Pericardial Thickening Research Articles

Markers of Subclinical Atherosclerosis in Severe Obesity and One Year after Bariatric Surgery.

Background: Aortic valve sclerosis (AVS), mitral valve sclerosis (MVS), remodeling of major arteries, and increased pericardial fat are associated with subclinical atherosclerosis. We assessed these markers of atherosclerosis in severely obese patients before and 1 year after bariatric surgery. Methods: Eighty-seven severely obese patients (43 ± 10 years, preoperative body mass index [BMI] 41.8 ± 5 kg/m2) underwent echocardiography before and 1 year after Roux-en-Y bypass surgery in the FatWest (Bariatric Surgery on the West Coast of Norway) study. We measured the end-diastolic aortic wall thickness (AWT), pericardial fat thickness at the right ventricular free wall, and AVS/MVS based on combined aortic leaflet thickness and hyperechoic valve lesions. Results: Postoperatively, patients experienced a reduction of 12.9 ± 3.9 kg/m2 in BMI, 0.5 ± 1.9 mm in AWT, 2.6 ± 2.3 mm in pericardial fat, and 45%/53% in AVS/MVS (p < 0.05). In multivariate regression analyses with adjustment for clinical and hemodynamic variables, less pericardial fat reduction was associated with male sex and higher 1-year blood pressure and BMI, and less AWT-reduction with higher age and 1-year BMI (p < 0.05). Persistent AVS and MVS were related to higher 1-year BMI and more advanced valve sclerosis preoperatively (p < 0.05). Conclusions: Markers of subclinical atherosclerosis decreases significantly 1 year after bariatric surgery, particularly in younger patients that achieve a BMI < 28 kg/m2.

A Case Of Recurrent Constrictive Pericarditis With Diffuse Fibrosis

<h3>Background</h3> Evaluation for etiology of constrictive pericarditis is essential in guiding management. Uncommon etiologies include fibrosing mediastinitis, which is caused by proliferation of fibrous tissue in the mediastinum and Erdheim-Chester disease (ECD) which is characterized by inflammatory infiltration of lesions by histiocytes, often with involvement of the pericardium and aorta. <h3>Case</h3> A 46-year-old male with a history of idiopathic retroperitoneal fibrosis with thoracic and abdominal infiltrative masses, recurrent constrictive pericarditis and pericardial effusions, and recurrent admissions for heart failure with preserved ejection fraction (HFpEF) exacerbations presented with worsening shortness of breath and lower extremity edema. He previously underwent pericardial window and steroid therapy with minimal improvement. He was diagnosed with ECD. CT scan revealed large bilateral pleural effusions, soft tissue infiltration surrounding the heart and retroperitoneum, and diffuse pericardial thickening. Echocardiography findings were suggestive of constrictive pericarditis and reduced ejection fraction of 40%. Cardiac MRI confirmed these findings. Cardiac catheterization was consistent with constrictive physiology (Figure 1 A-H). Endomyocardial biopsies revealed scattered lymphocytes with no fibrosis or histiocyte infiltration. He underwent pericardiectomy, from the superior vena cava to the inferior vena cava and phrenic nerve to left anterior descending artery, with repeat biopsies revealing acute and chronic inflammation with extensive fibrosis. Follow up echocardiography showed improvement of septal motion variation and elimination of respiratory effect on mitral valve motions. <h3>Discussion</h3> Imaging was initially concerning for ECD given cardiac findings with retroperitoneal fibrosis. However, biopsies were inconsistent with ECD. Due to constrictive physiology, he underwent pericardiectomy with repeat biopsies revealing acute and chronic inflammation with extensive fibrosis, yielding a more likely diagnosis of idiopathic fibrosing mediastinitis. Treatment for idiopathic fibrosing mediastinitis is symptomatic relief with surgical resection. <h3>Conclusion</h3> Recurrent constrictive pericarditis with extensive multiorgan fibrosis is uncommon and ECD and fibrosing mediastinitis should be differential diagnoses in order to guide appropriate management.

Pericardial Effusion on MRI in Autosomal Dominant Polycystic Kidney Disease.

Autosomal dominant polycystic kidney disease (ADPKD) has been associated with cardiac abnormalities including mitral valve prolapse and aneurysmal dilatation of the aortic root. Herein, we investigated the potential association of pericardial effusion with ADPKD. Subjects with ADPKD (n = 117) and control subjects without ADPKD matched for age, gender and renal function (n = 117) undergoing MRI including ECG-gated cine MRI of the aorta and heart were evaluated for pericardial effusion independently by three observers measuring the maximum pericardial effusion thickness in diastole using electronic calipers. Pericardial effusion thickness was larger in ADPKD subjects compared to matched controls (Mann–Whitney p = 0.001) with pericardial effusion thickness >5 mm observed in 24 of 117 (21%) ADPKD subjects compared to 4 of 117 (3%) controls (p = 0.00006). Pericardial effusion thickness in ADPKD was associated with female gender patients (1.2 mm greater than in males, p = 0.03) and pleural effusion thickness (p < 0.001) in multivariate analyses. No subjects exhibited symptoms related to pericardial effusion or required pericardiocentesis. In conclusion, pericardial effusion appears to be more prevalent in ADPKD compared to controls. Although in this retrospective cross-sectional study we did not identify clinical significance, future investigations of pericardial effusion in ADPKD subjects may help to more fully understand its role in this disease.

Constrictive pericarditis: rare but reversible cause of protein losing enteropathy.

Constrictive pericarditis is uncommon in children. It results from scarring and consequent loss of the normal elasticity of the pericardial sac and is most commonly seen as a late sequelae of idiopathic or viral pericarditis. Here, we report a case of protein losing enteropathy as a complication of constrictive pericarditis in a 2-year-old child. Pericardial thickening was demonstrated by cardiac MRI and subsequent pericardiectomy led to remarkable improvement and resolution of protein losing enteropathy.

Ventricular conduction improvement after pericardial fat reduction triggered by rapid weight loss in subjects with obesity undergoing bariatric surgery.

Obesity is considered a major cardiovascular risk factor. The excess of pericardial fat (PF) in patients with obesity has been associated with a variety of electrocardiographic alterations. In previous studies, we demonstrated that rapid weight loss and bariatric interventions result in decreased PF. The aim of this study is to report the changes in PF after bariatric surgery and its effect on ventricular conduction. US hospital, academic institution. A linear measurement of PF thickness on computed tomography scans was obtained for 81 patients, as well as a retrospective review of electrocardiographic changes before and after bariatric surgery. We compared the changes in PF thickness and electrocardiographic components before and after procedures. Common demographics and co-morbidities were collected along with lipid profiles preoperative and postoperative. A total of 81 patients had electrocardiograms done before and 1 year after bariatric surgery. Females comprised 67.9% (n = 55), and the average age for our population was 55.07 ± 14.17 years. Pericardial fat thickness before surgery was 5.6 ± 1.84 and 4.5 ± 1.62 mm after surgery (P = .0001). Ventricular conduction (QT and QT corrected [QTc] intervals) showed a significant improvement from 438.7 + 29 before to 426.8 + 25.3 after bariatric surgery (P = .006). We found a statistically significant association between the decrease in PF and the decrease in QTc intervals (P = .002). Obesity is a risk factor for arrhythmias and sudden cardiac death. Bariatric surgery and its effect on PF produce an improvement in ventricular conduction, which may reduce the ventricular electrical instability in patients with obesity.

Efficacy of anakinra on rebound of multisystem inflammatory syndrome.

Efficacy of anakinra on rebound of multisystem inflammatory syndrome.

Elucidation of Histological Features of Pericardium in Cases Clinically Presented as Constrictive Pericarditis: A Retrospective Observational Study

Introduction: Constrictive Pericarditis (CP) is an uncommon but important disease characterised by impaired diastolic ventricular filling and impaired ventricular ejection as a result of thickened, fibrosed and often calcified pericardium. Aim: To analyse histomorphological features of pericardial biopsy removed in patients with clinical and radiological features of constriction. Materials and Methods: The present study was a retrospective observational study conducted at LPS Institute of Cardiology and Cardiothoracic Vascular Surgery and Department of Pathology, GSVM Medical College, Kanpur, Uttar Pradesh, India. A total of 108 patients with CP were studied between a time period of January 2008 to June 2019. Clinical, demographic, laboratory and operative data of patients were retrieved from record section of mentioned departments and analysed. On histology the following parameter, if present, were recorded: inflammation and its type, granulation tissue, fibrosis, extracellular collagen deposition, granuloma, haemosiderin deposition, mesothelial hyperplasia, capillary proliferation, and calcification. Data was analysed using Microsoft Office Excel spread sheet. Results: Out of 108 cases, 98 cases (90.7%) had increased pericardial thickness and 10 cases (9.2%) had normal pericardial thickness, despite clinical and echocardiographic features of restriction. In majority of cases (96 cases, 88.9%), inflammation was of chronic type and only in 8 cases (7.4%), it was of acute nature. Tubercular pericarditis was the major cause in 46 cases (42.6%) followed by chronic non specific idiopathic in 39 cases (36.1%). Conclusion: The current study evaluated the histological features of CP in a semiquantitative grade manner thus helping clinician and pathologists to guide for other ancillary testing and thus guide toward accurate diagnosis. The current study evaluated the histological features of CP in a semiquantitative grade manner thus helping pathologists to guide for other ancillary testing and thus guide toward accurate diagnosis.

Outcome of Pericardiectomy for Constrictive Pericarditis: Single Center Experience

Background. Constrictive pericarditis is a rare chronic inflammatory disease that impairs diastolic filling, reduces cardiac output, and ultimately leads to heart failure. TB and post-pericardiotomy and idiopathic are the commonest causes. Multimodality imaging are essential for confirming the diagnosis Trans-thoracic echocardiography is the golden method of diagnosis. Computed tomography is another confirmatory diagnostic tool of pericardial thickness. Right side heart Cath and magnetic resonance imaging help in diagnosis of constrictive pericarditis from restrictive cardiomyopathy and confirm diastolic filling dysfunction of the heart. Pericardiectomy is the mainstay therapy, should be early and complete if feasible to provide symptoms relieve and adequate outcome Patients and methods. We retrospectively review medical records of 13 patients operated for pericardiectomy for constrictive pericarditis. Demographic and perioperative data were analyzed. Results. The mean age of patients was 49.9±7.8 years. All of our patients were symptomatic (NYHA class II-IV) with 7 months median duration of symptoms. TB was the commonest cause. Complete pericardiectomy was achieved in 11 patients (84.6%). Cardiopulmonary bypass was conducted in 5 patients (4 for associated cardiac procedure and one for repair of IVC injury). NYHA class improved to class I in 9 patients (75%). We had one case (7.6%) of mortality. The cause of death was sepsis and respiratory failure. Conclusion. Phrenic to phrenic pericardiectomy without bypass is safe and effective for treating constrictive pericarditis.

CONTRIBUTION OF CARDIAC IMAGING (CT AND MRI) IN THEDIAGNOSIS OF CHRONIC CONSTRICTIVE PERICARDITIS: A SERIES OF 76 CASES

Background:Constrictive pericarditis (CP) is an uncommon disease that is usually difficult to diagnose. Transthoracic echocardiography can sometimes fail to establish its diagnosis. The aim of our study is to prove that both Computed tomography (CT) and magnetic resonance (MR) imaging offer distinct advantages to confirm the diagnosis of CP and make therapeutic decisions for patients with this condition. Methods:Data of 76 patients who underwent MRI for a suspicion of CP from January 2009 to October 2021 were reviewed retrospectively Results:MRI and CT scan confirmed the diagnosis showing pericardial thickening in all cases, measuring 7.6 ± 3.2 mm on average circumferential in 62,7 %, and localized in 37,3 %, pericardial calcification in 50 % of cases and inferior vena cava plethora in all cases. An abnormal septal motion was found in all patients. Imaging data namely pericardial thickening, calcifications, as well as their topography, were confirmed by surgical exploration, and the results were consistent in 100% of cases. Conclusion:Although cardiac CT and CMR are recommended as second-line tests in the diagnostic workup of constrictive pericarditis, they offer distinct advantages to not only confirm the diagnosis but also make therapeutic decisions for patients with this condition. Nowadays, many studies prove that a modern approach for the management of pericardial diseases should include the use of different imaging modalities.

741 A complex clinical mosaic of severe autoimmune calcific constrictive pericarditis with striking haemodynamic response to immunosuppressive therapy

Abstract Autoimmune constrictive pericarditis constitutes a conundrum to modern cardiology with much uncertainty surrounding both pathophysiology and optimal treatment strategies. We hereby describe the case of a 35-year-old woman of Nigerian origin with severe right heart failure secondary to calcific constrictive pericarditis. Her past medical history included coagulation factor XI deficiency, leukopenia, 2nd trimester miscarriage and premature labour due to placenta previa with fibrin deposition. Further investigations revealed atrial fibrillation, severe biatrial enlargement, moderate tricuspid and mitral regurgitation, pericardial thickening, post-capillary pulmonary hypertension and right ventricular dip-and-plateau pattern, compatible with severe constrictive pericarditis. Extensive screening for infectious and autoimmune causes only revealed borderline positive ANA (1:80). Thereafter, the patient underwent complete surgical pericardiectomy with pericardial biopsies revealing fibrous thickening, diffuse calcification and lymphocyte/macrophage infiltrates, in the absence of giant multinucleated cells or granulomas. The patient was later discharged but soon experienced relapse of exertional dyspnoea presenting with right-sided haemo-pneumothorax (requiring pleural drainage), diffuse alveolar haemorrhage, large right-sided basal and infrascissural pleural effusion, and ascites. She was treated with high dose iv furosemide, oral ibuprofen and colchicine, suspension of rate control medications, achieving initial reduction in pulmonary oedema and ascites, relapsing however after attempts to switch to oral diuretic therapy. Due to the finding of persistent lymphopenia, further immunological tests were conducted, revealing raised IgG1 levels as well as altered peripheral lymphocyte populations (raised CD4+/CD8+ ratio and CD8+ central memory, reduced CD8 effector memory). This finding in conjunction with the history of factor XI deficiency, 2nd trimester miscarriage and placental fibrin deposition as well as the observation of painful cutaneous nodules at sites of venepuncture, suggestive of Koebner’s phenomenon, veered the diagnostic focus to a potential autoimmune aetiology and in particular to systemic lupus erythematosus (&amp;gt;10 ACR-EULAR score points with case reports describing all the above as potential disease manifestations). Furthermore, revision of thoracic CT scans, demonstrated bilateral migratory peribronchovascular nodules with ground-glass halo. CT- guided biopsies thereof were performed revealing focal alveolar damage with capillaritis and alveolar haemorrhage, further corroborating the clinical suspicion of autoimmune disease and justifying the introduction of high-dose oral corticosteroid therapy. In liaison with our tertiary rheumatology centre, the patient was later switched to mycophenolate with gradual weaning from corticosteroid. Concurrent cardiological follow-up revealed persistence of good haemodynamic status (NYHA class II, absence of pulmonary oedema and ascites) with oral diuretic therapy, regression of cutaneous symptoms and echocardiography demonstrating consistent reduction in both mitral and tricuspid regurgitation. This constitutes to our knowledge the first report of autoimmune calcific constrictive pericarditis with significant haemodynamic response to immunosuppressive therapy. Despite the relative rarity of this disease entity, early recognition and instatement of immunosuppressive treatment may prove fundamental to halt and potentially reverse the haemodynamic progression of this highly morbid condition.

Epicardial and pericoronary adipose tissue in severe COVID-19 infection

Objective To investigate the association between epicardial and pericoronary adipose tissue thicknesses measured with computed tomography (CT) and severity of COVID-19 infection. Methods We recruited 504 patients admitted with RT-PCR-proven diagnosis of COVID-19 infection and underwent simultaneous Chest CT scanning. Epicardial adipose tissue thickness (EAT) and pericardial adipose tissue thickness (PCAT) were measured by CT. Comparisons were performed between ICU admitting and non-ICU admitting patients were performed. Results Of 504 patients, 423 patients were hospitalised in normal wards or followed as outpatient, and 81 patients were admitted to ICU. EAT and PCAT were significantly increased in ICU patients (5.98[5.06–7.13] mm vs. 8.05[6.90–9.89] mm, p < 0.001 and 9.3[7.4–11.5] mm vs. 11.2[10.3–13.2] mm, p < 0.001, respectively). In multiple logistic regression analyses, EAT and PCAT were independent predictors of ICU admission. A cut-off point of 6.64 mm EAT has a sensitivity of 82.7% and a specificity of 66.7% (AUC = 0.789, 95% CI: 0.744–0.833, p < 0.001) and a cut-off point of 9.85 mm PCAT has a sensitivity of 91.4% and a specificity of 61.2% (AUC = 0.744, 95% CI: 0.700–0.788, p < 0.001). Conclusion We found that both increased EAT and PCAT were associated with the severity of COVID-19 infection defined as the need for ICU admission.

C21. Cardiac Complications in Immunocompromised Patient : A Case Report

Abstract Background Cardiovascular diseases in human immunodeficiency virus (HIV)-positive patients are becoming increasingly detected in developing countries. Pericardial involvement may be manifested as acute pericarditis, constrictive pericarditis, symptomatic pericardial effusion and cardiac tamponade. The aim of this report is to present a patient with AIDS clinical stage IV who developed pericarditis and pericardial effusion. Case Summary A 27-year-old male came to our ER with 7-day fever and delirium syndrome. He has been diagnosed with AIDS clinical stage IV for the past 3 years with the latest CD4 count was 6/mm3. Serial Transthoracic Echocardiography (TTE) revealed small to moderate circumferential pericardial effusion, thickening of pericardium and reduced left ventricular ejection fraction without signs of cardiac tamponade from TTE. Upon hospitalization, he developed signs of hypotension without distended jugular veins nor muffled heart sounds. It was decided to initiate supportive treatment and NSAIDs without pericardiocentesis. The patient recovered uneventfully. As an outpatient, no other cardiovascular complications developed. Discussion Pericardial conditions are the most frequent cause of heart disease in patient with HIV infection. Most cases are mild and asymptomatic. Pericardial effusion may be marker of end-stage HIV infection because it is associated with low CD4 cell count and is often caused by opportunistic infections and malignant neoplasms. Treatment of pericarditis in HIV patients is no different from that in general population. Asymptomatic patients with small pericardial effusion without tamponade require no intervention.

C21. Cardiac Complications in Immunocompromised Patient : A Case Report

Abstract Background Cardiovascular diseases in human immunodeficiency virus (HIV)-positive patients are becoming increasingly detected in developing countries. Pericardial involvement may be manifested as acute pericarditis, constrictive pericarditis, symptomatic pericardial effusion and cardiac tamponade. The aim of this report is to present a patient with AIDS clinical stage IV who developed pericarditis and pericardial effusion. Case Summary A 27-year-old male came to our ER with 7-day fever and delirium syndrome. He has been diagnosed with AIDS clinical stage IV for the past 3 years with the latest CD4 count was 6/mm3. Serial Transthoracic Echocardiography (TTE) revealed small to moderate circumferential pericardial effusion, thickening of pericardium and reduced left ventricular ejection fraction without signs of cardiac tamponade from TTE. Upon hospitalization, he developed signs of hypotension without distended jugular veins nor muffled heart sounds. It was decided to initiate supportive treatment and NSAIDs without pericardiocentesis. The patient recovered uneventfully. As an outpatient, no other cardiovascular complications developed. Discussion Pericardial conditions are the most frequent cause of heart disease in patient with HIV infection. Most cases are mild and asymptomatic. Pericardial effusion may be marker of end-stage HIV infection because it is associated with low CD4 cell count and is often caused by opportunistic infections and malignant neoplasms. Treatment of pericarditis in HIV patients is no different from that in general population. Asymptomatic patients with small pericardial effusion without tamponade require no intervention.

C87. Serial Cases of Cardiovascular Manifestation on Leptospirosis: A Tales of Unfortunate Events

Abstract Background Leptospirosis is a zoonosis disease caused by Leptospira species. It's endemic and has become a major public health issue, especially in tropical regions. Clinical manifestation varies from mild or asymptomatic to severe multiple organ failure. We report cases of severe leptospirosis which complicates supraventricular tachycardia and myoperdicarditis from Universitas Sebelas Maret Academic Hospital. Case Summary The first case was a 44-year-old man referred from Internal Medicine Department with Leptospira infection with Weil’s disease. On 5th daycare, the patient was reporting had an episode of tachyarrhythmia, the ECG show SVT-AVNRT, there was no history of arrhythmic events before admitted to the hospital, the echocardiography was normal. The second case was a 67-year-old man who was referred from emergency department with shortness of breath, the ECG reveals diffuse ST-segment elevation in all limb and precordial leads with reciprocal ST-depression at aVR and V1, there was also downsloping of the PR and TP segment on precordial leads (Spodick’s sign), with normal ejection fraction on echocardiographic examination with pericardial thickening. Both patients have hsTroponin levels rose above the normal limit and serological testing found positive leptospira IgM. Discussion Severe leptospirosis can cause multi-organ dysfunction including cardiac involvement. The patients, in this case, suffered from leptospirosis with SVT-AVNRT and myopericarditis. The exact pathophysiology is still unclear, but there are several hypotheses, such as cytokine storms and direct damage from leptospira endotoxins. Arrhythmias and cardiac disturbance in leptospirosis patients are associated with poor outcomes and higher mortality rates.

C87. Serial Cases of Cardiovascular Manifestation on Leptospirosis: A Tales of Unfortunate Events

Abstract Background Leptospirosis is a zoonosis disease caused by Leptospira species. It's endemic and has become a major public health issue, especially in tropical regions. Clinical manifestation varies from mild or asymptomatic to severe multiple organ failure. We report cases of severe leptospirosis which complicates supraventricular tachycardia and myoperdicarditis from Universitas Sebelas Maret Academic Hospital. Case Summary The first case was a 44-year-old man referred from Internal Medicine Department with Leptospira infection with Weil’s disease. On 5th daycare, the patient was reporting had an episode of tachyarrhythmia, the ECG show SVT-AVNRT, there was no history of arrhythmic events before admitted to the hospital, the echocardiography was normal. The second case was a 67-year-old man who was referred from emergency department with shortness of breath, the ECG reveals diffuse ST-segment elevation in all limb and precordial leads with reciprocal ST-depression at aVR and V1, there was also downsloping of the PR and TP segment on precordial leads (Spodick’s sign), with normal ejection fraction on echocardiographic examination with pericardial thickening. Both patients have hsTroponin levels rose above the normal limit and serological testing found positive leptospira IgM. Discussion Severe leptospirosis can cause multi-organ dysfunction including cardiac involvement. The patients, in this case, suffered from leptospirosis with SVT-AVNRT and myopericarditis. The exact pathophysiology is still unclear, but there are several hypotheses, such as cytokine storms and direct damage from leptospira endotoxins. Arrhythmias and cardiac disturbance in leptospirosis patients are associated with poor outcomes and higher mortality rates.

C29. Chronic Pericardial effusion associated with Cytomegalovirus

Abstract Pericardial effusion is one of the most challenging clinical condition to determine the etiologies. A 60 yo woman presented with atypical sign of pericardial effusion. She visited several physicians and without any clinical improvement. Echocardiography revealed 133.5 ml pericardial effusion and pericardial thickness of 12,14 mm. Cardiac MRI was then performed and indicated, thickening of pericardium (4.8-5.1mm) at lateral right atrium, RV free wall and apical RV. The thickened part of the pericardium at apical RV has rigid, immobile appearance. Moderate amount of pericardial effusion prominently located at basal of heart. Pericardial effusion was at superior and lateral right atrium, apical RV and LV, and lateral, inferior, anterior left ventricle. Serology tests Anti CMV IgG reactive, anti CMV IgM non reactive and TB quantiferon negative. These results confirmed the pericarditis associated with CMV infection. The biggest challenge for the clinician is to find out an etiologic diagnosis. The common causes of pericarditis are infection (viral, bacterial), metabolic (renal failure, hypothyroidsism), cancer, myocardial infarction, and post traumatic. Among infectious causes, the enteroviruses, herpesviruses and mycobacterium tuberculosis are the most common causes. Cytomegalovirus belongs to the herpesviruses group. Clinician should be aware about the possible etiologies, as chronic pericarditis is a condition that requires comprehensive and multidisciplinary approaches.

C29. Chronic Pericardial effusion associated with Cytomegalovirus

Abstract Pericardial effusion is one of the most challenging clinical condition to determine the etiologies. A 60 yo woman presented with atypical sign of pericardial effusion. She visited several physicians and without any clinical improvement. Echocardiography revealed 133.5 ml pericardial effusion and pericardial thickness of 12,14 mm. Cardiac MRI was then performed and indicated, thickening of pericardium (4.8-5.1mm) at lateral right atrium, RV free wall and apical RV. The thickened part of the pericardium at apical RV has rigid, immobile appearance. Moderate amount of pericardial effusion prominently located at basal of heart. Pericardial effusion was at superior and lateral right atrium, apical RV and LV, and lateral, inferior, anterior left ventricle. Serology tests Anti CMV IgG reactive, anti CMV IgM non reactive and TB quantiferon negative. These results confirmed the pericarditis associated with CMV infection. The biggest challenge for the clinician is to find out an etiologic diagnosis. The common causes of pericarditis are infection (viral, bacterial), metabolic (renal failure, hypothyroidsism), cancer, myocardial infarction, and post traumatic. Among infectious causes, the enteroviruses, herpesviruses and mycobacterium tuberculosis are the most common causes. Cytomegalovirus belongs to the herpesviruses group. Clinician should be aware about the possible etiologies, as chronic pericarditis is a condition that requires comprehensive and multidisciplinary approaches.

Incessant pericarditis as a risk factor for complicated pericarditis and hospital admission

Abstract Background Incessant pericarditis is defined as pericarditis with persistent symptoms without a symptom-free interval of 4 to 6 weeks despite therapy. On the contrary, recurrent pericarditis is characterized by recurring symptoms after a symptom-free interval of at least 4 to 6 weeks, allowing the completion of therapy. Aims The aim of this study is to assess the risk of complicated pericarditis and related hospitalizations according to the clinical pattern of incessant or recurrent pericarditis. Methods From January 2017 to December 2018, all consecutive patients admitted to AOU Città della Salute (Turin, IT) for pericarditis were included in a prospective cohort study with a clinical and echocardiographic follow-up at 1, 3, and 6 months, and then every 6 months. Results We included 147 patients (median age, 50.9 years [IQR, 28.5]; 49.7% women, 89% had idiopathic aetiology, 11% had pericarditis related to systemic inflammatory disease/postcardiac injury syndrome, 80% had pericardial effusion, and 62% had elevated C-reactive protein &amp;gt;5 mg/L). Patients were treated according to ESC guidelines. After a median follow-up of 14 months (IQR, 9 months), adverse events were recorded in 54/147 patients (36.7%): nonidiopathic/viral aetiology in 16 of 147 cases (10.9%), recurrent pericarditis/persistent symptoms in 53 of 147 cases (36.1%), cardiac tamponade in 4/147 cases (2.7%), persistent CP in 4/147 cases (2.7%), and hospitalization related to pericarditis in 38/147 cases (25.9%). An incessant course was reported in 18 of 147 cases (12%). The risk of complications was higher in patients with incessant pericarditis (Figure) – especially CP – compared to nonincessant course (22.2% versus 0%, respectively; P&amp;lt;0.001). Patients with incessant pericarditis more commonly had echocardiographic evidence of CP (77.8% vs. 9.3%; P&amp;lt;0.001) and thickened pericardium on multimodality imaging (66.7% vs. 4.7%; P&amp;lt;0.001). These findings were reversible with medical therapy with the use of anakinra (100 mg/d) and colchicine in all but 4 cases that progressed to persistent CP, which were referred for pericardiectomy. An analysis of risk factors for complicated pericarditis and hospitalization using Cox proportional hazards regression analysis identified the following risk factors: large pericardial effusion (hazard ratio, 7.63 [95% CI, 3.09–18.83]), elevated C-reactive protein &amp;gt;5 mg/L (hazard ratio, 5.55 [95% CI, 1.87–16.44]), and incessant course (HR, 17.10 [95% CI, 7.63–38.33]). Conclusions This study highlights that an incessant course of pericarditis is a possible new risk factor for complications and especially for developing constriction. In clinical practice, the detection of an incessant course, as well as imaging findings of constriction and pericardial thickening, should prompt more diagnostic testing, a close follow-up, and more aggressive therapy to prevent complications and persistent constriction. Funding Acknowledgement Type of funding sources: None. Figure 1

PERICARDIAL TB CAUSING RESTRICTIVE CARDIOMYOPATHY TREATED WITH RIFAMPIN, ISONIAZID, PYRAZINAMIDE, ETHAMBUTOL (RIPE) AND CORTICOSTEROIDS

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Pericardial tuberculosis presents in one to two percent of pulmonary tuberculosis (TB). Of these patients, approximately thirty to sixty percent develop constrictive pericarditis without treatment. This case presents a patient with constrictive pericarditis from reactivation of a prior pleural TB infection, treated with RIPE therapy and adjunctive steroids. CASE PRESENTATION: An 81 year old male from India with a history of pleural TB (treated with isoniazid, para-aminosalicylic acid and an unknown agent) and recent diagnosis of a large pericardial effusion without tamponade who presented with dyspnea. On presentation, he was hemodynamically stable. Physical exam was unremarkable. Labs significant for c-reactive protein of 166 mg/L and BNP of 508 pg/mL. Echocardiogram showed a small pericardial effusion with new constrictive pericarditis. Work up included a heart catheterization, consistent with constrictive physiology. Cardiac MRI revealed pericardial thickening, adhesions and fibrosis. A thoracoscopy with pericardial biopsy was performed and was negative for mycobacterium tuberculosis (MTB). Bronchoscopy with bronchoalveolar lavage was negative for MTB, however induced sputum post-bronchoalveolar was positive. He was treated with two months of RIPE therapy followed by four months of Isoniazid and Rifampin, in addition to prednisone 60 mg daily with a taper and Bactrim for Pneumocystis Jiroveci prophylaxis. After treatment initiation, sputum testing was negative. Repeat echocardiogram showed resolution of pericardial effusion without constriction. The patient tolerated treatment without complications. DISCUSSION: Tuberculosis pericarditis is diagnosed when any MTB is detected in the body in the setting of pericarditis. In this case, the patient underwent an extensive workup which revealed findings consistent with constrictive pericarditis, however the relation to tuberculosis was not established until his post-bronchoalveolar sputum despite negative pericardial biopsy. Negative pericardial biopsy results cannot rule out tuberculosis pericarditis as the sensitivity ranges from ten to sixty-four percent. A pericardiocentesis on initial presentation may have been helpful in an earlier diagnosis. Standard treatment is RIPE. However, the role of corticosteroids is controversial. Research supports the use of corticosteroids in patients who have or are at high risk of developing constrictive pericarditis. These patients include those with large pericardial effusions, high levels of inflammatory cells in pericardial fluid, and/or early signs of constriction. Corticosteroids have not become standard therapy due to significant side effects, with unclear benefits. CONCLUSIONS: Tuberculosis pericarditis is a rare and challenging diagnosis. Recommended treatment is with RIPE and the role of adjunct corticosteroids warrants further investigation. REFERENCE #1: Larrieu AJ, Tyers GF, Williams EH, Derrick JR. Recent experience with tuberculous pericarditis. Ann Thorac Surg 1980; 29:464. REFERENCE #2: Komsuoglu B, Goldeli O, Kulan K, Komsuoaylu SS. The diagnostic and prognostic value of adenosine deaminase in tuberculous pericarditis. Eur Heart J 1995; 16:1126. REFERENCE #3: Nahid P, Dorman SE, Alipanah N, et al. Official American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America Clinical Practice Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clin Infect Dis 2016; 63:e147. DISCLOSURES: No relevant relationships by Adetokunbo Adebayo, source=Web Response No relevant relationships by Alissa Ali, source=Web Response No relevant relationships by Jared Beaudin, source=Web Response No relevant relationships by Julie Nguyen, source=Web Response

Salvation to Hearts in Distress under Shells of Stress: Subtotal Pericardiectomy in a Series of 9 Patients with Constrictive Pericarditis

Objective: Chronic constrictive pericarditis (CCP) is a rare entity responsible of diastolic heart failure. The true prevalence is yet to be defined. The purpose of this study was to describe the clinical and para-clinical characteristics of patients with CCP, the therapeutic management, the outcomes and impacting factors. Materials and Methods: We conducted a retrospective descriptive study from 2017 to 2020 including 9 patients hospitalized for CCP in our cardiovascular surgery department. Results: The mean age was of 32.6 years. Majority were men (n=7). Dyspnea was the most common sign. Peripheral signs were dominated by signs of right heart failure. Cardiac ultrasonography showed pericardial thickening and calcifications with Doppler adiastolic signs in 90% of cases. Thoracic CT was performed in 7 patients, cardiac MRI in one patient, showing calcifications and measuring the pericardial thickening. Cardiac catheterization performed in 6 patients showed the aspect of Dip plateau. Tuberculosis etiology was retained in 55.6%; post-radiation origin in one patient and 33.4 % of cases were idiopathic. All of patients benefited from subtotal pericardiectomy with good results in the medium and long term. Two deaths occurred, the first patient died following multi-visceral failure, the second died 3 years later from neoplasia. Conclusion: The CCP is a rare condition with poor prognosis. The diagnosis should be raised when there are signs of right heart failure associated with signs of hemodynamic adiastolia. The echocardiography, with computed tomography or cardiac MRI and especially cardiac catheterization confirm the diagnosis and also etiological orientation. Tuberculosis and idiopathic etiologies were the most common at our country. Medical treatment options are limited. Pericardiectomy remains the only radical treatment with good results in immediate, medium and long term.