrictive pericarditis, asymptomatic pericardial effusion, and pericardial tamponade. Direct evidence on the pathophysiology of pericarditis in the context of rheumatic diseases is scant. It is theorized that immune perturbations within pericardial tissue result from the underlying central immunopathology of the respective autoimmune or autoinflammatory disease. Pericarditis management depends on acuity, the underlying cause and epidemiological features such as patient's immune status and geographic prevalence of infections such as tuberculosis. Immunosuppressive medications including biologics such as interleukin 1 blockers emerge as possible steroid sparing agents for pericarditis treatment.

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.