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24 Surgery forAtrial Fibrillation
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approach can be combined with various catheter ablation techniques resulting in a
“hybrid” approach [7, 8]. See Fig.24.2.
Management oftheLeft Atrial Appendage (LAA)
In patients with AF, the most dreaded complication is stroke as a result of thrombus
formation in the heart due to stasis of blood from the abnormal rhythm. In AF, it has
been well established that the LA appendage (LAA) is the main source of thromboembolism that can result in stroke. This is the reason for “occlusion” or ligation of
the LAA in patients with AF undergoing cardiac surgery. This is accomplished
through a variety of surgical techniques including amputation of the LAA and
suture closure, stapler occlusion, double-layer suture closure from inside the left
atrium, or epicardial occlusion with an FDA-approved device. In a recent randomized trial, patients with atrial brillation undergoing cardiac surgery were randomized to either have LAA occlusion or not. This trial of over 4000 patients showed a
lower risk of ischemic stroke with occlusion compared to no LAA occlusion [9].
References
1. Centers for Disease Control and Prevention, National Center for Health Statistics. In: About
multiple cause of death, 1999–2019. CDC WONDER online database website. Atlanta, GA:
Centers for Disease Control and Prevention; 2019.
2. Cohn LH.In: Cohn LH, editor. Cardiac surgery in the adult. 4th ed. McGraw-Hill Medical; 2012.
3. Benjamin EJ, Muntner P, Alonso A, Bittencourt MS, Callaway CW, Carson AP, etal. Heart
disease and stroke statistics—2019 update: a report from the American Heart Association.
Circulation. 2019;139(10):e56–528.
4. Ferguson TB Jr, Cox JL.Surgery for atrial brillation. In: Zipes DP, Jalife J, editors. cardiac
electrophysiology: from cell to bedside. 2nd ed. Philadelphia: Saunders; 1995. p.1567.
5. Cox JL.The surgical treatment of atrial brillation. IV.Surgical technique. J Thorac Cardiovasc
Surg. 1991;101:584.
6. Cox JL, Boineau JP, Schuessler RB, etal. Electrophysiologic basis, surgical development, and
clinical results of the maze procedure for atrial utter and atrial brillation. Adv Card Surg.
1995;6:1.
7. Bhadwar V, Rankin JS, Damiano R Jr, etal. The Society of Thoracic Surgeons 2017 clinical practice guidelines for the surgical treatment of atrial brillation. Ann Thorac Surg.
2017;103:329–41.
8. Brescia AA, Louis C.TSRA review of cardiothoracic surgery. 3rd ed. Independently published; 2021.
9. Whitlock RP, Belley-Cote EP, Paparella D, etal. Left atrial appendage occlusion during cardiac
surgery to prevent stroke. N Engl J Med. 2021;384(22):2081–91.
Chapter 25
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Pericardial Disease
AdamPaine, AkashPremkumar, andThoralfM.Sundt
Learning Objectives
• Natural history and etiology.
• Diagnostic criteria.
• Distinguishing between constrictive pericardial disease vs restrictive
cardiomyopathy.
• Indications for pericardiectomy.
• Operative technique.
Anatomy
There are two layers to the pericardium, the visceral and parietal, folded onto one
another creating a closed space between which there is normally a small amount of
serous uid (Fig.25.1) [1]. The visceral layer, more commonly referred to as the
epicardium, is normally thin and translucent, although it becomes markedly thickened in the setting of pericarditis. The parietal pericardium is more substantial, normally 1mm thick, and what is more commonly referred to as “the pericardium.”
The cephalad border of the parietal pericardium is its reection onto the superior
vena cava (SVC), aorta, and pulmonary artery (Fig.25.2). The caudal border is
opposed to the surface of the diaphragm. The lateral borders abut the bilateral pleural spaces with the pericardium reected around the four pulmonary veins. The
anterior border abuts the sternum and the posterior border abuts the posterior
A. Paine (*) · A. Premkumar · T. M. Sundt
Division of Cardiac Surgery, Massachusetts General Hospital, Boston, MA, USA
e-mail: apaine@partners.org; apremkumar@mgh.harvard.edu; tsundt@mgh.harvard.edu
Switzerland AG 2024
J. P. Bloom, T. M. Sundt (eds.), Cardiac Surgery Clerkship, Contemporary
Surgical Clerkships, https://doi.org/10.1007/978-3-031-41301-8_25
289© The Author(s), under exclusive license to Springer Nature
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A. Paine et al.
Pericardial
cavity
Endocardium
Myocardium
Fig. 25.1 Layers of the pericardium from the outermost brous pericardium with its adherent
inner parietal serous pericardium that lines the pericardial cavity and is in continuity with the visceral serous pericardium, synonymous with the epicardium
Fibrous
pericardium
Parietal layer
of serous
pericardium
Epicardium
(viceral layer
of serous
pericardium)
mediastinal structures including the descending thoracic aorta and the esophagus.
There are two potential spaces within the pericardial sac: the transverse sinus, which
is posterior to the aorta and the main pulmonary artery and anterior to the parietal
pericardium, and the oblique sinus, which is posterior to the left atrium, anterior to
the parietal pericardium, and anked by the four pulmonary veins. The transverse
sinus is of note to the cardiac surgeon as it can be used as a tunnel for a right internal
thoracic artery bypass graft to the lateral wall of the heart (see Chap. 11—
Management of Coronary Artery Disease).
Right common
Left internal jugular
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carotid artery
Right subclavian
artery
Innominate artery
Right
brachiocephalic
vein
Superior vena
cava
Transverse sinus
of pericardium
Right pulmonary
veins
Inferior vena cava
Fig. 25.2 Cephalad, caudal, lateral, and posterior borders of the pericardium including the oblique
and transverse sinuses
vein
Left subclavian vein
Left brachiocephalic
vein
Left subclavian artery
Left common carotid
artery
Arch of aorta
Ligamentum arteriosum
Pulmonary trunk
Left pulmonary veins
Oblique sinus of
pericardium
Etiology
Acute pericarditis is the most common disease of the pericardium and is most frequently caused by a systemic viral infection. Other causes include uremia, autoimmune disorders, and less commonly bacterial infections. The inammation of the
pericardium can lead to a reactive increase in the volume of pericardial uid termed
effusive pericarditis. Occasionally, if the effusion accumulates rapidly enough, it
can lead to tamponade physiology. Less than 1% of patients with pericarditis will
eventually go on to develop constrictive pericarditis [2].
Constrictive pericarditis is a bit of a misnomer as it occurs consequently to peri-
carditis but frequently exists absent active inammation. In the developing world,
constriction is most commonly caused by tuberculous pericarditis, however in
regions with a low prevalence of tuberculosis, constriction is commonly idiopathic
with or without a recognized episode of acute pericarditis. It also occurs in a small
percentage of cases following cardiac surgery and may become evident many years
after mediastinal radiation [3]. In this latter case, radiation cardiomyopathy often
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coexists making it difcult to determine if a patient’s signs and symptoms are secondary to constriction, restriction, or both. Rather than an external force on the
myocardium, restrictive cardiomyopathy is a condition inherent to the myocardium
itself that renders it non-compliant. Other causes of restrictive cardiomyopathy are
amyloidosis, sarcoidosis, and endomyocardial brosis [4].
A. Paine et al.
Physiology
Due to the relative non-compliance of the parietal pericardium, an increase in uid
volume within the pericardial sac results in reduced diastolic lling of the cardiac
chambers and subsequent reduced cardiac output (cardiac output = heart rate ×
stroke volume). When this results in hemodynamic compromise, it is referred to as
tamponade. Cardiac tamponade may be the result of uid collection secondary to
acute inammation, uremic pericarditis, or malignancy among non-surgical patients,
or secondary to postoperative bleeding in the post-surgical patient (See Chap. 34—
Principles of Perioperative Care). Pericardial constriction similarly restricts cardiac
lling but in a slowly progressive manner that makes its diagnosis often difcult and
delayed. Both constriction and restriction impair diastolic lling of the heart,
thereby reducing cardiac output and leading to symptoms of heart failure. It is critical to make the distinction of constrictive versus restrictive etiology of symptoms as
only constrictive pericardial disease will benet from pericardiectomy.
History
Patients with acute pericarditis present with severe chest pain, classically made
worse by leaning forward. There may or may not have been a preceding episode of
viral illness. Patients with constrictive pericarditis most commonly present with
slowly progressive symptoms of right-sided heart failure. Signs and symptoms
include dyspnea on exertion, orthopnea, ascites, and peripheral edema. Some will
complain of a sense of fullness in their head, especially when bending over, or may
notice jugular venous distension. Given the aforementioned causes of constriction,
a thorough history including inciting infections, mediastinal radiation, and cardiac
surgery should be elicited as well as potential causes of restrictive cardiomyopathy
such as sarcoidosis, cardiotoxic chemotherapy, etc.
Physical Exam
Acute pericarditis classically causes a loud friction rub best heard with the patient
leaning forward. In cases complicated by a signicant effusion (effusive pericarditis), there may be co-existing signs consistent with constrictive physiology
25 Pericardial Disease
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including evidence of right-sided heart failure such as peripheral edema, hepatomegaly, and ascites. Kussmaul’s sign, a paradoxical increase in jugular venous distention with inspiration, can be seen in patients with restricted right ventricular
lling including both constriction and restriction. Patients with constriction may
have a pericardial knock on auscultation, which is caused by abrupt cessation of
ventricular lling during diastole once the point of physical constriction has been
reached.
Imaging
The diagnosis of acute pericarditis is principally clinical with supportive laboratory
evidence of elevated inammatory markers and potentially echocardiographic evidence of an effusion. The diagnosis of tamponade or constriction, however, is often
made by imaging studies. Enlargement of the cardiac silhouette may be seen in the
presence of an effusion, although echocardiography is the diagnostic test of choice.
In the setting of constriction, pericardial calcication seen on chest X-ray is essentially diagnostic, although it is present in less than 25% of cases [5] (Fig.25.3).
Cross-sectional imaging with computed tomography (CT) and magnetic resonance
imaging (MRI) may demonstrate pericardial calcication, but almost invariably
demonstrates pathologic thickening (>4mm) (Fig.25.4). Cardiac MRI can be helpful in identifying tethering of the myocardium by pericardial adhesion as well as
evidence of active inammation of the pericardium, inltrative myocardial processes causing restriction, and can demonstrate impaired diastolic lling [6, 7].
Echocardiography is a required diagnostic test in all patients presenting with
heart failure symptoms as the differential is broad. While constriction is uncommon, it is important to consider as a potentially curable cause. When tamponade is
Fig. 25.3 Pericardial calcication on chest X-ray, although seen in less than 25% of cases, is
highly suggestive of constrictive pericarditis in the appropriate clinical context
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Fig. 25.4 Computed tomography demonstrating pericardial calcication and pathologic thickening (>4mm) is highly suggestive of constrictive pericarditis in the appropriate clinical context
A. Paine et al.
present, in addition to obvious uid in the pericardial space, there will be right
ventricular collapse and inferior vena cava dilatation without respiratory variation.
Evidence of right heart failure, including inferior vena cava distention with
decreased respiratory variation, can also be seen on the echocardiogram of patients
with either constriction or restrictive cardiomyopathy. Echocardiography may
identify pericardial thickening and will pathognomonically demonstrate increased
ventricular interdependence in constriction. Given a xed volume that can be
accommodated within the non-compliant pericardium, as one cardiac chamber volume increases, another chamber must have a corresponding decrease in volume.
Ventricular interdependence is demonstrated on echocardiography as interventricular septal bounce where the septum bows toward the left ventricle during inspira-
tion as the pulmonary venous return declines with pooling of blood in the lungs
permitting rapid lling of the right ventricle at the expense of left. Conversely,
during expiration, the left lls at the expense of the right, resulting in reversal of
hepatic venous ow [8] (Fig.25.5).
Cardiac catheterization is invasive but denitive. It is not always necessary
to diagnose constriction; however, in cases where imaging and history do not
adequately differentiate constriction and restriction, it is indicated. Ventricular
pressure tracings in constriction demonstrate the square root sign which corre-
sponds to a ventricle that lls rapidly in early diastole until meeting the xed
resistance of the non-complaint pericardium (Fig. 25.6). Additional specic
ndings supportive of constriction include equalization of left ventricular end
diastolic pressure (LVEDP) and right ventricular end diastolic pressure (RVEDP),
both of which are abnormally elevated [9]. Most characteristic of constriction as
compared with restriction is systolic discordance, with a decline in systemic
pressure and increase in pulmonary artery pressure during inspiration and the
reverse in expiration in the setting of constriction due to the changes in lling
noted above.
noitaripxEnoitaripsnI
ventricular interdependence
Copyright © McGraw-Hill Education. All rights reserved
Pressure (mm Hg)
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RV LV
Fig. 25.5 Echocardiography demonstrating ventricular interdependence is seen in constrictive
pericarditis. Ventricular interdependence is demonstrated on echo by the interventricular septum
bowing toward the left ventricle during inspiration and toward the right ventricle on expiration
Fig. 25.6 Ventricular
pressure tracing
demonstrating the square
root sign consistent with a
diagnosis of constrictive
pericarditis. This tracing
results from a ventricle that
lls rapidly in early
diastole until meeting the
xed resistance of the
non-complaint pericardium
25
20
15
10
5
0
Source: Lawrence H, Cohn, David H, Adams:
Cardiac Surgery in the Adult, Fifth Edition
RV LV
LV RV
Square-root sign
Indication forSurgery
Surgical intervention is not indicated in acute pericarditis unless there is a signicant effusion with evidence of tamponade. In this case either a subxiphoid or lateral
thoracoscopic window may be therapeutic, although increasingly percutaneous
drainage is employed if possible. In the setting of constriction, there is no effective
medical management. Optimizing volume status with diuretics may improve symptoms; however, medications will not reverse the xed constriction of the pericardium. In properly selected patients, pericardiectomy improves functional status
with an acceptable risk prole with most series reporting an operative mortality
between 2.5 and 9% [10, 11]. Factors that are associated with poor outcomes following pericardiectomy include prior radiation (as these patients commonly have a
component of radiation-induced restrictive cardiomyopathy which will not benet
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A. Paine et al.
from pericardiectomy) renal insufciency, reduced ventricular function, high pulmonary artery pressures, and NYHA class IV symptoms.
Operative Technique
The standard approach to pericardiectomy is via a median sternotomy. The tenet to
a successful outcome is near complete removal of the pericardium leaving only a
small portion of pericardium posterior to the right phrenic nerve, a narrow strip
along the left phrenic nerve, and the inaccessible portion of posterior pericardium
within the oblique sinus. As removal of certain parts of the pericardium requires
manipulation of the heart that can lead to signicant hemodynamic changes, the use
of cardiopulmonary bypass (CPB) may be necessary. With an experienced surgeon
and cardiac anesthesiologist, a complete pericardiectomy can often be performed
without the use of CPB, however it is typically necessary in a reoperative setting and
one should not compromise on the adequacy of pericardiectomy just for the sake of
avoiding CPB.It is critical to preserve the bilateral phrenic nerves which innervate
the diaphragm as injury can result in respiratory failure. Accordingly, the patient
should not be paralyzed during pericardiectomy. The phrenic nerves can be tested
with a nerve stimulator both for identication and to determine their integrity postpericardial resection. Finally, it is critical to remove both the parietal and visceral
pericardium as both can contribute to impaired diastolic lling. There is often a very
appealing plane of dissection between the layers, however this will fail to treat the
disease. The visceral pericardium requires meticulous dissection off the myocardium, as it can be quite adherent. Adequate visceral pericardial dissection is demonstrated by clearly visible epicardial coronary arteries at the conclusion of the
pericardiectomy [12] (Fig.25.7).
Fig. 25.7 Pericardiectomy requires near complete removal of the visceral and parietal pericardium
leaving only a small portion posterior to the right phrenic nerve, a narrow strip along the left phrenic
nerve, and the inaccessible portion of posterior pericardium within the oblique sinus(Copyrighted
and used with permission of Mayo Foundation for Medical Education and Research)
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References
1. Rodriguez ER, Tan CD.Structure and anatomy of the human pericardium. Prog Cardiovasc
Dis. 2017;59(4):327–40.
2. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, etal. 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(42):2921–64.
3. Myers RBH, Spodick DH.Constrictive pericarditis: clinical and pathophysiologic characteristics. Am Heart J. 1999;138:219–32.
4. Muchtar E, Blauwet LA, Gertz MA.Restrictive cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis, and therapy. Circ Res. 2017;121(7):819–37.
5. Cosyns B, Plein S, Nihoyanopoulos P, Smiseth O, Achenbach S, Andrade MJ, etal. European
Association of Cardiovascular Imaging (EACVI) position paper: multimodality imaging
in pericardial disease On behalf of the European Association of Cardiovascular Imaging
(EACVI) and European Society of Cardiology Working Group (ESC WG) on Myocardial and
Pericardial diseases.
6. Masui T, Finck S, Higgins CB.Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging. Radiology. 1992;182(2):369–73.
7. Gupta A, Singh Gulati G, Seth S, Sharma S.Cardiac MRI in restrictive cardiomyopathy. Clin
Radiol. 2012;67(2):95–105.
8. Yang R, Smith J, Mokadam NA.Pericardial disease. In: Baumgartner WA, Jacobs JP, Darling
GE, editors. STS cardiothoracic surgery E-book. Chicago: Society of Thoracic Surgeons; 2020.
9. Feins EN, Walker JD.In: Cohn LH, Adams DH, editors. Cardiac surgery in the adult, pericardial disease. 5th ed. McGraw Hill Education; 2017. p.1225–42.
10. Vistarini N, Chen C, Mazine A, Bouchard D, Hebert Y, Carrier M, etal. Pericardiectomy for
constrictive pericarditis: 20 years of experience at the Montreal heart institute. Ann Thorac
Surg. 2015;100:107–13.
11. Gillaspie EA, Stulak JM, Daly RC, Greason KL, Joyce LD, Oh J, et al. A 20-year experience with isolated pericardiectomy: analysis of indications and outcomes. J Thorac Cardiovasc
Surg. 2016;152:448–58.
12. Villavicencio MA, Dearani JA, Sundt TM. Pericardiectomy for constrictive or recurrent
inammatory pericarditis. Oper Tech Thorac Cardiovasc Surg. 2008;13(1):2–13.
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