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Acute and Chronic Pulmonary Embolism: Perspectives on Diagnosis and Management Chapter | 24 365
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Chapter 25
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Surgical Management of Cardiovascular
Thrombotic Conditions
Michael Magarakis, Alejandro E. Macias, Ali Ghodsizad and Tomas A. Salerno
University of Miami Miller School of Medicine and Jackson Memorial Hospital, Miami, Florida, USA
INTRODUCTION
The focus of contemporary treatment of cardiovascular thrombotic conditions is on the application of percutaneous devices
and pharmacotherapy. Nevertheless, there are major clinical conditions and thrombotic scenarios which still require surgical treatment, either as “first in line” option or as a secondary option in case the abovementioned methods fail to achieve
the treatment goals or cannot be applied. In addition to the established role of artificial cardiac valves the recent
advancement of mechanical cardiac assist devices into the main stream of cardiovascular treatment is considered a major
development, yet, their susceptibility to thrombosis is of major concern. Thus, the participation of cardiothoracic surgeons
in the management of patients who present with thrombotic cardiac conditions is an essential integral of the modern “ heart
team “ approach. Accordingly, this chapter provides the perspectives of cardiothoracic surgery on the management of
various cardiac thrombotic conditions.
SURGICAL MANAGEMENT OF ACUTE PULMONARY EMBOLISM
Pulmonary embolism (PE) is an uncommon condition with a variable clinical presentation. It refers to obstruction of the
pulmonary artery, or one of its branches, by thrombus, tumor, air, or fat that usually originates somewhere else in the body.
The incidence of PE in the general population ranges between 50 and 100 cases per 100,000 people per year [1,2].
PE can be classified based on timing of presentation (acute, subacute, or chronic), presence or absence of hemodynamic
stability (massive, submassive, low risk), anatomic location (saddle, lobar, segmental, subsegmental), and last, presence or
absence of symptoms (symptomatic or asymptomatic). The most critical and time sensitive of all of these is the identification of a massive PE. Massive PE is suspected when the systolic blood pressure is <90 mmHg for a period of >15 min
and/or hypotension that requires vasopressors and cannot be explained by any other causes is present. As a result, the word
“massive” does not describe the size of the PE, but its hemodynamic effect.
The pathogenesis of PE is identical to that of venous thromboembolic disease, i.e., venous stasis, endothelial injury, and
hypercoagulable state. Most PEs arise from the lower extremity venous system and about 50% of patients who present with
a PE also have venous thrombosis at the time of presentation [3e7]. The pathophysiologic response to PE includes
pulmonary infarction with concomitant inflammatory response [8], impaired gas exchange from mechanical obstruction of
the pulmonary vascular bed affect ing the ventilation/perfusion balance, and last, cardiovascular compromise due to
diminished stroke volume as a result of obstructed pulmonary vasculature.
Clinical presentation varies and patients with PE may in fact present with no symptoms at all. The most common
symptom is dyspnea followed by chest pain, cough, and rarely hemoptysis. In the case of a massive PE, patients may present
with hypotension and shock. In hemodynamically normal patients, the diagnosis of PE is confirmed by computed tomographic angiogram of the thorax (Fig. 25.1). Oftentimes, however, the patient is too unstable and there may be no time to
proceed to the computed tomography (CT) scanner. At the same time, resuscitation transthoracic echocardiography may help
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Copyright © 2018 Elsevier Inc. All rights reserved.
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FIGURE 25.1 Computed tomography of a patient with a massive pulmonary embolus of the right main pulmonary artery (red arrows).
establish the diagnosis. The presence of new right-ventricular strain or direct visualization of thrombus within the heart does
not make a definitive diagnosis of PE. Treatment is often started based upon these findings in an unstable patient.
The mainstay of management in patients presenting with a PE includes anticoagulation therapy. In hemodynamically
stable patients who do not have evidence of right-heart strain or troponin leak (low-risk PE), unfractionated heparin with
eventual transition to vitamin K antagonists or direct thrombin inhibitors is usually adequate treatment. Those with
contraindications to anticoagulation will require placement of an inferior vena cava filter.
Acute, submassive, or massive PE is a life-threatening condition and rapid response with appropriate intervention is needed.
Among 2392 patients from the International Cooperative Pulmonary Embolism Registry (ICOPER), the 90-day mortality rates
were 52.4% in patients presenting with massive PE [9]. There are several options to consider in treating these patients, but the
goal is the same: relieve the mechanical obstruction from the pulmonary vasculature and restore normal physiology.
The modalities used in cases of a massive or submassive PE include three broad categories: systemic thrombolytics,
catheter-directed therapies, and surgical embolectomy. The consensus guidelines, as of this writing, from the American
Heart Association and European Society of Cardiology highlight that surgical treatment for the management of PE should
be reserved for hemodynamically unstable PE, particularly in patients with absolute contraindications to thrombolytic
therapy or failed systemic thrombolysis or catheter-based treatments [10,11].
The treatment algorithm described previously is based on limited data from small surgical series, and these practice
patterns may be more reflective of scarce surgical expertise and availability rather than the standard of care provided in major
academic centers. Indeed, increasing evidence suggests that pulmonary embolectomy might be considered first-line therapy
for select patients [12e14]. There is promising evidence that early surgical embolectomy in patients with documented
central PE and signs of right-ventricular strain may be beneficial before the onset of hemodynamic collapse [15e20].
At the University of Miami/Jackson Memorial Hospital we use the algorithm depicted in Fig. 25.2. If a patient presents
with a massive PE and a central thrombus we proceed with surgical embolectomy (see images) (Fig. 25.3). If the patient
presents without hemodynamic instability but has evidence of right-heart strain on echocardiography and a central
thrombus, then a multidisciplinary approach for surgery versus catheter-directed thrombolysis is implemented. The Seattle
II trial is the largest and best-designed trial describing the efficacy and safety of catheter-directed low-dose fibrinolysis in
patients with massive (20% of the cohort) and submassive (80% of the cohort) PE. The authors report a 4.7% 30-day
mortality, 10% major vascular complication rate, and significant reduction in the mean pulmonary artery systolic pressure (51.4 mmHg vs. 36.9 mmHg; P < .0001).
Oftentimes however, the patient is too unstable for time-consuming catheter-based therapies and immediate surgical
embolectomy is needed. In the current era the practicing cardiac surgeon will often consider extracorporeal membrane
oxygenation (ECMO) in patients with massive PE presenting in extremis in an effort to stabilize the hemodynamics and
operate in a more controlled setting. Since 2004, ECMO has been increasingly used for patients as a b ridge to embolectomy, with the majority of the reports showing satisfactory results [21e26].
Once the patient is confirmed to have a massive, central PE, and is deemed to be a surgical candidate, we proceed to the
operating room. The open heart team has been called in advance. The surgery is performed through median sternotomy
with cardiopulmonary bypass under normothermic conditions and without cross clamping the aorta. A single, dual-stage
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FIGURE 25.2 University of Miami/Jackson Memorial Hospital protocol for the management of a patient with acute massive embolism. BP, blood
pressure; ECMO, extracorporeal membrane oxygenation; PE, pulmonary embolism.
FIGURE 25.3 Extracted thrombus from the right and left main pulmonary artery after surgical embolectomy.
venous cannula is placed in the right atrium. Bicaval cannulation may facilitate exploration of the right atrium or ventricle
for clot and allows closure of any patent foramen ovales. The first step of the operation is to perform a longitudinal
arteriotomy of the main pulmonary artery trunk. The clot is extracted with a combination of ring forceps and suction. It is
of paramount importance to remove all of the thrombus to prevent propagation of the clot and/or chronic pulmonary
hypertension due to organization of the thrombus later on. An inferior vena cava filter is inserted immediately after the
operation to prevent recurrent PE. Intravenous (i.v.) heparin is started on postop erative day 1 after appropriate hemostasis
has been confirmed. The patient is then bridged to warfarin therapy for a total duration of 6 months.
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In terms of outcomes, there are several surgical series that have demonstrated the efficacy and safety of surgical embolectomy in patients with massive PE. One of the largest and most recent (2015) was by Neely et al. [27]. The authors reviewed
the outcomes in 115 patients who presented with massive or submassive PE after surgical embolectomy. Operative mortality for
the combined groups was 6.6%. Patients with massive PE had a mortality of 10.2% versus 3.6% for patients with submassive
PE. These numbers clearly show that these patients can often be saved and that the mortality may be decreased significantly
from 55% to less than 10% with expeditious treatment and restoration of blood flow through the pulmonary vasculature.
The most recent comprehensive meta-analysis, at this writing, from Kalra et al. [28], reviewed all studies from 1945 to
2015, involving 1579 patients who underwent 1590 surgical embolectomies for PE. The in-hospital mortality in all patients
was 26.3%. When interpreting this number, one needs to take into account that this review included all studies published
over the past 70 years. The reported mortality, however, is still significantly better than the 90-day mortality rate of 52.4%
from the ICOPER. In this registry only 3 of the 108 patients with massive PE underwent surgical embolectomy.
In conclusion, PE can be a life-threatening condition, and prompt diagnosis of massive PE is of paramount importance.
The literature suggests that mortality can be decreased exponentially with rapid surgical embolectomy in the subgroup of
patients with massive PE. Pulmonary embolectomy deserves greater consideration as first-line therapy for select patients with
acute, central, massive, and submassive PE, and the best practices are yet to be determined by randomized controlled trials.
MANAGEMENT OF PROSTHETIC HEART VALVE THROMBOSIS
Prosthetic valve thrombosis (PVT) is described as any thrombus near or attached to a functioning valve, in the absence of
infection, which interferes with valvular function or occludes part of the blood flow. Although PVT is rare, it can be a lifethreatening complication of valve replacement [29,30].
The incidence of PVT has been reported to be 0.03% in bioprosthetic valves, 0.5%e8% in mechanical valves in the
aortic and mitral positions, respectively, and as common as 20% in mechanical tricuspid valves [29,31e33]. In general,
tricuspid prostheses are more likely to be involved compared with mitral prostheses, which in turn are more involved than
prostheses in the aortic position. Although the most commonly affected design is the old-type “tilting-disk” mechanical
valve, even new-generation prostheses can be affected by this complication [30,32,33].
There are several factors that may lead to PVT: thrombogenicity of the prosthesis, abnormal transprosthetic blood flow,
left-atrial geometry and function (i.e., atrial fibrillation), and most importantly, inadequate anticoagulation. The molecular
interaction between plasma components and the prosthesis can cause absorption of plasma proteins, particularly adhesive
proteins. In addition, altered transprosthetic blood flow may cause turbulent flow producing shear stress and downstream
recirculation; also, subclinical hemolysis with subsequent ADP release eventually activates the coagulation system. It is
important to note that prothrombotic factors play a significant role in the development of PVT, such as abnormal atrial
contractions, drugs (e.g., contraceptives), systemic lupus erythematosus, malignant tumors, and incomplete endothelialization of a valve’s ring. Although all of these play a role in the pathogenesis of PVT, the most common etiology of PVT is
inadequate anticoagulant therapy [29e35]. The clinical presentation may vary and usually includes dyspnea, peripheral
embolism, and symptoms of heart failure, among others.
The American College of Cardiology/American Heart Association 2014 Guidelines for the Management of Patients
With Valvular Heart Disease has given the following recommendations with different classes of evidence [34]. In terms of
the diagnosis of PVT, the only established/class I evidence is the use of transesophageal echocardiography (TEE).
However, new diagnostic modalities have risen. In regard to management, left-sided PVT with New York Heart Association (NYHA) class III to IV symptoms has class I evidence for urgent surgery. Nevertheless, the guidelines provide with
weaker (class IIa) evidence for the remaining recommendations of PVT management. Treatment modalities include i.v.
unfractionated heparin, fibrinolytic therapy, and/or urgent surgical intervention. For left-sided PVT urgent surgical intervention is needed, unless the thrombus is less than <0.8 cm
mobile thrombus requires surgical intervention. Right-sided PVT is always treated with fibrinolytics (class IIa evidence).
As mentioned earlier, although TEE has been the gold standard for the diagnosis of PVT, four-dimensional computerized
tomography (4DCT) is gaining increasing popularity. The US FDA has approved two studies comparing outcomes of surgical
and transcatheter aortic valve replacement (TAVR). Both of these trials used 4DCT to analyze valve anatomy, leaflet mobility,
and valve thrombosis. If PVT was identified, follow-up 4DCT was performed to assess for thrombus resolution [36e38].
There continues to be debate on how to approach PVT; and this argument is hardly settled. This may be due to its low
incidence rate or merely that a single list of recommendations does not yet display superiority over other recommendations
made throughout the literature. Medical management of PVT is anticoagulation therapy combined with fibrinolytics
(Fig. 25.4). However, obstruction caused by pannus formation will not be effectively treated by medical therapy and valve
replacement is necessary [29,30].
Left-sided PVT is very often associated with embolic stroke, and valve replacement is likely to be a better option for
these patients. Even with the use of fibrinolytics, the incidence of embolic stroke is between 12% and 15% [29,30,32e35].
2
, in which case, fibrinolytic therapy can be used. Of note, any
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(A) (B)
FIGURE 25.4 Fluoroscopy. (A) Systolic frame of a patient’s aortic prosthetic valve on presentation. Only one of two valve leaflets open. (B) Systolic
frame of the same aortic prosthetic valve after complete thrombus resolution with fibrinolytic therapy.
As a result, fibrinolytic therapy is reserved for those who have contraindications to surgery, in whom surgery carries a
higher risk than medical therapy. In patients who are NYHA functional class I or II and who have a small thrombus, shortterm i.v. heparin and/or continuous infusion of fibrinolytic therapy should be sufficient. The dimensional threshold for this
recommendation has not been defined because of the discrepancies described in small studies (some say between 5 and
10 mm), as well as the lack of large cohort studies. The use of recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase has been supported in studies. Most centers will administer unfractionated heparin as soon as PVT is
suspected, then discontinue it during fibrinolysis, and later resume heparin after the completion of thrombolysis. The most
widely used protocols of fibrinolytic therapy are the following [29e35]:
l recombinant tPA, 10-mg bolus followed by 90-mg infusion over 2e6h,
or
l streptokinase slow infusion over 12e48 h, with occasional extension to 72e120 h,
or
l urokinase slow infusion over 6e 48 h.
Risk factors for unfavorable outcomes with fibrinolytic therapy include active internal bleeding, recent cranial trauma
or tumor, history of hemorrhagic stroke, large or mobile thrombi, hypertension (>200/120 mmHg), hypotension or shock,
and symptoms of NYHA IIIeIV. Complete resolution of PVT with fibrinolytic therapy should be followed by i.v. heparin
with subsequent transition to warfarin. Low-dose aspirin is recommended in all patients after fibrinolytic therapy [34,35].
Roudaut et al. [32] reported their 23-year experience with thrombosed mechanical prosthetic valves in 110 patients.
Thrombolytic therapy resulted in total resolution of PVT in 71% of patients, partial resolution in 17%, and complete failure
in 12% of patients. Furthermore, aortic prosthetic valves were found to respond more favorably (80%) to fibrinolytic
therapy than mitral valve prostheses (65%). Fibrinolytic therapy was associated with systemic embolism in 15%, and
severe hemorrhagic complications occurred in 5% of patients. Recurrent PVT occurred in 20% of patients and overall
mortality in this series was 12%.
One of the most comprehensive studies comparing surgical management with thrombolytic therapy was also done by
Roudaut et al. [33]. The authors included 210 patients who had PVT: 110 patients wer e treated with fibrinolysis, 99
patients had primary surgery, and 37 patients had secondary surgery due to fibrinolytic therapy failure. The fibrinolytic
therapy group achieved complete resolution in 71% (80% in aortic PVT, 65% in mitral PVT, and 100% in tricuspid PVT);
overall mortality was 11.8% for this group. The surgical group had complete PVT resolution in 89% of patients with a
mortality rate of 10.3%. Hemodynamic success was significantly better in the surgical group (89% vs. 70.9%, P < .001),
embolic episodes were significantly more frequent in the fibrinolysis group (15% vs. 0.7%, P < .001), and overall
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complications were more common in the fibrinolytic group (25.2% vs. 11.1%, P ¼ .005). Outcomes of this study suggest
that surgery has better results compared with fibrinolytic therapy, significantly lower rate of embolic events, and lower
overall complication rate: surgery should be the treatment of choice in left-sided PVT.
In the recent era, TAVR has become the treatment of choice for high-risk patients with severe aortic stenosis. Hansson
et al. [38] have published the largest series that assessed TAVR (Edwards Sapien XT or Sapien 3) PVT in 405 patients. The
patients were evaluated by multidetector CT and echocardiography 1e3 months post-TAVR. PVT was found in 7% of
patients (85% was subclinical and 15% was clinically overt). In multivariate analysis, TAVR using a valve of 29 mm was
associated with PVT, as well as the absence of warfarin therapy post-TAVR. This study also demonstrated that 85% of
cases resulted in complete resolution with a combination of warfarin and antiplatelet therapy.
In the largest series evaluating surgical aortic valve replacement (SAVR) and TAVR subclinical PVT, Chakravarty
et al. [39] assessed 931 patients with CT imaging. A total of 890 patients (752 patients with TAVR and 138 patients with
SAVR) had interpretable CT scans. The overall PVT rate for the cohort was 12% (4% in SAVR pati ents vs. 13% in TAVR
patients). Subclinical PVT was more frequent in patients receiving dual antiplatelet therapy alone, compared with patients
treated with anticoagulants (novel oral anticoagulants and warfarin), 15% and 4%, respectively. Patients who used warfarin
had complete PVT resolution (36/36, 100%) versus patients who did not receive anticoagulants (2/22, 9%). As a result of
these data, anticoagulation therapy (novel oral anticoagulants and warfarin) is effective in prevention and/or treatment of
subclinical PVT.
In previous years, medical treatment of PVTs with fibrinolysis was often the first-line treatment in most institutions.
This was mainly due to the high risks that were originally associated with surger y. Later on, TEE was introduced and
more accurate assessment of the t hrom bu s character ist ics was possible. As a result, surgery was revisited and later
became the preferred therapeutic strategy. Because of the low incidence of PVT, randomized prospective trials are
difficult to perform, and definite therapeutic recommendations are lacking. That being said, there is good evidence to
support that left-sided PVTs often require surgical intervention, especially in patients with large or mobile thrombi.
Right-sided PVTs can be treated medically. Finally, subclinical PVTs in surgical and transcatheter valves can be prevented with oral anticoagulant therapy. Last, the future of valve prosthesis is looking promising with tissue-engineered
valves; although these valves are in their early stages of clinical trial, at this writing, no animal or clinical study has
reported any PVTs. More studies are needed to further elucidate this complex clinical entity for standardizing management to improve patient outcomes.
LEFT-VENTRICULAR ASSIST DEVICE THROMBOSIS: NATURAL HISTORY, DIAGNOSIS,
AND SURGICAL TREATMENT
Ventricular assist devices (VADs) are not fully biocompatible, and therefore are predisposed to device thrombosis, which
can lead to subsequent pump dysfunction. Significant hemolysis can occur as a result of device thrombosis, but can also be
caused by other factors.
First-generation pulsatile VADs, including the Thoratec (HeartMate I) device, were relatively large, so any thrombus
created in part of the pump could be dislodged and cause an embolic stroke. Newer continuous-flow left-ventricular assist
devices (CF LVADs) are much smaller and have less volume holding the various pump components [38]. So pump
thrombosis can be found in CF LVADs, where the clot stays in the device, leading to increased hemolysis and device
dysfunction (Fig. 25.5).
A number of different factors can lead to pump thrombosis (in CF LVADs), including pump material, coagulation
management, and patient-specific factors (Table 25.1). Coagulat ion management protocols for VAD patients are institution
dependent, and unfortunately, there is large variability among the different groups.
A decrease in anticoagul ation thresholds [40] has been postulated to have resulted in an increase in CF LVAD
thrombosis [41]. Over- and under-anticoagulation can cause major adverse events, including bleeding, such as gastrointestinal bleeding and intracranial hemorrhage; hemolysis; pump thrombosis; and ischemic/embolic strokes.
At the Miami Transplant Institute we have consistently followed an anticoagulation protocol to target the therapeutic
window of warfarin therapy with an international normalized ratio goal of 2e3, 5, and 80e325 mg depending on the
required aspirin dose. The clinical diagnosis of pump thrombos is is established at our center by observing various
parameters, including plasma hemoglobin, LDH (lactate dehydrogenase) (LDH > 800) and a positive ramp study (on
minimal RPMs the aortic valve does not stay closed), if the left-ventricular end diastolic diameter does not show any
change in size, dark urine, and signs of heart failure. Intravenous heparin is not used to bridge to per oral Coumadin
application at our center.
Surgical Management of Cardiovascular Thrombotic Conditions Chapter | 25 373
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FIGURE 25.5 Thrombosed left-ventricular assist device.
TABLE 25.1 Factors Leading to Pump Thrombosis
Pump
Axial vs. centrifugal pump design, influencing the flow pattern
Pump material with variable compatibility
Magnetically levitated vs. regular bearings (bearing cooling is not maintained when the blood flow is reduced)
Patient
Age
Gender
Concerns about compliance
Hypercoagulable state (factor V Leidendhomozygous vs. heterozygous)
Physician
Anticoagulation
Likelihood of thrombosis
Mechanical issues from stenosed or malpositioned inflow cannula directed to septum
Lower pump speed
Patients with VAD thrombosis can present with:
l significant hemolysis, which causes fatigue, dark urine, or scleral icterus;
l device alarms, including variations in the pulsatility index;
l cardiogenic shock in patients with totally VAD-dependent flow.
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Laboratory Workup for Ventricular Assist Device Thrombosis
1. LDH: elevation of levels to more than 2.5 times that of the baseline should be investigated.
2. Haptoglobin: reduced in LVAD patients due to chronic hemolysis - not useful for VAD thrombosis diagnosis.
3. Plasma free hemoglobin: can effectively be used for pump thrombosis diagnosis.
4. Total bilirubin: usually elevated with significant hemolysis, but one needs to exclude other causes such as liver insuf-
ficiency in right-heart failure, hepatitis, and cirrhosis.
5. Serum creatinine: can be elevated as a result of hemoglobinuria and cause acute kidney failure.
Chest X-Ray
Chest X-ray can be used to assess changes in pump position.
Echocardiography: Transthoracic, Transesophageal
An echocardiogram is a very useful tool to diagnose pump thrombosis. Transthoracic echocardiography alone does not
provide sufficient detail, whereas TEE can give more information. Usually, patients have a baseline ramp TEE after VAD
implantation. It helps to adjust the optimal pump speed and to assess device malfunction. In cases of suspected VAD
thrombosis, a TEE should be done and compared with the baseline study. It is also critical to acknowledge diminished or
absent cannula diastolic flow velocity, as well as increased systolic-to-diastolic velocity ratio. These two parameter changes
have been described as predictors for suspected pump thrombosis [42,43].
Computed Tomographic Angiography
The application of computed tomographic angiography (CTA) as a diagnostic tool has been shown to be helpful for
evaluation of patients with suspected VAD dysfunction. CTA scan can visualize kinking of the outflow graft and enables
three-dimensional reconstruction and also can define inflow cannula positioning. It can be used as a sensitive marker to
show preserved outflow graft patency [44].
Cardiac Catheterization
The assessment of intraaortic pressures by cardiac catheterization can demonstrate any pressure gradient in the outflow
graft caused by graft kinking or possible stenosis. Fluoroscopy has been used during the initial experience episode to treat
graft thrombosis and to treat by local tPA application. Echocardiogram is the major important imaging modality in
evaluating pump thrombosis. Other imaging, like CTA and cardiac catheterization, should be considered if the diagnosis is
unclear.
Medical Treatment of Left-Ventricular Assist Device Thrombosis
Different approaches, including i.v. tPA administration as well as starting i.v. heparinization, are used to treat LVAD
thrombosis.
Surgical Approaches for Treatment of Left-Ventricular Assist Device Thrombosis
Pump exchange can be carried out via different surgical approaches depending on the failing part of the pump and may
require extracorporeal circulation.
We use the following surgical approaches:
Isolated subxiphoid approach: This approach is used for replacement of the inflow cannula or pump exchange, espe-
cially using the HeartWar e pump.
Subxiphoid approach and addit ional small left anterior thoracotomy: In cases in which the inflow graft requires
replacement and the so-called left-ventricular apex does not require recoring, the operation should be accomplished
through a left anterior fourth to fifth intercostal incision.
Redo sternotomy: More extensive corrections require a redo sternotomy.
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