A 57-Year-Old Man With Insidious Dyspnea [602428]

A 57-Year-Old Man With Insidious Dyspnea
and Nonpleuritic Chest and Back Pain
Kenta Nakamura, MD; George A. Alba, MD; Jonathan A. Scheske, MD; Nandini M. Meyersohn, MD;
James R. Stone, MD, PhD; Gus J. Vlahakes, MD; Cameron D. Wright, MD;
Brian B. Ghoshhajra, MD; and David M. Dudzinski, MD, JD
A 57-year-old man with a history of DVT and pulmonary embolism, transient ischemic attacks,
prior 60 pack-year smoking history, and oxygen-dependent COPD presented with insidiouslyworsening dyspnea associated with new pleuritic chest and back pain.
CHEST 2016; 150(2):e41-e47
Case Presentation
Three years before presentation, the patient developed
left lower extremity edema shortly following air travel
and he was ultimately diagnosed with a DVT and
concomitant pulmonary embolism (PE). Additional
evaluation revealed emphysema, COPD, and hypoxemia
necessitating 3 to 4 L/min of supplemental oxygen. He
was anticoagulated with Coumadin until 1 year before
presentation when he suffered a mechanical fall with
multiple rib fractures and anticoagulation was
discontinued. He was otherwise treated for suspected
oxygen-dependent COPD until the index presentation
with acutely worsened dyspnea and chest pain.
On presentation, vital signs were remarkable for
hypotension to 87/59 mm Hg, tachypnea to 24
breaths/min, and hypoxemia requiring 6 L/min
supplemental oxygen by nasal cannula to maintain an
oxygen saturation of 96%; he was afebrile and heart rate
was 89 beats/min. Cardiac auscultation was remarkable
for a III/VI holosystolic murmur best appreciated along
the left sternal border and intensi fied with inspiration.
Right ventricular (RV) lift and pulmonary artery “tap”
were absent. Jugular venous pressure was elevated at13 cm H 2O (8 cm above the sternal angle of Louis).
There was 2 țpitting edema of the bilateral lower
extremities. Initial laboratory studies were notable for
acute renal failure (creatinine, 2.1 mg/dL; reference,
0.60-1.50 mg/dL), elevated aminotransferases (aspartate
transaminase, 2,801 U/L; alanine transaminase, 1,275
U/L; reference, 10-40 U/L; 10-55, U/L, respectively),
elevated lactate (4.7 mmol/L; reference, 0.5-2.2 mmol/L),
and elevated D-dimer (4970 ng/mL; reference, 110-250
ng/mL). Electrocardiogram revealed normal sinus
rhythm with an ectopic atrial focus and premature atrial
contraction, biatrial enlargement, nonspeci fic ST/T-wave
changes in the right precordial (V1-4) leads, and right
bundle branch block ( Fig 1 ).
An anteroposterior chest radiograph was
underpenetrated but remarkable for diffuse interstitial
pulmonary markings suggestive of pulmonary edema,
prominence of the pulmonary arteries, and suggestion of
enlarged cardiac silhouette ( Fig 2 ). Transthoracic
echocardiogram demonstrated a 5.4-cm serpiginous
echodensity seen in the both right and left atria
straddling a probable patent foramen ovale (PFO)(Fig 3 A,3B;Video 1 ). The interatrial septum was
AFFILIATIONS: From the Division of Cardiology, Department of
Medicine (Drs Nakamura and Dudzinski); Division of Pulmonary andCritical Care Medicine, Department of Medicine (Drs Alba and
Dudzinski); Cardiovascular Imaging, Department of Radiology (Drs
Scheske, Meyersohn, and Ghoshhajra); Department of Pathology(Dr Stone); Division of Thoracic Surgery (Dr Wright), and Division ofCardiothoracic Surgery (Dr Vlahakes), Department of Surgery, Mas-sachusetts General Hospital, Harvard Medical School, Boston, MA.CORRESPONDENCE TO: David M. Dudzinski, MD, JD, Massachusetts
General Hospital, Corrigan Minehan Heart Center and PulmonaryEmbolism Response Team, 55 Fruit St, Yawkey 5B, Boston, MA 02114;
e-mail: ddudzinski@mgh.harvard.edu
Copyright /C2112016 American College of Chest Physicians. Published by
Elsevier Inc. All rights reserved.
DOI: http://dx.doi.org/10.1016/j.chest.2016.02.680[Chest Imaging and Pathology for Clinicians ]
journal.publications.chestnet.org e41

displaced leftward in both systole and diastole and the
right ventricle appeared dilated and hypokinetic with
interventricular septal flattening. Moderate tricuspid
regurgitation and a markedly elevated estimated
pulmonary artery systolic pressure of 59 mm Hg plus
estimated central venous pressure were noted. Contrast-
enhanced CT imaging of the chest showed a hypodense
mobile mass traversing the interatrial septum and
additional filling defects in the RV apex ( Fig 3 C) and theright pulmonary arteries ( Fig 4 A). Mosaic attenuation
(Fig 4 B) and occlusive thrombi of segmental arteries
were noted in the lower lobes of the right lung. The main
pulmonary artery was enlarged at 37 mm in diameter
(normal, <29 mm1). The right atrium and ventricle
again appeared dilated with interventricular septal
flattening and probable RV hypertrophy. Extensive
emphysema and pulmonary edema were also noted.
Given the inherently unstable nature of thrombus-in-
transit across the interatrial septum and in the RV
cavity, the patient was taken for comprehensive surgicalthromboembolectomy to remove thrombi from both
atria and the right ventricle; thromboendarterectomy of
the pulmonary, lobar, and subsegmental arteries; and
closure of the PFO. Thrombus-in-transit was con firmed
in the right atrium extending into the left atrium
through a large PFO. Upon gross inspection, the right
pulmonary artery and tributaries were occluded with
extensive subacute and chronic material ( Fig 5 A).
Following endarterectomy, the artery appearedthickened and in flamed with substantial scar tissue.
Histology of the thrombus retrieved from the pulmonary
artery revealed both organizing and unorganized
thrombus with focal areas of intimal hyperplasia
suggestive of at least a subacute process, consistent with
presence of thrombosis of varying ages from acute to
chronic ( Fig 5 B,5C).I
II
IIIaVR
aVL
aVFV1
V2
V3V4
V5
V6
V1
25mm/s 10mm/mV 100Hz
Figure 1 –Electrocardiogram showing biatrial enlargement and right bundle branch block.
Figure 2 –Chest radiograph showing diffusely increased reticular
markings, prominence of the pulmonary arteries, and enlarged cardiac
silhouette.
e42 Chest Imaging and Pathology for Clinicians [150#2 CHEST AUGUST 2016 ]

What is the diagnosis?
Figure 3 –Transthoracic echocardiogram showing a 5.4-cm linear echodensity in the right atrium and left atrium straddling a patent foramen ovale
(A, apical four-chamber view; B, subcostal four-chamber view). See Video 1 for cine. Contrast-enhanced CT scan of the chest shows a mobile mass
extending across a patent foramen ovale as well as right atrial and right ventricular dilation and right ventricular hypertrophy (C), with a lowattenuation filling defect in the RV apex concerning for thrombus. LA ¼left atrium; LV ¼left ventricle; RA ¼right atrium; RV ¼right ventricle.
Figure 4 –A, Contrast-enhanced CT imaging for pulmonary embolism showed a large eccentric filling defect in the main right-sided pulmonary artery
as well as signi ficantly dilated pulmonary artery. B, Color-inverted CT image showed a pattern of mosaic attenuation in the lower lobes of the right
lung, suggestive of chronic thromboembolic pulmonary hypertension.
Figure 5 –A, Gross photograph of material retrieved from the right-sided pulmonary artery and tributaries included extensive subacute and chronic
thrombus. Histology of the thrombus shows both unorganized (B) and organized (C) thrombus components. Intimal hyperplasia was also noted,
consistent with the presence of organized thrombus and suggestive of chronicity (yellow arrows).
journal.publications.chestnet.org e43

Diagnosis: VTE causing acute, subacute, and
chronic PE complicated by chronicthromboembolic pulmonary hypertension(CTEPH).
Discussion
Clinical Discussion
The history of signi ficant hypoxemia and signi ficant
pulmonary hypertension should raise suspicion
for alternative diagnoses other than COPD. A
comprehensive evaluation for additional etiologies of
persistent hypoxemia and pulmonary hypertension
following VTE and PE was warranted, including
consideration for CTEPH. In review of the patient ’s chart,
an echocardiogram that had been performed at the time of
initial PE several years before presentation revealedelevated estimated pulmonary artery systolic pressure. In
the absence of evidence for left heart failure, such as
enlarged left atrium, aortic or mitral valvulopathy, or left
ventricular dysfunction, an echocardiogram suggestive of
pulmonary hypertension warrants additional diagnostic
investigation. Preliminary evaluation typically includes
pulmonary function tests, ventilation-perfusion ( _V/ _Q)
(or perfusion-only) scintigraphy scan, overnight oximetry
and polysomnography, and laboratory testing including
autoimmune serologies, HIV, and liver function tests.
2-4
_V/ _Q scanning has been longer established than contrast-
enhanced CT scanning for chronic thromboemboli; in
this case, the CT scan is clearly preferable in this patient
with extensive COPD and abnormal underlying lung
parenchyma and ventilation, both factors that are known
to decrease the sensitivity of scintigraphy. Although
COPD was diagnosed at the time, the severity of
hypoxemia was disproportionate to the parenchymal
findings, and evaluation of pulmonary hypertension and
consideration for con firmatory right heart catheterization
were appropriate.The patient ’s current unstable presentation 3 years later
was consistent with acute PE as manifested clinically by
chest pain, tachypnea, and hypoxemia. The prior history
of VTE was an important historical risk factor for
recurrence. Hypotension with biochemical evidence of
end-organ dysfunction constituted shock resulting from
cardiovascular compromise. The patient was felt to have
“massive ”5or“high-risk ”6PE based on hemodynamic
instability and prolonged hypotension. Classi fication of
PE strati fies patients into those at high risk for death
that warrant consideration of invasive and/orthrombolytic therapies as opposed to conservative
management with anticoagulation alone.
5-7However,
the presence of thrombus-in-transit with embolization
to the left heart, presumably acute, as visualized on
echocardiography and CT imaging, presented an urgent
need for procedural intervention to mitigate risk of
further embolization with high likelihood of systemic
embolization. Thrombus-in-transit is a relatively rare
finding, observed in 4% of all patients with PE,8but in
18% in those requiring intensive care.9Transit of
thrombus through an intracardiac shunt into the left
atrium is rarer. The scenarios of mobile thrombus are
not directly addressed in treatment guidelines5,6;
however, thrombus-in-transit carries high mortality and
warrants aggressive intervention.10-12Treatment strategy
for mobile thrombus may be generally strati fied
according to hemodynamic status ( Table 1 ), but requires
careful multidisciplinary discussion and care
coordination.11-13At our institution and others, a
Pulmonary Embolism Response Team has beenorganized for questions such as mobile thrombus where
patient-speci fic decision-making is required to integrate
comorbidities, hemodynamic status, burden of disease,
need for additional surgical or percutaneous procedures,
institutional-speci fic expertise with surgical or
percutaneous procedures, and risk of undertreatment
with anticoagulation alone or a percutaneous
approach.
11-14Given impaired hemodynamics and
TABLE 1 ]Proposed Treatment Strategy for Thrombus-in-Transit (Right Heart Thrombi) in Acute Pulmonary Em-
bolism, Classi fied According to Hemodynamic Status and Surgical Riska,10,11,29-31
Acceptable Surgical Risk Unacceptable Surgical Risk
Hemodynamically
stableConsider surgical thrombectomy Consider anticoagulation alone or
percutaneous aspiration thrombectomy
Hemodynamically
unstableConsider surgical thrombectomy or systemic or
catheter-directed thrombolysis or percutaneousaspiration thrombectomyConsider systemic or catheter-directed
thrombolysis or percutaneous aspirationthrombectomy
aOptimal treatment strategy requires patient-speci fic, multidisciplinary discussion and care coordination. There are no consensus guidelines because of a
paucity of data and so treatment must be individualized for high-risk patient scenarios, for example in the case of impending systemic embolization a si n
the patient presented.
e44 Chest Imaging and Pathology for Clinicians [150#2 CHEST AUGUST 2016 ]

oxygen exchange, this patient would likely not have
tolerated the additional burden of emboli to the
pulmonary circulation and ongoing risk of paradoxical
arterial embolization predisposing to myocardial
infarction and further stroke.12,15,16
Imaging Discussion
Echocardiography and contrast-enhanced CT clearly
demonstrated thrombus-in-transit with dramatic
visualization of a highly mobile and unstable right atrialthrombus traversing a PFO and reaching into the left
atrium ( Fig 3 ). CT also revealed a large thrombus in the
RV apex not clearly visualized on echocardiogram,
highlighting the importance of multimodality imaging in
the management of complex thromboembolic disease.
The large eccentric filling defect in the main right-sided
pulmonary artery ( Fig 4 A) and occlusive thrombi in the
segmental arteries of the right middle and lower lobes
were consistent with both acute/subacute and chronicPE, respectively. Furthermore, the mosaic pattern of
attenuation noted on the right lower lung field suggests
irregular perfusion and strongly supports CTEPH
(Fig 4 B), albeit confounded in this case by the expected
hypoperfusion in segments with underlying
parenchymal abnormality resulting from emphysema.
17
The imaging is suggestive of both acute and chronic RVfailure. A signi ficantly dilated main pulmonary artery at
37 mm (normal, <29 mm
1) together with RV dilation
and septal flattening may suggest acute RV strain.
Demonstration of RV hypertrophy supports acomponent of chronic cardiopulmonary insult because
hypertrophy cannot develop immediately following
acute PE. The estimated pulmonary artery systolic
pressure in excess of 50 mm Hg makes pulmonary
hypertension a likely explanation.
4The absence of left
atrial enlargement argues against chronically elevated
left ventricular filling pressure or volume as an etiology
of both right heart failure and elevated pulmonary artery
pressure. In considering the patient ’s prior history of
VTE and PE, his preexisting oxygen dependence may
have been better explained by occult CTEPH thanCOPD alone.
PFO is a congenital vestige of the left-to-right atrial
shunt physiologically necessary in utero but may persist
in up to one-third of adults.
18The slitlike flap of the
interatrial septum typically seals shortly after birth with
reversal of right- and left-sided filling pressures
following the first breaths of life and dramatic reduction
in pulmonary vascular resistance. The majority of PFOs
are undetected and asymptomatic because higher leftatrial pressure prevents right-to-left flow of blood
under normal physiologic conditions. However,
increased right heart chamber pressures may cause
paradoxical right-to-left flow across the PFO. The
systolic murmur with respiratory augmentation suggests
a right-sided lesion and taken together with left sternal
location is highly suggestive of tricuspid regurgitation,
consistent with RV dysfunction, dilation, and pressure
overload. We believe that the patient in our study
presented with preexisting RV pressure overload
resulting from occult CTEPH and was thus at increasedrisk for paradoxical embolism through the PFO; this
phenomenon may also explain the patient ’s history of
transient ischemic attacks.
Pathologic Discussion
Gross pathology of the pulmonary artery thrombectomyspecimen was consistent with subacute and chronic
thromboemboli with evidence of remodeling and scar
formation of the right-sided pulmonary and segmental
arteries. Histopathology supported this diagnosis as
evidenced by organized thrombus, though thethrombus-in-transit retrieved from the atria showed
components of unorganized and thus acute thrombus.
Extensive involvement of the proximal pulmonary
vasculature was consistent with the diagnosis of
CTEPH as opposed to primary pulmonary arterial
hypertension, which typically involves distal, smaller
arteries <300
mm in size.19The development of CTEPH
is thought to be a secondary arteriopathy,20grossly
mediated by thromboemboli resulting in arterialocclusion, inadequate thrombus resolution, and
inflamed and scarred arterial tissue. Right-sided
cardiomyopathy is observed with CTEPH, likely through
the pathophysiology of increased pulmonary vascular
resistance leading to RV dilation and dysfunction.
21,22
Given the chronicity of CTEPH, the right ventricleadversely remodels; both dilation and hypertrophy
were observed in the patient in our study, findings
that would be unusual for an isolated acute process.
T h em i x e da c u t ea n dc h r o n i cn a t u r eo ft h i s
patient ’s thromboembolic pathologies is explained by
thromboembolic phenomena over the course of hours
to years. In summary, this patient likely developed
CTEPH in the years following initial VTE and PE and
presented several years later with recurrent acute and
subacute PE and thrombus-in-transit.
Treatment Discussion
In general, the sequelae of acute PE, even those withhemodynamic signi ficance and RV compromise,
journal.publications.chestnet.org e45

typically normalize with anticoagulation within 6 weeks
of PE and resolves without signi ficant long-term
sequelae.23A small minority of acute PE patients,
approximately 1% to 8%,20progress to CTEPH. Given
the persistent involvement of the larger, proximal
vasculature typically observed in CTEPH, there is an
opportunity for surgical revascularization with
pulmonary thromboendarterectomy to confer a survival
benefit.4,24If deemed inoperable, balloon angioplasty or
medical therapy alone may be considered as
alternatives.25The patient in our study underwent
thromboendarterectomy at the time of
thromboembolectomy for acute thrombi. Despite this
aggressive revascularization of all lobar and
subsegmental pulmonary arteries, a _V/ _Q scintigraphy
scan performed 1 week following surgery revealed an
unmatched _V/ _Q defect in the right lower lobe ( Fig 6 )
consistent with persistent chronic thromboembolism,
likely from distal thrombotic burden or irreversible
vasculopathy not reversible with surgery alone.A 2-week postoperative echocardiogram revealed a
persistently dilated and hypokinetic RV with an elevated
pulmonary artery systolic pressure of 69 mm Hg plus
central venous pressure. Right heart catheterization
revealed persistent precapillary pulmonary hypertension
(pulmonary artery systolic pressure 55 mm Hg, mean
pulmonary artery pressure of 37 mm Hg, pulmonary
artery occlusion pressure of 10 mm Hg, pulmonary
vascular resistance of 7.8 Wood units, and reduced
cardiac index of 1.89 L/min/m
2). The patient was
ultimately discharged to home on the inhaledvasodilator treprostinil four times daily, oral sildena fil,
and continued supplemental oxygen at 6 L/min.
Persistent pulmonary hypertension following
pulmonary thromboendarterectomy occurs in up to
one-third of patients at 3 month follow-up resultingfrom distal, surgically inaccessible thrombus or
irreversibly impaired vasculopathy.
26-28Nevertheless,
surgical intervention confers mortality bene fit compared
with medical therapy alone despite persistence of
pulmonary hypertension.
Conclusions
The patient in our study exhibited a spectrum of acute,subacute, and chronic PE, representing thromboembolicevents hours, days to weeks, and years after initial
VTE, respectively. Initial management focused on
hemodynamic stabilization and prophylactic retrieval of
a right- to left-sided thrombus that posed a catastrophic
risk of both pulmonary and systemic embolization.
Suspected by history and con firmed at the time of
surgery, CTEPH was appropriately considered, and the
patient underwent concomitant thromboembolectomy,
thromboendarterectomy, and PFO closure.
Multidisciplinary expertise and multimodality
imaging were instrumental in diagnosis and ultimatelyidentifying the optimal management strategy for this
complicated patient.
Acknowledgments
Financial/non financial disclosures: The authors have reported to
CHEST the following: J. R. S. has received payments for expert witness
testimony involving cases of PE. None declared (K. N., G. A. A.,
N. M M., G. J. V., C. D. W., B. B. G., D. M. D.).
Other contributions: CHEST worked with the authors to ensure
that the Journal policies on patient consent to report informationwere met.
Additional information: The Video can be found in the Multimedia
section of the online article.
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