In the UK, pericardectomy is performed at various heart and chest hospitals. Notable centres include Royal Brompton Hospital London, Liverpool Heart and Chest Hospital and Royal Papworth Hospital. Pericardectomy is rarely performed outside of specialist centres in the UK and therefore anaesthetic trainees may have limited experience of this procedure. Those trainees who as part of OOPE or for altruistic reason, plan to go abroad and gain experience in this procedure, are advised to take a look at this article.
Sher Mohammad and anaesthetic colleagues from Peshawar (referral centre not only for residents but for the people from across the border in Afghanistan), regularly perform cardiac procedures and share their experience of pericardectomy.
Erstwhile notable clinicians who mentioned pericardium and related pathologies
- The sac around the heart was known to Hippocrates, but it was Giovanni Morgagni in 1700s, who first associated the symptoms of heart failure with a thickened pericardium on autopsy [1].
- In the first half of 1800s, Jean Nicolas Corvisart and Sir Richard Bright mentioned the relationship between constrictive pericarditis and advanced renal disease. In the 1870s, Richard Volkmann coined the term ‘constrictive pericarditis’ and postulated that thickened pericardium contributed directly to decrease pump performance. Nuanced physical findings were later mentioned by Adolph Kussmaul, Sir William Osler and Hermann Pick.
- Dr.Sauerbruch resected a portion of pericardium in 1913 and the first pericardiectomy is generally attributed to Dr.Wilhelm Rehn in 1920. In the 1950s, invasive haemodynamic features of constrictive pericarditis were described and in 1955, William Dressler reported a case series documenting successful treatment of pericarditis with aspirin and steroids [2-4]. Soon, indomethacin and colchicine were added to the treatment regime [4-7].
- In 1979, echocardiographic criteria for constrictive pericarditis were described and by the end of 20th century, both cardiac MR and cardiac computed tomography emerged as complementary imaging modalities [8-13].
- In 2005, clinical trials of combination of colchicine with conventional therapy for managing acute and recurrent pericarditis [14-18] were studied. In 2009, initial reports of successful treatment of autoimmune-associated recurrent pericarditis using IL-1 receptor antagonist anakinra [21-23].
Anatomy of the pericardium
The normal pericardium is situated in the anterior mediastinum surrounding the heart and proximal parts of great vessels. It consists of an outer fibrous layer and an inner serous layer. The fibrous pericardium contains a dense network of collagen fibres that stabilise the position of the heart and associated vessels within the mediastinum.
The serous pericardium is a two-layered membrane composed of an outer parietal layer and an inner visceral layer. The visceral layer is also known as the epicardium. The potential, fluid-filled space between these two serous layers is the pericardial cavity. In normal states, approximately 15-50 ml of fluid is contained within the pericardial sac. This fluid is produced by visceral mesothelial cells and is drained from the pericardial sac via lymphatics into the right side of the heart.
The pericardial fluid minimises friction exerted on pericardium from normal heart movements during the cardiac cycle and serves to balance hydrostatic pressures over the surface of the heart.
Normal pericardial thickness is 1-2 mm (the thickness of the pericardium before surgery was 7.42±2.31mm and after surgery 5.20±2.15 mm in a Chines study).
Diagram showing the Anatomy of the Heart and Pericardium (Courtesy of Dr. Arshad Khan who drew and contributed the picture)
Physiology of the pericardium
Although normal cardiovascular function can occur in the absence of pericardium, it does have certain physiological benefits.
- The pericardium stabilises the heart in its anatomic position and limits excessive movement within the chest cavity.
- The pressure exerted on the cardiac chambers by the pressure within the intrapericardial space prevents acute distension of the chambers and helps optimise atrial and ventricular coupling and filling.
- The pericardial sac serves as a physical barrier against the spread of infection or cancer within the mediastinum.
- Prostaglandins are secreted by mesothelial and endothelial cells of the pericardium that regulate autonomic cardiac reflexes, myocardial contractile function, and influence epicardial coronary artery tone.
Prevalence of constrictive pericarditis
In the developed world, pericarditis is often idiopathic in origin or occurs secondary to cardiac surgery or radiotherapy.
In Asia and Africa, tuberculosis continues to be the most common cause of constrictive pericarditis. The true incidence of tuberculous constrictive pericarditis in the developing world is, in all likelihood, underestimated owing to the challenges in establishing a definite diagnosis of TB during effusive stage of the disease.
Uncommon causes include rheumatological diseases, malignancy and trauma.
Causes of constrictive pericarditis
It is unknown why constrictive pericarditis appears to be three times more common in males than females. Multiple aetiologies of constrictive pericarditis include tuberculosis, infection(viral), postoperative haemorrhage, rheumatic disease, trauma, tumours, mediastinal radiotherapy and idiopathy [25,26]. In rare instances, constrictive pericarditis may occur after sclerotherapy for oesophageal varices.
See table-1 for factors causing constriction of the PERICARDIUM
Table-1: Factors causing Constrictive Pericarditis
Constrictive pericarditis and COVID-19
With the spread of the pandemic COVID-19 and SARS-CoV-2 vaccines, cardiovascular involvement, has been reported. The pericardial disease primarily associated with these situations is known to be acute pericarditis. [27,28] However, it was found in >10 case reports of constrictive pericarditis following the diagnosis of COVID-19 or the administration of mRNA-vaccine, [29,30] with a temporal relationship ranging from 4 days to 7 months, and without predilection for age groups. All cases reported an effusive–constrictive pericarditis, suggesting an acute-on-chronic or subacute mechanism, except for two cases, in which a transient constriction was described. In more than half of cases, a cardiac comorbidity was present, with a predominance of arterial hypertension.
Constrictive Pericarditis/Pericardial tethering
In normal conditions, the two layers of the pericardium slide over each other during the cardiac cycle. When pericardial adherence is present, due to fibrosis or calcification, the independent motion of the visceral and parietal pericardium is lost.
Constrictive pericarditis is a potentially curable cause of diastolic heart failure. The scarred, and non-compliant pericardium causes restraint to the early diastolic ventricular filling, resulting in equalisation of intracardiac diastolic filling pressures, producing the so-called “single diastolic chamber”. Ventricular filling pressures become markedly elevated and predominantly right heart failure ensues. The two hallmark physiological features of constrictive pericarditis are enhanced ventricular interdependence and dissociation of intrathoracic and intracardiac pressures.
Clinical Presentation
Signs and symptoms are usually non-specific and mimic right ventricular failure making diagnosis difficult [31, 32, 33, 34,35]. Tachycardia is the predominant sign because of the fixed stroke volume state. Arrhythmias, especially atrial fibrillation, are not uncommon. Fluid overload ranging from peripheral oedema to anasarca is a usual finding. This is due to venous hypertension which is often worsened by protein-losing enteropathy in decompensated disease. Patients may have associated cachexia, indicating a chronic and insidious disease process. Decreased cardiac output with shortness of breath and fatiguability are almost always elicited on thorough enquiry. Table-2 explains a succinct summary of clinical presentation.
Table-2: Clinical features of Constrictive Pericarditis, A , B , C
*Friedreich’s sign is the exaggerated drop in diastolic central venous pressure seen in constrictive pericarditis (particularly with a stiff calcified pericardium) and manifested as abrupt collapse of the neck veins or marked descent of the central venous pressure waveform.
Auscultatory findings in constrictive pericarditis include a pericardial knock, which is a high-pitched sound occurring in early diastole before the third heart sound. It indicates that the ventricular filling at the end of the early diastole does not happen.
Kussmaul’s sign is a paradoxical increase in jugular venous pressure on inspiration. It reflects an increase in right atrial preload from an increase in intra-abdominal pressure during inspiration. The increase in preload cannot be accommodated because of the fixed pericardial constriction, and the back pressure is transmitted to the systemic venous system. This is detected clinically as increased pressure in the jugular vein.
Special investigations
The diagnosis of constrictive pericarditis remains challenging, and the clinical picture of unexplained venous congestion should be clarified with multiple imaging modalities to ensure accurate and efficient diagnosis [31, 32, 33, 34, 35].
ECG may show low voltages, non-specific upward sloping ST-T wave changes, atrial fibrillation and P mitrale, indicating chronic atrial hypertension.
CT scan and MRI are both useful to confirm pericardial thickening and calcification [31, 35]. CT scan can delineate and quantify the degree of calcification based on CT scan score, and MRI has a 93% accuracy for differentiating constrictive pericarditis from restrictive cardiomyopathy based on a pericardial thickness of >4 mm.
The gold standard for diagnosis is cardiac catheterisation with analysis of intra-cavitary pressure curves, which are high and, in end-diastole, equal in all chambers.
Complications
- Pulmonary hypertension
- Hepatomegaly and liver dysfunction
- Metabolic acidosis
- Hypoxia
- Shock
- Death
Treatment Options for Constrictive Pericarditis
If there is evidence of active inflammation, a trial of anti-inflammatory medications (NSAIDs, colchicine) is recommended before surgery. Tuberculous pericarditis should be treated with anti-TB medications for two months prior to surgery.
A subset of patients may have spontaneous resolution or may respond to medical management, and they are said to have transient constrictive pericarditis. Patients with newly diagnosed constrictive pericarditis who are haemodynamically stable and do not have stigmas of chronic constriction may be treated with anti-inflammatory agents for up to three months with close monitoring. If these patients develop signs of chronic constriction and haemodynamic instability, they should undergo prompt surgery.
While drug therapy is often used to relieve the symptoms, pericardiectomy is the only way to restore normal cardiac physiology in patients with constrictive pericarditis [37,38]. Early pericardiectomy improves the overall clinical outlook and can prevent the development of cardiac cachexia, severe liver dysfunction and myocardial atrophy. A recent study indicates that pericardectomy has a high safety margin and favourable clinical outcomes for the treatment of constrictive pericarditis [39].
Diuretics have been used to reduce oedema or elevated venous pressure before surgery or for palliative control of symptoms in patients who cannot be treated surgically.
If a decision is made to proceed with pericardectomy, effort should be made to remove as much of the pericardium as possible. Extensive penetration of the myocardium by fibrosis and calcification is associated with poor prognosis. Operative mortality ranges from 10% to 20%.
Anaesthetic Management for Surgeries other than pericardectomy
Anaesthetic management of patients with constrictive pericarditis varies when undergoing non-cardiac surgery. Peripheral surgery on limbs for plastic and orthopaedic procedures are better carried out under plexus blocks and sedation. Central neuraxial blockade could result in profound hypotension and is better avoided. Other surgical procedures can be carried out under GA with patient spontaneously breathing (IPPV interferes with haemodynamic).
Surgery for Pericardectomy
Pericardectomy is indicated for chronic or irreversible constrictive pericarditis, refractory recurrent pericarditis despite optimal treatment, or partial agenesis of the pericardium with a complication (herniation of heart).
The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved[40] ,with mortality rates of 6% or higher in major referral centres[41].
A poor outcome is almost always the result after a pericardectomy is performed for constrictive pericarditis whose origin was radiation-induced, furthermore some patients may develop heart failure post-operatively[42].
Anaesthetic Management for Pericardectomy
A multidisciplinary approach involving cardiologist, surgeon, anaesthetist and critical care specialist is needed to provide optimal peri-operative care and a good outcome. Diagnostic tools, especially the role of echocardiography, that add in the diagnosis and management of these high-risk patients is of paramount importance.
Providing safe anaesthesia care for these patients is challenging because of their primary pericardial pathology and significant co-morbidities affecting other organ systems. A thorough understanding of the pathophysiology of the pericarditis and its effect on overall haemodynamic variables is necessary before formulating a care plan. The anaesthetist should be well drilled to tackle a life-threatening catastrophe.
Situational awareness and vigilance are extremely important about:
- CVS Collapse can happen at induction (BIS monitor advisable to titrate the dose of anaesthesia and take precautions to minimise myocardial depression and bradycardia i.e. because of fixed stroke volume state).
- Bronchial blocker is preferred over double lumen tube.
- Mechanical ventilation may increase right ventricular afterload and decrease forward flow through the right ventricular outflow tract. This will in turn increase right ventricular end-diastolic pressures, worsen interventricular septal shift, further compromise left ventricular filling and negatively impact cardiac output. With an appropriate ventilatory strategy, however, the effect of mechanical ventilation can be minimised. The lowest possible inspiratory pressures and PEEP to maintain minute volume and oxygenation should be used [42].
- Surgical handling may cause arrhythmias.
- Surgeon may make a hole in the heart while removing fibrotic tissues from myocardium.
- Perioperative bleeding can happen and may need re-exploration. Because of liver dysfunction, vitamin-K may be needed prior to surgery to improve the synthesis of coagulation factors. Tranexamic acid can also reduce the bleeding. Transfusion triggers and the need for intraoperative administration of blood and clotting factors should be discussed and decided by the multidisciplinary team before start of procedure.
- Post-op ventilation for 12- 24 hours is advisable.
- Low cardiac output syndrome identified and treated.
See Table-3 shows a succinct summary of anaesthetic management for Pericardectomy.
Table-3 explains A……..Z anaesthetic approach for pericardectomy
*Fluid management
When the atrophied LV is freed off the restraint of the scarred pericardium, it can easily be overwhelmed with sudden increase in volume return from the dilated venous system. Additionally acute fluid shift can occur as the venous pressure drops and interstitial fluid is pulled back into the systemic circulation. Meticulous intraoperative fluid management is critical to the overall success of the procedure. Minimizing intraoperative fluid and using diuretics from the beginning of the surgery are effective. This way low CO syndrome could be avoided.
**Inotropes such as adrenaline (fast HR preferred around 100 beats per minute, allows the atrophic heart to recover under an affordable load, β blockers and calcium antagonists if needed should be used judiciously).
*** The patient may need to go on CPB
Conclusion and future
This complex clinical syndrome has been known to clinicians for centuries but the diagnosis remains challenging both to identify and then manage. The perioperative management is challenging not only to the attending anaesthetist but also the surgeons, nursing staff and critical care specialists. Anticipation and vigilance for post-op complications is extremely important.
Recent advances in cardiac imaging along with an expanding armamentarium of treatment options have improved the quality and precision of care for patients with constrictive pericarditis.
New developments in treating constrictive pericarditis include medications like IL-1 blockers [44] in conjunction with colchicine. Furthermore, imaging-guided therapy [45], particularly using cardiac magnetic resonance imaging (CMR), is increasingly used to assess inflammation and guide the treatment.
Robot assisted pericardiectomies have been undertaken in some centres. The minimally invasive robotic approach to pericardiectomy offers advantages in visualisation and complete removal of the constricting pericardium [46].
Conflict of Interest Non-declared
Diagram and Illustrations: Author’s own
Authors and Contributors:
Dr.Sher Mohammad1,Dr.Mujahid Ul Islam2,Dr.Muhammad Sheharyar Ashraf3, Dr.Parhaizgar Khan4 , Dr.Ijaz Hussain5, Dr.Arshad Khan6, Dr.Salman Yahya7, Dr.Emad Abo Ebeid8
1.Consultant Anaesthetist(retired), STH NHS FT Sheffield
2.Professor of Anaesthesia, Rehman Medical College, Peshawar
3.Assistant Professor, Anaesthesia and ICU, Lady Reading Hospital. Peshawar
4.Professor of Anaesthesia, Pak International Medical College Peshawar
5.Resident Physician, Lady Reading Hospital Peshawar
6.Clinical Research Fellow (Pulmonary Hypertension), Royal Hallamshire Hospital,Sheffield
7.Consultant Anaesthetist(locum), York and Scarborough Teaching Hospitals NHS FT
8.Consultant Anaesthetist(locum), Airdale General Hospitals, Keighley
Correspondence Address: smyousafzai@doctors.org.uk
References
1. Morgagani GB. De sedibus et causis morborum per anatomen indagatis. Venice: Remondini; 1761.
2. Lin TK, AnacheM.Rightheart pressurepatternsinconstrictive pericarditis: mechanism of formation and significance. Am Heart J 1956;51:340–50.
3. Yu PN, Lovejoy FW, Joos HA, Nye RE, Mahoney EB. Right auricular and ventricular pressure patterns in constrictive pericarditis. Circulation 1953;7:102–7.
4. Dressler W. Idiopathic recurrent pericarditis. Am J Med 1955;18:591–601.
5. McGinn JT, Rosati M, McGinn TG. Indomethacin in treatment of pericarditis. N Y State J Med 1970;70:1783–9.
6. McGinn JT. Indomethacin for pericarditis. N Engl J Med 1968;279:436.
7.Zemer D, Cabili S, Revach M, Shahin N. Constrictive pericarditis in familial Mediter ranean fever. Isr J Med Sci 1977;13:55–8.
8. Vaitkus PT, Kussmaul WG. Constrictive pericarditis versus restrictive cardio myopathy: a reappraisal and update of diagnostic criteria. Am Heart J 1991; 122:1431–41.
9. Sechtem U, Tscholakoff D, Higgins CB. MRI of the abnormal pericardium. AJR Am J Roentgenol 1986;147:245–52.
10. Shimamoto H, Okamoto M, Sakura E, Yokote Y, Amioka H, Tsuchioka Y, et al. Complementary diagnosis by Doppler echocardiography and CT in a case with con strictive pericarditis. Jap J Clin Radiol 1986;31:1139–42
11. Rienmuller R, DoppmanJL, Lissner J, Kemkes BM, Strauer BE. Constrictive pericardial disease: prognostic significance of a nonvisualized left ventricular wall. Radiology 1985;156:753–5.
12, Gouliamos A, Andreou J, Steriotis J, Kalovidouris A, Vlahos L, Papavassiliou C. Detec tion of pericardial heart disease by computed tomography. Clin Radiol 1984;35: 397–400.
13. Shubrooks SJ. Echocardiographic features of constrictive pericarditis and echo eval uation of septal myectomy in IHSS. Circulation 1979;60:215–6.
14. Imazio M, Brucato A, Cemin R, Ferrua S, Maggiolini S, Beqaraj F, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med 2013;369:1522–8.
15. Imazio M, Brucato A, Cemin R, Ferrua S, Belli R, Maestroni S, et al. Colchicine for recur rent pericarditis (CORP): a randomized trial. Ann Intern Med 2011;155:409–14.
16. Imazio M,Bobbio M, CecchiE, DemarieD,Demichelis B,Pomari F, etal. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation 2005;112:2012–6.
17. Imazio M, Bobbio M, Cecchi E, Demarie D, Pomari F, Moratti M, et al. Colchicine as f irst-choice therapy for recurrent pericarditis: results of the CORE (COLchicine for REcurrent pericarditis) trial. Arch Intern Med 2005;165:1987–91.
18. Imazio M, Belli R, Brucato A, Cemin R, Ferrua S, Beqaraj F, et al. Efficacy and safety of colchicine for treatment of multiple recurrences of pericarditis (CORP-2): a multi centre, double-blind, placebo-controlled, randomised trial. Lancet 2014;383:2232–7.
19. Chae JJ, Wood G, Masters SL, Richard K, Park G, Smith BJ, et al. The B30.2 domain of pyrin, the familial mediterranean fever protein, interacts directly with caspase-1 to modulate IL-1β production. Proc Natl Acad Sci U S A 2006;103:9982–7.
20.ShohamNG,CentolaM,MansfieldE,HullKM,WoodG,WiseCA,etal.Pyrinbinds the PSTPIP1/CD2BP1 protein,definingfamilial Mediterraneanfever and PAPA syndrome as disorders in the same pathway. Proc Natl Acad Sci U S A 2003;100:13501–6.
21. Picco P, Brisca G, Traverso F, Loy A, Gattorno M, Martini A. Successful treatment of idiopathic recurrent pericarditis in children with interleukin-1β receptor antagonist (anakinra): an unrecognized autoinflammatory disease? Arthritis Rheum 2009;60: 264–8.
22. Cantarini L, Lucherini OM, Cimaz R, Galeazzi M. Recurrent pericarditis caused by a rare mutation in the TNFRSF1A gene and with excellent response to anakinra treatment. Clin Exp Rheumatol 2010 ;28:802.
23. Scott IC, Hajela V, Hawkins PN, Lachmann HJ. A case series and systematic literature review of anakinra and immunosuppression in idiopathic recurrent pericarditis. J Cardiol Cases 2011;4:e93–7.
24. Brucato A, Imazio M, Gattorno M, Lazaros G, Maestroni S, Carraro M, et al. Effect of anakinra on recurrent pericarditis among patients with colchicine resistance and corticosteroid dependence: the AIRTRIP randomized clinical trial. JAMA 2016;316: 1906–12.
25.Devasia T, Kareem H, Prasad R, Razak A. Crescent-shaped extensive pericardial calcification. BMJ Case Rep. 2014;2014:bcr2014205334.
26.Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: the Task Force for the diagnosis and management of Pericardial Diseases of the European Society of Cardiology (ESC)endorsed by: the European Association for Cardio-Thoracic surgery (EACTS). Eur Heart J. 2015;36:2921–64.
27.Diaz-Arocutipa C, Saucedo-Chinchay J, Imazio M. Pericarditis in patients with COVID-19:A systematic review. J Cardiovasc Med (Hagerstown) 2021;22:693–700. doi: 10.2459/JCM.0000000000001202. [DOI] [PubMed] [Google Scholar]
28.Collini V, Imazio M, De Biasio M, Sinagra G. Coronavirus disease 2019 vaccination-related pericarditis:A single tertiary-center experience. J Cardiovasc Med (Hagerstown) 2022;23:779–83. doi: 10.2459/JCM.0000000000001365. [DOI] [PMC free article] [PubMed] [Google Scholar]
29.Diana D, Cardillo I, Polizzi V, Musumeci F. 544 Two cases of constrictive pericarditis temporally associated with mRNA-1273 COVID-19 vaccination. Eur Heart J Suppl. 2021;23 suab142.014. [doi:10.1093/eurheartj/suab142.014] [Google Scholar]
30.Yousafzai Ok, Raza A, Zaman Mo, Silber Dj, Balani B, Hollenberg Sm, et al. A rare case of constrictive pericarditis following COVID-19 Exposure And Vaccination. J Am Coll Cardiol. 2022;79:2342. [Google Scholar]
31.Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Current Problems in Cardiology. 2004;29(9):503-567
32.Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2015;36(42):2921-2964
33.Grocott HP, Gulati H, Srinathan S, Mackensen GB. Anesthesia and the patient with pericardial disease. Canadian Journal of Anesthesia/Journal canadien d’anesthésie. 2011;58(10):952
34.Grecu L. Cardiac tamponade. International Anesthesiology Clinics. 2012;50(2):59-77
35.Verhaert D, Gabriel RS, Johnston D, Lytle BW, Desai MY, Klein AL. The role of multimodality imaging in the management of pericardial disease. Circulation. Cardiovascular Imaging. 2010;3(3):333-343
36 . Nikolaus Friedreich.
37.Murashita T, Schaff HV, Daly RC, et al. Experience with pericardiectomy for constrictive Pericarditis over eight decades. Ann Thorac Surg. 2017;104:742–50.
38.Di Lazzaro D, Di Bella I, Pasquino S, Berti V, Da Col U. Pericardiectomy for constrictive pericarditis. Multimed Man Cardiothorac Surg. 2020;2020.
39.Nachum E, Sternik L, Kassif Y, et al. Surgical Pericardiectomy for Constrictive Pericarditis: a single Tertiary Center Experience. Thorac Cardiovasc Surg. 2020;68:730–6.
40 Cinar B, Enc Y, Goksel O, Cimen S, Ketenci B, Teskin O, Kutlu H, Eren E (2006). “Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy”. Int J Tuberc Lung Dis. 10 (6): 701–6. PMID 16776460.
41^ Chowdhury UK, Subramaniam GK, Kumar AS, Airan B, Singh R, Talwar S, Seth S, Mishra PK, Pradeep KK, Sathia S, Venugopal P (2006). “Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques”. Ann Thorac Surg. 81 (2): 522–9. doi:10.1016/j.athoracsur.2005.08.009. PMID 16427843.
42^ Greenberg, Barry H. (2007). Congestive heart failure (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. p. 410. ISBN 978-0-7817-6285-4. Archived from the original on 12 January 2023. Retrieved 21 September 2015.
43.O’Connor CJ, Tuman KJ. The intraoperative management of patients with pericardial tamponade. Anesthesiology Clinics. 2010;28(1, 1):87-96
44.S.Lo Presti, T.K.Elajami, R.Reyaldeen, C.Anthony, M.Imazio, A.L.Klein Emerging therapies for recurrent pericarditis: IL-1 inhibitors J Am Heart Assoc,10(19),article e021685
45. S.Kumar,S.Khubber,R.Reyaldeen,et al. Advances in imaging and targeted therapies for recurrent pericarditis:a review JAMA Cardiol,7(9)(2022),pp.975-985.10.1001/jamacardio.2022.2584
46.Jett GK,Nguyen AB,Squires JJ,Robinson K, Shih E. Total Robotic Pericardiectomy for Constrictive Pericarditis.December 2023, Doi:10.25373/ctsnet.24747234
