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23 Acute andChronic Pulmonary Embolism
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Fig. 23.1 Computed
tomography pulmonary
angiogram (CT-PA)
demonstrating large
occlusive clot within the
proximal right and left
main pulmonary arteries
(arrows)
277
Risk Stratication
• After the diagnosis of acute PE has been established, rapid risk stratication is
critical in guiding appropriate management. PE is classied into three main cat-
egories: low risk, intermediate risk or submassive PE, and high-risk or mas-
sive PE [3].
• Low risk: Patients are normotensive with normal RV function and cardiac bio-
markers (troponin, pro-BNP). They have an excellent prognosis once anticoagu-
lation is established.
• Intermediate risk (submassive): Patients have evidence of RV dysfunction and/or
myocardial injury (elevated troponin/BNP) but without hypotension or shock.
• High risk (massive): Patients are persistently hypotensive (systolic blood pres-
sure [SBP] <90mmHG or a decrease in SBP >40mmHg for ≥15min), with RV
dysfunction and signs of obstructive shock and end-organ hypoperfusion includ-
ing altered mental status, cold/clammy skin, oliguria, increased lactate, or car-
diac arrest. Mortality in this group can be as high as 30–50%.
Treatment ofAcute Pulmonary Embolism
• Low risk: Anticoagulation with low-molecular-weight heparin (LMWH) or
direct acting oral anticoagulants (DOACs) is considered rst-line treatment in
patients with low-risk PE.
• Intermediate risk: Systemic anticoagulation is recommended over systemic or
catheter-directed thrombolysis in most patients with intermediate risk PE.
– The pulmonary embolism thrombolysis trial showed that patients treated with
thrombolysis had less hemodynamic deterioration but no improvement in
mortality and an increased risk of major bleeding (6%) and intracranial hemorrhage (2%) [4].
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– Intermediate risk patients deemed at increased risk of impending clinical
deterioration (based on vital signs, severity of RV dysfunction, or gas
exchange) may be considered for additional interventions including catheterdirected thrombolysis or catheter embolectomy.
• High risk: Management begins with cardiorespiratory stabilization, which may
include extracorporeal membrane oxygenation (ECMO) in patients with
profound hemodynamic compromise. Systemic thrombolysis remains the main-
stay of therapy. In patients with contraindications to thrombolysis or in whom
cardiogenic shock is likely to precede the effect of systemic thrombolysis,
catheter- directed therapy or surgical embolectomy can be considered.
A. L. Axtell et al.
Indications forSurgery
• Surgical pulmonary embolectomy should be considered in patients with interme-
diate or high-risk PE with any of the following:
– Profound RV failure and cardiogenic shock.
– Treatment failure of systemic thrombolysis.
– Contraindication to thrombolysis (history of intracranial hemorrhage, intra-
cranial mass or aneurysm, stroke within the past 3 months, major surgery
within the last month, brain or spinal surgery within the past 2months).
– Patent foramen ovale.
– Pregnancy.
– Thrombus in transit within the right atrium or ventricle.
Operative Technique forPulmonary Embolectomy
• A median sternotomy is performed, and bicaval and ascending aortic cannulation
are established. If additional cardiac procedures are required (i.e., extraction of
intracardiac thrombus, PFO closure), cardioplegic arrest and aortic crossclamping may be required.
• Once cardiopulmonary bypass (CPB) is established, a longitudinal incision is
made in the main PA 1–2cm from the pulmonary valve which can be extended
to the proximal left PA.
• Clot is carefully extracted using forceps, suction catheters, or Fogarty balloon
catheters (Fig.23.2).
• A separate incision in the right PA can be made longitudinally between the SVC
and the aorta to remove additional thrombus located in the right PA beyond the
bifurcation.
• If necessary, additional maneuvers can be performed to remove more peripheral
thrombi. This includes opening the pleural spaces bilaterally and manually compressing each lung to mobilize additional clot and retrograde perfusion via the
23 Acute andChronic Pulmonary Embolism
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279
Fig. 23.2 Surgical pulmonary embolectomy specimen
pulmonary veins to retrograde ush thrombotic material into the more proximal
pulmonary arteries.
• When sufcient thrombus has been removed, the arteriotomies are closed primarily and CPB is weaned.
Chronic Thromboembolic Disease
Pathogenesis
• CTEPH is a pulmonary vascular disease that results from incomplete thrombolysis of an acute PE.Fibrin within the embolus becomes progressively more cross
linked and organized over time leading to incorporation and endothelialization.
This leads to pulmonary vascular obstruction, redistribution of blood ow, and
accompanying small vessel vasculopathy that drives progressive pulmonary
hypertension and eventually right heart failure and death.
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• Risk factors for CTEPH include previous PE, younger age, unprovoked PE, splenectomy, venoarterial shunt or infected pacemaker, and antiphospholipid antibody syndrome. While many hypercoagulable disorders have been documented
in patients with CTEPH (antithrombin III deciency, protein C and/or S deciency, Factor V Leiden, Prothrombin gene mutation), they are not more prevalent than in patients with primary pulmonary hypertension [5].
A. L. Axtell et al.
Presentation andDiagnosis
• The most common presenting symptoms include dyspnea on exertion, atypical
exertional angina, exercise intolerance, exertional pre-syncope or syncope, and
hemoptysis. Patients commonly have sequelae of right heart failure with lower
extremity edema, hypoxemia, and occasionally pulmonary artery ow murmurs.
• Echocardiogram: Can conrm signicant pulmonary hypertension, estimate RV
size and function, and screen for other cardiac disorders.
• Ventilation-Perfusion (V/Q) scanning: Will show segmental defects in CTEPH.A
normal V/Q scan essentially eliminates CTEPH from further diagnostic
consideration.
• CT pulmonary angiogram: Will demonstrate pulmonary artery anatomy and can
screen for other pulmonary disease processes. Finding suggestive of CTEPH
includes a mosaic perfusion pattern of the lung parenchyma, peripheral infarcts,
and narrowed pulmonary arteries with pulmonary artery cutoffs.
• Cardiac catheterization: A right heart catheterization is performed to measure the
hemodynamics of the pulmonary circulation and to perform a pulmonary angiogram. Typical ndings include delayed lling of vessels, branch occlusions,
webs, pouches, and narrowed vessels (Fig.23.3).
• CTEPH is dened as precapillary pulmonary hypertension with a mean pulmo-
nary artery pressure ≥25 mmHg and a pulmonary arterial occlusion pressure
≤15mmHg in the presence of organized ow-limiting thrombi or emboli in the
pulmonary arteries after at least 3months of therapeutic anticoagulation [6].
Indications forSurgery
• PTE is the only curative intervention for patients with CTEPH, and 3-year survival approaches 90% [7].
• PTE should be considered in all patients but especially those who are symptomatic, have signicant pulmonary hypertension, have proximal or segmental disease, and who do not have prohibitive comorbidities.
• In most cases, if the disease is obstructing the main, lobar, or proximal segmental
pulmonary arteries, PTE is feasible and likely successful. If the disease is limited
to distal segmental and subsegmental branches, PTE is technically more
challenging.
23 Acute andChronic Pulmonary Embolism
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Fig. 23.3 Pulmonary
angiogram in a patient with
CTEPH demonstrating
lower lobe predominant
occlusive disease (arrow)
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Operative Technique forPulmonary Thromboendarterectomy
• A median sternotomy is performed, and bicaval and ascending aortic cannulation
with left PA and aortic root venting is established. Adequate visualization is
accomplished using CPB and periods of circulatory arrest. This allows for a
bloodless eld by diverting pulmonary arterial blood ow and reducing collateral ow.
• Once cardiopulmonary bypass (CPB) is established, and the desired core temperature (usually 18°C to 20°C) has been reached, the aorta is cross-clamped
and cardioplegia is administered.
• A longitudinal incision is made in the right main PA between the SVC and
the aorta.
• The endarterectomy is undertaken by entering the proper plane between the
intima and the media (Fig.23.4a). The plane should appear smooth and pearly
white. The specimen is dissected circumferentially and followed distally as far as
possible, following each subsegmental branch individually until it ends in a tail
(Fig.23.4b).
• When blood return obscures the dissection eld, deep hypothermic circulatory
arrest should be instituted, which improves exposure of the interior of the pulmonary artery. Periods of circulatory arrest are limited to 20min at a time.
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Fig. 23.4 (a) Initiation of the endarterectomy plane, (b) typical PTE specimen demonstrating
abnormal intimal thickening and obstruction of numerous segmental arteries
A. L. Axtell et al.
• Once the right side is completed, hypothermic reperfusion is reinstituted and the
pulmonary arteriotomy is closed primarily.
• Next, a left pulmonary arteriotomy is made. The endarterectomy plane is initiated and the specimen dissected into each segmental and subsegmental branch
under an additional period of circulatory arrest.
• Once both sides are completed, circulation is reinstituted and full rewarming is
begun. If other cardiac procedures are needed (i.e., PFO closure, valve repair),
these are performed during the rewarming period.
• When the patient is rewarmed, CPB is weaned and the patient decannulated.
References
1. Licha CRM, McCurdy CM, Maldonado SM, Lee LS.Current Management of Acute Pulmonary
Embolism. Ann Thorac Cardiovasc Surg. 2020;26:65–71.
2. LeVarge BL, Wright CD, Rodriguez-Lopez JM.Surgical Management of Acute and Chronic
Pulmonary Embolism. Clin Chest Med. 2018;39:659–67.
3. Rivera-Lebron BN, Rali PM, Tapson VF.The PERT concept: a step-by-step approach to managing pulmonary embolism. Chest. 2021;159:347–55.
4. Meyer G, Vicaut E, Danays T, etal. Fibrinolysis for patients with intermediate-risk pulmonary
embolism. N Engl J Med. 2014;370:1402–11.
5. Vlahakes GJ, Wright CD. Chronic thromboembolic pulmonary hypertension. In: Atlas
of cardiac surgical techniques: a volume in the surgical techniques atlas series. Saunders/
Elsevier; 2010.
6. Kratzert WB, Boyd EK, Saggar R, Channick R. Critical Care of Patients after Pulmonary
Thromboendarterectomy. J Cardiothorac Vasc Anesth. 2019;33:3110–26.
7. Papamatheakis DG, Poch DS, Fernandes TM, Kerr KM, Kim NH, Fedullo PF.Chronic thromboembolic pulmonary hypertension: JACC focus seminar. J Am Coll Cardiol. 2020;76:2155–69.
Chapter 24
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Surgery forAtrial Fibrillation
SarahM.Nisivaco andJamesL.Cox
Surgery forAtrial Fibrillation
Intro
Atrial brillation (AF) is the most commonly seen cardiac arrhythmia, with a lifetime risk of 25% above 40years of age. In the US, it accounts for over 500,000
hospital admissions and 160,000 deaths per year [1, 2]. Patients with AF can be
asymptomatic or experience a wide range of symptoms including palpitations,
lightheadedness, chest pain, shortness of breath, or fatigue.
The morbidity and mortality associated with AF can be largely attributed to 3
main sequelae: (1) symptomatic irregular heartbeat causing patient discomfort, (2)
potential for compromised hemodynamics due to atrioventricular (AV) dyssynchrony, and (3) risk for thromboembolism and stroke due to stasis of blood in the
left atrium [3].
While various pharmacotherapies exist for the treatment of AF, they have limited
success given the lack of efcacy of most medications, as well as bothersome side
effects. Given this, there has been great interest in the development of alternative
approaches to treating AF including catheter-based and surgical interventions [4].
S. M. Nisivaco (*) · J. L. Cox
Division of Cardiac Surgery, Bluhm Cardiovascular Institute, Northwestern Medicine and
Northwestern University Feinberg School of Medicine, Chicago, IL, USA
e-mail: sarah.nisivaco@nm.org; James.Cox@nm.org
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_24
283© The Author(s), under exclusive license to Springer Nature
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S. M. Nisivaco and J. L. Cox
Atrial Fibrillation Classication
• Paroxysmal: episodes of AF lasting less than 7days.
• Persistent: episodes of AF lasting longer than 7days and less than 1year.
• Long-standing persistent: episodes of AF lasting longer than 1year.
Surgical Treatment Options
Dr. Cox and his team of researchers began their historical work in the understanding
of the electrophysiology of AF in the 1980s. This research formed the groundwork
of all present day surgical and catheter-based interventions aimed at treating AF.
The current surgical treatment options for AF include:
1. Cut-and-sew Cox-Maze III procedure
2. Minimally invasive CryoMaze III procedure
3. Cox-Maze IV procedure
4. Modied CryoMaze III procedure
5. Robotic CryoMaze III procedure
6. Hybrid Maze Procedure
7. Robotic CryoMaze III procedure
8. Totally Thoracoscopic (TT) Modied Maze IV procedure
9. TT Modied Maze IV/Catheter Hybrid procedure
10. Convergent Hybrid procedure [5]
Cox-MAZE
The primary surgical treatment of AF, the Cox-Maze procedure, was introduced into
clinical practice in 1987 after extensive research investigation on animal models [3].
Through this work, Dr. Cox and colleagues outlined the atrial macro re-entrant circuits that occur in persistent and long-standing persistent atrial brillation. The
Cox-Maze procedure used knowledge of these re-entrant circuits to create a “maze”
of surgical incisions in the atria that interrupt the drivers perpetuating AF.In addition to interrupting these macro-reentrant circuits, this specic maze pattern of surgical incisions allows the SA node to continue to propagate signals throughout the
entirety of both atria and then to the AV node, thus maintaining sinus rhythm and AV
synchrony and allowing the atria to function properly [4].
The Cox-Maze surgical procedure is successful for both persistent and long-
standing persistent AF.The reason for this is behind the pathophysiology of persistent versus paroxysmal AF.In paroxysmal AF, the underlying pathophysiology is
focal triggers that induce self-limited episodes of atrial brillation. The treatment
for this (discussed in detail below under “pulmonary vein isolation”) is isolation of
the triggers in order to lessen the probability of these triggers inducing AF. In
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Fig. 24.1 Objectives of AF Surgery. PAF paroxysmal atrial brillation, N-PAF non-paroxysmal
atrial brillation
contrast, patients with persistent AF have established episodes of AF that are sustained by the aforementioned macro-reentrant drivers, and are independent of triggers [5]. Therefore, the treatment for this is a surgical cure that rids the atrium of
these drivers and allows the atria to be activated and responsive to sinus rhythm. See
Fig.24.1.
The original Cox-Maze procedure underwent a series of evolutions to result in
the current surgical options listed above. The Cox-Maze III procedure is preserved
as the gold standard for surgical treatment of AF.It originally created transmural
lesions via a “cut- and- sew” method, but eventually transitioned to creation of
lesions through a variety of alternative energy techniques. The most common energy
techniques used are cryoablation and bipolar radiofrequency ablation. The CoxMaze IV is the most commonly performed procedure today [6]. It results in the
same functional lesion pattern as the Cox-Maze III procedure but the lesions are
created with surgical ablation devices to shorten the procedure time.
The Cox-Maze procedure is performed on cardiopulmonary bypass (CPB) and
can be done through a median sternotomy, a less invasive right mini-thoracotomy,
or the most minimally invasively through a totally endoscopic robotic approach. Of
the macro-reentrant drivers present in persistent AF episodes, 70% are located in the
left atrium and 30% in the right atrium. Therefore, a bi-atrial lesion set is ideally
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S. M. Nisivaco and J. L. Cox
performed. However in certain cases—such as higher-risk patients or when trying
to minimize CPB time in complex cases—a left atrial lesion set only can be performed. Bi-atrial lesion sets include those in the left atrium, right atrium, and a box
lesion around the pulmonary veins (PVs) which acts to electrically “isolate” the
pulmonary veins (PVI). All lesions created should be full thickness, transmural
lines whether they are created from the endocardium or epicardium.
The left atrial set includes the PVI set, as well as lines connecting to the mitral
valve annulus, LAA, and coronary sinus.
The right atrial lesion set includes lines to the SVC, IVC, TV annulus, and RAA.
Pulmonary Vein Isolation (PVI)
PVI is an option for surgical treatment of paroxysmal AF.The pulmonary veins
have been well established as a common trigger point in a majority of AF cases. The
PVs can be electrically isolated as “islands” with independent lesion sets around the
right and left PVs, with or without a connecting lesion between the two islands.
More commonly, the PVs are isolated as a combined “box” with a single lesion set
going around all four PVs and the posterior left atrial wall. Unlike the Cox-Maze
procedure, PVI does not require opening of the left atrium or any part of the heart,
thus allowing for avoidance of CPB.Like the Cox-Maze procedure, it can be performed with minimally invasive techniques such as robotically or thoracoscopically.
Surgical PVI, often combined with a left atrial appendage occlusion as discussed
below, is often performed for patients with concomitant AF who are undergoing
cardiac surgery for other reasons. In patients not already undergoing cardiac surgery, a catheter PVI can be performed which is successful in decreasing the likelihood that these triggers will induce episodes of paroxysmal AF.Finally, this surgical
Fig. 24.2 Overview of
interventional treatment of
AF. PAF paroxysmal atrial
brillation, N-PAF
non-paroxysmal atrial
brillation, PVI pulmonary
vein isolation, LAAO left
atrial appendage ligation
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