scholarly journals Idiopathic pericardial effusion in patients with hypertrophic cardiomyopathy

2021 ◽  
Author(s):  
Sarinya Puwanant ◽  
Veraprapas Kittipibul ◽  
Nattakorn Songsirisuk ◽  
Sakun Santisukwongchote ◽  
Patita Sitticharoenchai ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Pericardial Effusion ◽  
Heart Surgery ◽  
Chronic Kidney Disease Stage ◽  
Pressure Overload ◽  
Pericardial Fluid ◽  
Right Atrial ◽  
Disease Stage ◽  
Fluid Analysis ◽  
Septal Thickness

AbstractThe aims of this study were to examine the prevalence of moderate to large (moderate–large) idiopathic pericardial effusion (i-PEF) in patients with hypertrophic cardiomyopathy (HCM) and to identify clinical and echocardiographic hemodynamic profiles associated with pericardial effusion. A total of 292 adult patients with HCM were studied. Fifteen patients with a history of factors associated with pericardial effusion including myocardial infarction, heart surgery or cardiac procedure within the last 12 months, autoimmune disease, hydralazine use, chronic kidney disease stage 3–4, tuberculosis, and malignancy were excluded. Of 277 eligible patients with HCM, 11 patients (4%) with moderate-large i-PEF were identified. Clinical tamponade was present in 1 patient. Compared to patients with HCM who had no or small pericardial effusion, patients with moderate-large i-PEF were younger and more likely to have right ventricular (RV) hypertrophy and reverse septal curvature. These patients also exhibited a greater maximal septal thickness, mean and systolic pulmonary pressure, and right atrial pressure (p < 0.05 for all). Pericardial fluid analysis and histopathological exams were performed in 7 and 3 patients, respectively. All examinations revealed transudative and nonspecific etiology of pericardial effusion. Idiopathic pericardial effusion and cardiac tamponade in patients with HCM was uncommon. The pathophysiology involved in pericardial effusion remains undetermined. Patients with moderate-large i-PEF frequently exhibited a phenotype of pulmonary hypertension and RV pressure overload.

scholarly journals Idiopathic Pericardial Effusion in Patients with Hypertrophic Cardiomyopathy

2021 ◽  
Author(s):  
Sarinya Puwanant ◽  
Veraprapas Kittipibul ◽  
Nattakorn Songsirisuk ◽  
Sakun Santisukwongchote ◽  
Patita Sitticharoenchai ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Pericardial Effusion ◽  
Heart Surgery ◽  
Chronic Kidney Disease Stage ◽  
Pressure Overload ◽  
Pericardial Fluid ◽  
Right Atrial ◽  
Disease Stage ◽  
Fluid Analysis ◽  
Septal Thickness

Abstract Objectives: The aims of this study were to examine the prevalence of moderate to large (moderate-large) idiopathic pericardial effusion (i-PEF) in patients with hypertrophic cardiomyopathy (HCM) and to identify clinical and echocardiographic hemodynamic profiles associated with pericardial effusion. Methods: A total of 292 adult patients with HCM were studied. Fifteen patients with a history of factors associated with pericardial effusion including myocardial infarction, heart surgery or cardiac procedure within the last 12 months, autoimmune disease, hydralazine use, chronic kidney disease stage 3-4, tuberculosis, and malignancy were excluded. Results: Of 277 eligible patients with HCM, 11 patients (4%) with moderate-large i-PEF were identified. Clinical tamponade was present in 1 patient. Compared to patients with HCM who had no or small pericardial effusion, patients with moderate-large i-PEF were younger and more likely to have right ventricular (RV) hypertrophy and reverse septal curvature. These patients also exhibited a greater maximal septal thickness, mean and systolic pulmonary pressure, and right atrial pressure (p<0.05 for all). Pericardial fluid analysis and histopathological exams were performed in 7 and 3 patients, respectively. All examinations revealed transudative and nonspecific etiology of pericardial effusion. Conclusions: Idiopathic pericardial effusion and cardiac tamponade in patients with HCM was uncommon. The pathophysiology involved in pericardial effusion remains undetermined. Patients with moderate-large i-PEF frequently exhibited a phenotype of pulmonary hypertension and RV pressure overload.

scholarly journals P1262 If anything can go wrong, it will: management of a pericardial effusion in a young patient

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
J P Dias Ferreira Reis ◽  
T Mendonca ◽  
T Mano ◽  
G Portugal ◽  
P Silva Cunha ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Pericardial Effusion ◽  
Accessory Pathway ◽  
Pericardial Fluid ◽  
Nucleic Acid Amplification ◽  
Right Atrial ◽  
Oral Steroid ◽  
Large Pericardial Effusion ◽  
Increased Risk ◽  
Oncologic Patients

Abstract Case Report A 25 year-old male patient with an unremarkable past medical history presented to the Emergency Department due to a hemodynamically stable wide complex tachycardia at 260bpm with no response to adenosine, which was successfully treated with synchronized electrical cardioversion. Post cardioversion EKG revealed a pre excitation pattern and the transthoracic echocardiogram showed a large pericardial effusion with diastolic right atrial collapse. The patient was admitted in the Cardiology Department for emergent pericardiocentesis and further investigation. A total of 800 mL of bloody pericardial fluid was removed, compatible with an exudate, but fluid culture and cytology were inconclusive. Due to a rapid reaccumulation of pericardial fluid, the patient underwent a pericardial window, after which he developed an intractable pleuritic thoracalgia, refractory to the combination of ibuprofen, colchicine and oral steroid, despite the resolution of the pericardial effusion. He was also submitted to an electrophysiologic study with successful ablation of a right sided accessory pathway. Analysis of the pericardial fluid and biopsy were inconclusive once again, including a low level of adenosine deaminase and negative acid-fast bacilli test and nucleic acid amplification test for Mycobacterium tuberculosis. The patient was afebrile and denied any constitutional symptoms or relevant epidemiological context. The remainder etiological study was unremarkable, with the exception of fluctuating antibody titers for adenovirus, Borrelia burgdorferi and Mycoplasma pneumoniae, which were interpreted as a result of cross-reactivity. Nevertheless, a course of 21 days of doxycycline was tried without any significant improvement. Thoracic-abdominal-pelvic CT and PET scan were normal. Direct inoculation in guinea pig led to positive results for Mycobacterium tuberculosis and antituberculous therapy was started. Despite pathogen directed antibiotic treatment, there was no clinical improvement and the pericardial effusion gradually relapsed, evolving to cardiac tamponade requiring emergent drainage. Histologic examination of pericardial fragments finally revealed massive infiltration by an undifferentiated malignant tumor compatible with a malignant epithelioid hemangioendothelioma. Due to the patient’s poor performance status and rapidly deteriorating clinical course, it was decided not to start chemotherapy. The patient eventually died, 6 months after his admission to the ED and 2 weeks after the neoplasm’s diagnosis. Conclusion In regions with a high Tuberculosis incidence, there should be a high degree of suspicion for tuberculous pericarditis, especially in cases of recurrent pericardial effusion. Immunosuppressed individuals, such as oncologic patients, are at an increased risk for tuberculosis. The management of relapsing pericardial effusion remains a diagnostic challenge as described in this clinical case.

scholarly journals Tubercular Pericardial Effusion Presenting as Cardiac Tamponade

2021 ◽  
Vol 18 (4) ◽  
pp. 795-797
Author(s):  
Alok Pradhan ◽  
Ranjit Babu Jasaraj ◽  
Bhesh Raj Karki ◽  
Anish Joshi
Keyword(s):  
Chest Pain ◽  
Pericardial Effusion ◽  
Cardiac Tamponade ◽  
Adenosine Deaminase ◽  
Heart Sound ◽  
Venous Pressure ◽  
Pericardial Fluid ◽  
Jugular Venous Pressure ◽  
Fluid Analysis ◽  
Extra Pulmonary

Pericardial effusion is an uncommon extra-pulmonary manifestation of tuberculosis, tamponade being even rarer. Here, a 14-year female presented with cough, chest pain and fever. She had raised jugular venous pressure, hypotension, and muffled heart sound, suggestive of cardiac tamponade, confirmed by echocardiogram. She underwent pericardiocentesis with continuous pericardial fluid drainage. Her jugular venous pressure normalized after the aspiration. The high adenosine deaminase level in pericardial fluid analysis was suggestive of tuberculosis for which she was treated with antitubercular therapy and steroid. This case highlights the importance of adenosine deaminase for diagnosing the etiology of a rare presentation.Keywords: Adenosine deaminase; echocardiography; pericardial effusion; tamponade; tuberculosis

Abstract 17341: A 19-Year-Old Female with Recurrent Chylopericardium

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Cheng-Han Chen ◽  
Angela Kleiber ◽  
Christine Megerdichian ◽  
Gregg C Fonarow ◽  
Arnold S Baas
Keyword(s):  
Pericardial Effusion ◽  
Thoracic Duct ◽  
Correct Diagnosis ◽  
Pericardial Fluid ◽  
Shortness Of Breath ◽  
Pericardial Window ◽  
Percutaneous Embolization ◽  
Fluid Analysis ◽  
Large Pericardial Effusion ◽  
Work Up

A 19-year-old female initially presented to an outside hospital with worsening shortness of breath over the course of hours. Echocardiogram revealed a large pericardial effusion with tamponade physiology. An urgent pericardiocentesis followed by a pericardial window yielded 600cc of cloudy fluid, and work-up for infectious, auto-immune, and malignant etiologies was unrevealing. She was discharged home, but over the next four weeks developed a repeat pericardial effusion requiring another pericardiocentesis yielding 750cc of cloudy fluid. She then presented to our hospital two weeks later with progressive shortness of breath. Echocardiogram revealed a large pericardial effusion with evidence of early tamponade physiology. Our differential diagnosis for her recurrent pericardial effusions remained broad, with infectious and malignant etiologies at the top of consideration. Computed tomography of the chest demonstrated the pericardial effusion and mild mediastinal adenopathy. She underwent another pericardial window with removal of 600cc of milky fluid, and fluid analysis was notable for a markedly elevated triglyceride level consistent with a diagnosis of chylopericardium. Work-up for malignancy as an etiology for recurrent chylopericardium was negative. A percutaneous lymphangiogram was then performed, which revealed a significant leak in the superior aspect of the thoracic duct into the pericardial space. Percutaneous embolization of the thoracic duct was performed using detachable coils along with embolic glue, resulting in resolution of the leak. She has since remained asymptomatic, and follow-up echocardiogram was without recurrence of any pericardial effusion. This case of idiopathic recurrent chylopericardium as the cause for pericardial effusion represents a rare manifestation of a relatively common cardiac condition. It illustrates the importance of routine pericardial fluid analysis for triglycerides, as this led to her correct diagnosis of chylopericardium. The use of percutaneous thoracic duct embolization has only recently been reported as a novel approach for treatment of chylous leak, and may emerge as a useful alternative to surgery for recurrent chylopericardium.

scholarly journals Imatinib-induced pericardial effusion in a child

2019 ◽  
Vol 12 (9) ◽  
pp. e229975 ◽  
Author(s):  
Charlotte Terry ◽  
Pascale Avery ◽  
Sarah Morton ◽  
Jon Aron
Keyword(s):  
Differential Diagnosis ◽  
Pericardial Effusion ◽  
Kinase Inhibitor ◽  
Pericardial Fluid ◽  
Ultrasound Scan ◽  
Shortness Of Breath ◽  
Graft Versus Host ◽  
Fluid Analysis ◽  
Large Pericardial Effusion

A 12-year-old boy presented with central chest pain, shortness of breath and type 1 respiratory failure. He had a background of graft versus host disease (GvHD), which was currently managed with imatinib therapy. A focused bedside ultrasound scan was performed revealing a large pericardial effusion. The child was referred to a tertiary paediatric cardiology centre where he underwent emergency pericardiocentesis, draining a total of 800 mL of pericardial fluid. Fluid analysis excluded infection, and with no other concerns for a GvHD flare the diagnosis of an imatinib-induced pericardial effusion was made. On terminating the therapy, the pericardial collection did not reaccumulate. Tyrosine kinase inhibitor-induced pericardial and/or pleural effusion should be considered as a differential diagnosis in paediatric patients on this therapy presenting in a similar manner.

Phosphate binders in patients with chronic kidney disease: Between the new and the old.

2019 ◽  
pp. 2-3
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Phosphate Binders ◽  
Advanced Chronic Kidney Disease ◽  
Phosphate Retention ◽  
Stage 4 ◽  
Dietary Phosphate

Impaired phosphate excretion by the kidney leads to Hyperphosphatemia. It is an independent predictor of cardiovascular disease and mortality in patients with advanced chronic kidney disease (stage 4 and 5) particularly in case of dialysis. Phosphate retention develops early in chronic kidney disease (CKD) due to the reduction in the filtered phosphate load. Overt hyperphosphatemia develops when the estimated glomerular filtration rate (eGFR) falls below 25 to 40 mL/min/1.73 m2. Hyperphosphatemia is typically managed with oral phosphate binders in conjunction with dietary phosphate restriction. These drugs aim to decrease serum phosphate by binding ingested phosphorus in the gastrointestinal tract and its transformation to non-absorbable complexes [1].

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