Case Records of the Massachusetts General Hospital

Case 32-2023: A 62-Year-Old Woman with Recurrent Hemorrhagic Pericardial Effusion

Evin Yucel, M.D., Nilay K. Patel, M.D., Daniela R. Crousillat, M.D., Vinit Baliyan, M.D., Arminder S. Jassar, M.B., B.S., Igor Palacios, M.D., Ignacio Inglessis, M.D., and R. Neal Smith, M.D., Ph.D.

2023-10-19T00:00:00-04:00N Engl J Med20233891511152010.1056/NEJMcpc211584538916

A Woman with Recurrent Hemorrhagic Pericardial Effusion

A 62-year-old woman was evaluated for recurrent hemorrhagic pericardial effusion. Fourteen years earlier, she had undergone transcatheter closure of an atrial septal defect. A diagnosis was made.

Presentation of Case

Dr. Nilay K. Patel: A 62-year-old woman was evaluated at this hospital because of recurrent hemorrhagic pericardial effusion.

The patient had been in her usual state of health until 3 months before the current admission, when pleuritic pain and tightness in her chest developed suddenly while she was eating. The chest pain persisted and began to radiate to the neck and back. The symptoms did not abate with aspirin or acetaminophen. Within an hour after symptom onset, she noticed that the pain worsened with exertion and when she was in the supine position; she was also unable to take a full breath and had dizziness with exertion. She presented to the emergency department of another hospital.

On examination, the temporal temperature was 36.5°C, the heart rate 104 beats per minute, the blood pressure 120/91 mm Hg, the respiratory rate 16 breaths per minute, and the oxygen saturation 95% while the patient was breathing ambient air. Except for the finding of tachycardia, the examination was reportedly normal. The prothrombin time, international normalized ratio, and blood levels of electrolytes were normal, as were the results of tests of liver and kidney function; other laboratory test results are shown in Table 1.

An electrocardiogram (ECG) reportedly showed ST-segment elevation and T-wave inversion in the anterior and inferior leads. A chest radiograph reportedly showed a mildly enlarged cardiac silhouette. Intravenous heparin was administered. Four hours later, computed tomography (CT) of the chest, performed according to a pulmonary embolism protocol, reportedly ruled out pulmonary embolism; it also revealed a moderate circumferential pericardial effusion with an attenuation level of 34 to 50 Hounsfield units, a mildly dilated ascending aorta (at a diameter of 37 mm; normal diameter, <36 mm on the basis of the patient’s sex and body-surface area), and a pulmonary nodule in the right lower lobe that measured 4 mm in diameter. Intravenous heparin was stopped, and protamine sulfate was administered. The patient was transferred to the emergency department of a second hospital 3 hours later.

On arrival at the second hospital, the temporal temperature was 36.5°C, the heart rate 101 beats per minute, the blood pressure 108/75 mm Hg, the respiratory rate 24 breaths per minute, and the oxygen saturation 95% while the patient was receiving supplemental oxygen through a nasal cannula at a rate of 4 liters per minute. Pulsus paradoxus measured 16 mm Hg. The jugular venous pressure was 12 cm of water. Auscultation revealed tachycardia and a pericardial friction rub. The remainder of the examination was normal. The erythrocyte sedimentation rate and the level of troponin were normal. An ECG showed sinus tachycardia and right-axis deviation, with minor nonspecific ST-segment and T-wave abnormalities.

Dr. Daniela R. Crousillat: A transthoracic echocardiogram (TTE) showed a small-to-moderate circumferential pericardial effusion primarily abutting the right atrium and right ventricle with right atrial inversion and intermittent diastolic inversion of the right ventricle (Figure 1A). There was increased respiratory variation in the mitral inflow velocities and a dilated inferior vena cava with reduced respirophasic collapse; both these features were suggestive of the presence of physiologic characteristics of early tamponade (Figure 1B and Video 1). Colchicine and ibuprofen were administered, and the patient was admitted to the second hospital.

Dr. Patel: The next morning, pericardiocentesis was performed under fluoroscopic guidance with the use of a subxiphoid approach, and 200 ml of bloody fluid was drained; the intrapericardial pressure decreased from 12 mm Hg to 4 mm Hg. Analysis of the pericardial fluid revealed 4,700,000 erythrocytes per microliter and 12,010 nucleated cells per microliter, of which 78% were neutrophils, 13% monocytes, 8% lymphocytes, and 1% eosinophils. Gram’s staining revealed neutrophils and no organisms. The pericardial fluid albumin level was 3.0 g per deciliter, the total protein level 4.7 g per deciliter, the lactate dehydrogenase level 614 U per liter, the glucose level 71 mg per deciliter (3.9 mmol per liter), and the amylase level 31 U per liter.

Dr. Vinit Baliyan: On the second hospital day, a CT angiogram (CTA) of the chest showed a reduction in hemopericardium, and a pericardial drain was visible; there was no aortic dissection. There was an atrial septal occluder device in place that appeared to be in an appropriate position. The device appeared to be relatively large and abutted the aortic root anteriorly (Figure 1C). However, there was no evidence of erosion of the device into the aortic wall (known as device erosion) or pseudoaneurysm formation (Figure 1D).

Dr. Patel: On the third hospital day, no pericardial effusion was detected on TTE. Cytologic analysis of the pericardial fluid revealed reactive mesothelial cells, neutrophils, histiocytes, and eosinophils, with no malignant cells. The patient was discharged home with prescriptions for colchicine and ibuprofen.

Ten days after discharge from the second hospital, the patient had a follow-up visit with her cardiologist and reported that the chest pain and dyspnea had resolved. The heart rate was 94 beats per minute, the blood pressure 159/88 mm Hg, and the oxygen saturation 97% while she was breathing ambient air; the remainder of the examination was normal. The antinuclear antibody titer was 1:160, with a homogeneous pattern, and a test for rheumatoid factor was negative. CT of the chest, performed before and after the administration of intravenous contrast material, revealed small-volume pericardial effusion, mild bronchial wall thickening, and a 4-mm pulmonary nodule in the right lower lobe. Colchicine treatment was stopped.

Six weeks before the current admission, the patient called her primary care physician to report recurrent back pain and dyspnea that she noted were similar to her previous presentation; treatment with colchicine was resumed. During the next 12 days, sinus pressure, myalgias, nasal congestion, and cough productive of green sputum developed, and she was seen by her primary care physician. On examination, the temporal temperature was 36.7°C, the heart rate 112 beats per minute, the blood pressure 140/90 mm Hg, and the oxygen saturation 94% while she was breathing ambient air. The remainder of the examination was reportedly normal. A screening test for respiratory viruses was negative. A chest radiograph reportedly showed clear lungs. Doxycycline was prescribed.

Four days before the current admission, the patient was evaluated by her cardiologist at this hospital and reported ongoing cough and dyspnea. The heart rate was 87 beats per minute, and the blood pressure was 138/100 mm Hg. The remainder of the examination was normal.

Dr. Crousillat: A TTE showed recurrence of a moderate pericardial effusion, measuring up to 14 mm in end diastole, that was adjacent to the right ventricular free wall. There was evidence of right ventricular diastolic inversion that was suggestive of the physiologic characteristics of tamponade (Figure 2A and 2B). The patient was admitted to the cardiology floor of this hospital.

Dr. Patel: On evaluation, the patient reported that she had had episodes of dyspnea and cough with sputum production and a decrease in exercise tolerance in the weeks before this admission. She had no known sick contacts.

The patient’s medical history was notable for postoperative pulmonary embolism, hypertension, dyslipidemia, recurrent episodes of syncope with cardioinhibitory and vasodepressor responses on tilt testing, asthma, obstructive sleep apnea (for which she used a continuous positive airway pressure device), obesity, tubular adenomas (colonic polyps), hepatic steatosis, hiatal hernia, osteopenia, and cataracts. She also had a history of chronic obstructive pulmonary disease; on previous pulmonary-function testing, the forced expiratory volume in 1 second (FEV₁) was 0.92 liters (39% of the predicted value), and the ratio of FEV₁ to forced vital capacity was 47%.

Five and a half years before the current admission, the patient had undergone laparoscopic sleeve gastrectomy and abdominoplasty that had resulted in postoperative hemorrhage; she had lost 44 kg of weight after the sleeve gastrectomy. Fourteen years before this admission, the patient had undergone percutaneous transcatheter closure of a fenestrated atrial septal defect (ASD) with an interatrial septal aneurysm and a right-to-left shunt that was possibly related to recurrent transient ischemic attacks; the procedure had been performed with a 30-mm Amplatzer septal occluder device. She had had mammography and cervical cancer screening within the 16 months before this admission.

Medications included colchicine, apixaban, losartan, theophylline, calcium, vitamin D, vitamin B₁₂, a multivitamin, and inhaled tiotropium and mometasone–formoterol, as well as furosemide and albuterol as needed. Topiramate had caused paresthesia. The patient lived in Massachusetts with her husband and was a business owner. She had a 40-pack-year history of cigarette smoking and had quit smoking 10 years earlier; she did not drink alcohol or use other substances. Her family history was notable for coronary artery disease in her mother and father, stroke in her maternal grandmother and paternal grandfather, and seizure in a nephew.

The temporal temperature was 36.9°C, the heart rate 120 beats per minute, the blood pressure 126/81 mm Hg, the respiratory rate 20 breaths per minute, and the oxygen saturation 94% while the patient was breathing ambient air. Pulsus paradoxus measured 10 mm Hg. The height was 163 cm and the weight 67 kg; the body-mass index (the weight in kilograms divided by the square of the height in meters) was 25.2. On examination, the jugular venous pressure was 10 cm of water. Auscultation revealed tachycardia, with no murmur or rub. The remainder of the examination was normal.

The prothrombin time, international normalized ratio, and blood levels of electrolytes were normal, as were the results of tests of liver and kidney function; other laboratory test results are shown in Table 1. An ECG showed irregular tachycardia of uncertain underlying rhythm, low voltage in the limb leads, nonspecific ST-segment and T-wave changes, and a rightward axis.

Diagnostic tests were performed, and management decisions were made.

Differential Diagnosis

Dr. Evin Yucel: This 62-year-old woman, with a history of laparoscopic sleeve gastrectomy, a complicated abdominoplasty, and percutaneous transcatheter closure of a fenestrated ASD, presented with recurrent symptomatic hemorrhagic pericardial effusion. Her presentation was subacute, with evidence of the physiologic characteristics of tamponade on TTE.

Cardiac Tamponade

Cardiac tamponade is a cardiac emergency, in which there is often rapid accumulation of pericardial fluid resulting in a sudden increase in intrapericardial pressure. When the intrapericardial pressure exceeds the intracardiac pressures, the atrial and ventricular walls invert, which initially results in a decrease in diastolic filling and eventually a decrease in cardiac output. If cardiac tamponade is left untreated, cardiogenic shock ensues, which can result in death. Depending on the clinical scenario, pericardiocentesis can be performed for both therapeutic and diagnostic purposes.

Hemorrhagic Pericardial Effusion

Although there are many causes of pericardial effusion, in this patient, we can quickly narrow the differential diagnosis on the basis of the hemorrhagic nature of the effusion. Viral infections, metabolic abnormalities (e.g., uremia and hypothyroidism), and autoimmune diseases (e.g., systemic lupus erythematosus, systemic sclerosis, and mixed connective-tissue disease) are common causes of pericardial effusion; however, these conditions often lead to transudative and nonhemorrhagic effusions.

Aortic dissection leading to aortic-wall injury and penetrating trauma are two devastating causes of hemorrhagic pericardial effusion and usually develop very abruptly. This patient did not have a recent history of trauma, and aortic dissection was ruled out with the CTA scan of the chest.

Myocardial infarction complicated by free-wall rupture resulting in cardiac tamponade also develops suddenly. This patient’s ECG did not show any ischemic changes, her troponin levels were normal, and TTE did not reveal any wall-motion abnormalities; these findings make this diagnosis unlikely.

Although uncommon in the United States, tuberculous pericarditis can occur in patients with tuberculosis and could cause hemorrhagic pericardial effusion.¹ This patient did not have constitutional symptoms before her initial presentation, and chest imaging did not show findings consistent with pulmonary tuberculosis. However, some studies have shown that patients with tuberculous pericarditis may not have classic signs and symptoms of pulmonary tuberculosis.^2,3 Another clue to assist in the diagnosis of tuberculous pericarditis would be a lymphocytic and monocytic cell predominance in the pericardial fluid; however, this patient’s pericardial fluid had a predominance of neutrophils. Diagnosis of tuberculous pericarditis can be challenging because a mycobacterial (acid-fast bacilli) smear of the pericardial fluid can be negative in up to 60% of patients with this condition.⁴ Additional testing of adenosine deaminase activity in the pericardial fluid could be performed.^2,5

In the United States, metastatic disease is a common cause of symptomatic hemorrhagic pericardial effusion. Lung, breast, and esophageal cancers are the most common, whereas melanoma, lymphoma, leukemia, and acquired immunodeficiency syndrome–related Kaposi’s sarcoma are less common.^6,7 The diagnostic utility of cytologic analysis of pericardial fluid is well established; although its sensitivity for the diagnosis of malignant effusion is variable, it has a specificity of 100%, and therefore it is important to perform this analysis in all patients with hemorrhagic effusion.^6,8,9 In addition, immunohistochemical staining could detect malignant cells and can aid in differentiating among various tissues of origin. Pericardial biopsy is reserved for patients with a high probability of cancer who have already undergone nondiagnostic cytologic analysis and immunohistochemical staining of the pericardial fluid. This patient had a recent negative mammogram and cervical cancer screening. Although she had been a smoker, there was no lymphadenopathy on chest imaging, and only a 4-mm nodule in the right lower lobe was noted. Cytologic testing of the pericardial fluid was reportedly negative for cancer. Therefore, a malignant pericardial effusion is unlikely.

Percutaneous cardiac procedures, such as pacemaker implantation, coronary angioplasty, procedures that involve interatrial septostomy, and transcatheter valve interventions, can also cause hemorrhagic pericardial effusion and often result in a sudden onset of this condition. This patient had undergone percutaneous ASD closure 14 years earlier. Device erosion leading to cardiac perforation has been described and most often occurs within 6 months after the closure procedure, although there are case reports documenting the occurrence of device erosion up to 3 years after the closure procedure.^10,11

For this patient, it would be helpful to review the original intraprocedural echocardiographic imaging to evaluate the anterior interatrial septal tissue rim, since a deficient anterior rim has been proposed as one of the predictors of device erosion into the aorta. On the CT scan, the Amplatzer septal occluder device appeared to be too large for the size of her current interatrial septum, a finding that also introduces the possibility of device erosion. In addition, the patient had had successful weight-loss surgery more than 8 years after the implantation of the device. A few reports have shown a clinically significant reduction in the left atrial area and volume among patients who have undergone weight-loss surgery.^12,13 Lastly, we know that the patient had had complications after abdominal surgery. It would be essential to review the imaging findings with the radiologist to evaluate for diaphragmatic paralysis, which, if present, could also have distorted her cardiac anatomy and led to erosion of the device.

My diagnosis is device erosion due to remodeling of the left atrium, leading to the subacute accumulation of pericardial fluid. Transesophageal echocardiography (TEE), cardiac CT, or cardiac magnetic resonance imaging could be helpful in establishing a definitive diagnosis; however, given that the patient’s presentation was subacute, flow into the pericardium may not be visualized with these imaging studies.

Clinical Impression

Dr. Igor Palacios: The patient’s echocardiographic findings 14 years before this admission were consistent with a complex ASD on the basis of the presence of an interatrial septal aneurysm and fenestrated communication with two distinct holes and a pulmonary-to-systemic blood-flow ratio of 2:1. The percutaneous transcatheter closure of the complex secundum ASD was performed with the use of a single 30-mm Amplatzer septal occluder device. However, she lost 44 kg of weight after laparoscopic sleeve gastrectomy more than 8 years after placement of the device. The recurrent hemorrhagic pericardial effusion was suggestive of device erosion, given the possible changes in atrial size and geometry. TEE and cardiac CTA were performed, and the cardiac surgery service was consulted.

Clinical Diagnosis

Recurrent hemorrhagic pericardial effusion probably due to erosion of an atrial septal defect closure device.

Dr. Evin Yucel’s Diagnosis

Recurrent hemorrhagic pericardial effusion probably due to erosion of an atrial septal defect closure device.

Diagnostic Imaging

Dr. Crousillat: TTE (Figure 3A, 3B, and 3C and Videos 2 through 4, available with the full text of this article at NEJM.org) revealed a well-aligned and appropriately positioned Amplatzer septal occluder device. There was no evidence of impingement or distortion of the aorta by the device. The disks of the device appeared to protrude posteriorly into the visceral pericardium, without evidence of active extravasation of blood into the pericardial space on color Doppler imaging.

Dr. Baliyan: Gated cardiac CTA (Figure 3D, 3E, and 3F and Videos 5 and 6) revealed a moderate hemorrhagic pericardial effusion. The Amplatzer septal occluder device appeared unchanged in position relative to the previous CTA. The device again abutted the aortic root anteriorly and the atrial wall posteriorly. However, there was no evidence of active extravasation of contrast material into the pericardial space.

Discussion of Surgical Management

Dr. Arminder S. Jassar: I was asked to evaluate this patient for recurrent hemorrhagic pericardial effusion and possible device erosion. I elected to surgically remove the Amplatzer septal occluder device because erosion cannot be corrected with a percutaneous approach. Intraoperatively, a moderate hemorrhagic pericardial effusion was identified and drained. The device was visualized and carefully excised. There was an area of erosion of the device into the epicardial fat on the lateral aspect of the device close to the right superior pulmonary vein, although no transmural defect could be identified. The endocardia of the left and right atria were reapproximated to buttress the edges of the septal defect. A patch of autologous pericardium was sewn to the edges of the defect. The right atrium was closed, and the patient was weaned from cardiopulmonary bypass. There was no residual shunt visualized on postoperative TEE. The patient did well after the surgical procedure and was discharged home on postoperative day 4.

Pathological Evaluation

Dr. R. Neal Smith: The lower right outside portion of the ASD rim consisted of yellow pericardial fat, which indicated that the device had eroded through the pericardium (Figure 4).

Pathological Diagnosis

Erosion of an Amplatzer septal occluder device through the pericardium.

Discussion of Management

Dr. Ignacio Inglessis: For any patients undergoing percutaneous transcatheter closure of ASDs, our usual practice is to perform a clinical evaluation, ECG, and echocardiography before hospital discharge, at 1 month and 6 months after discharge, annually for 5 years, and every 1 to 2 years thereafter for life. If any new symptoms develop that are suggestive of erosion or impending erosion, such as chest pain or pericardial symptoms, immediate follow-up with a cardiologist is recommended. This patient’s prompt attention to her symptoms afforded diagnostic evaluation and treatment before the hemorrhagic pericardial effusion exerted additional deleterious effects.

Device erosion is a very rare but serious complication of percutaneous transcatheter closure of ASDs. The true incidence of device erosion is unknown; however, it has been estimated to occur after 0.05 to 0.3% of all procedures.^11,14

The following risk factors have been associated with an increased risk of device erosion: deficient anterior (aortic) and superior (superior vena cava) tissue rims abutting the ASD (<5 mm thick), an oversized device (defined as a device measuring >5 mm larger than the ASD diameter or the presence of a higher ratio of patient weight to device size or a higher ratio of patient age to device size), and the use of aggressive balloon sizing for device selection (an increased difference in size between the balloon and the static defect).^10,14 Device erosion can occur in both pediatric and adult patients. The median time from device placement to device erosion is 14 days, with 30% of cases occurring within 1 day after the procedure and only 5% of cases occurring beyond 5 years after the procedure. By far, the most common clinical presentation is hemopericardium or cardiac tamponade, with a minority of patients presenting with a fistula between the atrium and the aorta without pericardial fluid accumulation. Device erosion can be fatal; death occurs within the first day after diagnosis in half of affected patients and is more common in adults or in patients with an aortoatrial fistula.

Surgical intervention is the standard of care for patients presenting with device erosion after percutaneous transcatheter closure of any cardiac defect and should be performed urgently in patients with cardiac tamponade. The procedure usually involves device resection and patching of the erosion site. Nevertheless, conservative management, with close observation after pericardiocentesis, has been reported to be successful in a small number of patients.

The very late occurrence of device erosion observed in this patient (14 years after the procedure) is rare. The clinically significant weight loss before her presentation, with a resulting decrease in atrial size, may have increased the risk of device erosion by approximating the device to the atrial wall.

Follow-up

Dr. Patel: In the year after the patient’s corrective surgical procedure, she has done well, with resolution of her chest pain and dyspnea. Additional testing for alternative causes of the recurrent hemorrhagic pericardial effusion has been unrevealing. Outpatient TTE performed 4, 12, and 24 months after her surgery revealed no pericardial fluid.

Final Diagnosis

Amplatzer septal occluder device erosion.

[1] Presented atThis case was presented at the Medicine Case Conference.
[2] Financial disclosureDisclosure forms provided by the authors are available with the full text of this article at NEJM.org.

[1] Presented atThis case was presented at the Medicine Case Conference.

[2] Financial disclosureDisclosure forms provided by the authors are available with the full text of this article at NEJM.org.

We thank Dr. Muthiah Vaduganathan for his assistance in writing the case presentation.

We thank Dr. Muthiah Vaduganathan for his assistance in writing the case presentation.

Disclosure Forms

Disclosure Forms

References

1

Larrieu AJ, Tyers GF, Williams EH, Derrick JR. Recent experience with tuberculous pericarditis. Ann Thorac Surg 1980;29:464-468.7377888

2

Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol 1988;11:724-728.3351140

3

Strang JI, Kakaza HH, Gibson DG, et al. Controlled clinical trial of complete open surgical drainage and of prednisolone in treatment of tuberculous pericardial effusion in Transkei. Lancet 1988;2:759-764.2901610

4

Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608-3616.16330703

5

Reuter H, Burgess L, van Vuuren W, Doubell A. Diagnosing tuberculous pericarditis. QJM 2006;99:827-839.17121764

6

Saab J, Hoda RS, Narula N, et al. Diagnostic yield of cytopathology in evaluating pericardial effusions: clinicopathologic analysis of 419 specimens. Cancer Cytopathol 2017;125:128-137.28207201

7

Wilkes JD, Fidias P, Vaickus L, Perez RP. Malignancy-related pericardial effusion: 127 cases from the Roswell Park Cancer Institute. Cancer 1995;76:1377-1387.8620412

8

Wiener HG, Kristensen IB, Haubek A, Kristensen B, Baandrup U. The diagnostic value of pericardial cytology: an analysis of 95 cases. Acta Cytol 1991;35:149-153.2028688

9

Meyers DG, Meyers RE, Prendergast TW. The usefulness of diagnostic tests on pericardial fluid. Chest 1997;111:1213-1221.9149572

10

Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv 2004;63:496-502.15558755

11

Moore J, Hegde S, El-Said H, et al. Transcatheter device closure of atrial septal defects: a safety review. JACC Cardiovasc Interv 2013;6:433-442.23702008

12

Abed HS, Wittert GA, Leong DP, et al. Effect of weight reduction and cardiometabolic risk factor management on symptom burden and severity in patients with atrial fibrillation: a randomized clinical trial. JAMA 2013;310:2050-2060.24240932

13

Tuluce K, Kara C, Tuluce SY, et al. Early reverse cardiac remodeling effect of laparoscopic sleeve gastrectomy. Obes Surg 2017;27:364-375.27431666

14

McElhinney DB, Quartermain MD, Kenny D, Alboliras E, Amin Z. Relative risk factors for cardiac erosion following transcatheter closure of atrial septal defects: a case-control study. Circulation 2016;133:1738-1746.27002094

References

References

1

Larrieu AJ, Tyers GF, Williams EH, Derrick JR. Recent experience with tuberculous pericarditis. Ann Thorac Surg 1980;29:464-468.7377888

2

Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol 1988;11:724-728.3351140

3

Strang JI, Kakaza HH, Gibson DG, et al. Controlled clinical trial of complete open surgical drainage and of prednisolone in treatment of tuberculous pericardial effusion in Transkei. Lancet 1988;2:759-764.2901610

4

Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608-3616.16330703

5

Reuter H, Burgess L, van Vuuren W, Doubell A. Diagnosing tuberculous pericarditis. QJM 2006;99:827-839.17121764

6

Saab J, Hoda RS, Narula N, et al. Diagnostic yield of cytopathology in evaluating pericardial effusions: clinicopathologic analysis of 419 specimens. Cancer Cytopathol 2017;125:128-137.28207201

7

Wilkes JD, Fidias P, Vaickus L, Perez RP. Malignancy-related pericardial effusion: 127 cases from the Roswell Park Cancer Institute. Cancer 1995;76:1377-1387.8620412

8

Wiener HG, Kristensen IB, Haubek A, Kristensen B, Baandrup U. The diagnostic value of pericardial cytology: an analysis of 95 cases. Acta Cytol 1991;35:149-153.2028688

9

Meyers DG, Meyers RE, Prendergast TW. The usefulness of diagnostic tests on pericardial fluid. Chest 1997;111:1213-1221.9149572

10

Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv 2004;63:496-502.15558755

11

Moore J, Hegde S, El-Said H, et al. Transcatheter device closure of atrial septal defects: a safety review. JACC Cardiovasc Interv 2013;6:433-442.23702008

12

Abed HS, Wittert GA, Leong DP, et al. Effect of weight reduction and cardiometabolic risk factor management on symptom burden and severity in patients with atrial fibrillation: a randomized clinical trial. JAMA 2013;310:2050-2060.24240932

13

Tuluce K, Kara C, Tuluce SY, et al. Early reverse cardiac remodeling effect of laparoscopic sleeve gastrectomy. Obes Surg 2017;27:364-375.27431666

14

McElhinney DB, Quartermain MD, Kenny D, Alboliras E, Amin Z. Relative risk factors for cardiac erosion following transcatheter closure of atrial septal defects: a case-control study. Circulation 2016;133:1738-1746.27002094