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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3902_Библиотеки_им_академика_М_И_Перельмана
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151
PCWP 6mmHg; PA saturation 67.3%; cardiac output 4.5L/
min with a cardiac index 2.43L/min/m
2
; transpulmonary gra-
dient was 19mmHg.
Concurrent with her catheterization, pulmonary angiogra-
phy was obtained. This demonstrated pronounced filling
defects in the left lower pulmonary arteries and smaller filling
defects in the segmental and subsegmental levels; there were
filling defects in the right upper, middle, and lower lobe pul-
monary arteries at the lobar and segmental levels (Fig.16.4).
By hospital day 12, she was discharged in stable condition.
She was at a therapeutic level on warfarin therapy (patient
refused Eliquis). She was hemodynamically stable and ambu-
latory. Thrombolytic therapy was never given, as the consen-
sus of opinions was that she had acute pulmonary emboli on
top of significant chronic thrombi. The oral contraceptive
(OCP) drugs were discontinued on admission.
F . Several unmatched, large perfusion defects, particularly
apparent throughout the right lung and medial left lower lobe (pos-
terior view)
Chapter 16. Case 16: Acute Versus Chronic …
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152
Six weeks after hospital discharge the patient was working
full-time in a restaurant in her hometown, was increasing her
activities and doing well. She was stable on 8mg of warfarin
daily. By eleven weeks after hospital discharge, the patient
was feeling fine with no complaints. She was participating in
a yoga class and sailing. She also underwent a HAST study
for a planned vacation trip to San Diego and did not require
oxygen for the flight. She denied dyspnea with her activities,
though still had not regained her usual physical activity level
yet. Her physical examination was unremarkable.
Hypercoagulable lab studies all came back negative. A lim-
ited echocardiogram showed normal RV size, with mildly
decreased systolic function (40%), and a PA systolic pressure
estimated at 23mmHg, Chest radiograph findings were “nor-
mal” and a lung ventilation-perfusion scan documented reso-
lution of the previously observed perfusion defects (Fig.16.5).
At the time of her six month follow up, the patient was
clinically doing well and had resumed all prior activities
including the exercise required by ROTC training. She dis-
continued her warfarin without recurrence of any concerning
symptoms (WHO Functional Class I). Echocardiogram find-
ings: normal RV size and function; PASP 21mmHg, TAPSE
26mm, normal IVC, and no effusion.
F . Intraluminal filling defects apparent (arrows) in both
descending pulmonary arteries, as well as in the segmental vessels of
the right upper lobe, right lower lobe and lingula
D. L. Zwicke et al.
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153
Radiographic Interpretation
CTPA demonstrates acute and subacute pulmonary embo-
lism. There are central filling defects surrounded by rim of
contrast medium in multiple segmental pulmonary artery
branches, characteristic of acute emboli. Clot retraction to the
periphery of the vessel in the distal right main pulmonary
artery is likely due to clot reorganisation and recanalization
and is indicative of the subacute nature of the process. There
is near complete occlusion of left lower lobe and right upper
lobe arteries. Whilst this can be seen with both acute and
chronic thromboembolic disease, the vessel is typically dis-
tended in acute PE and becomes fibrosed and attenuated with
progression to CTEPH. Other angiographic features of
CTEPH include pouch defects, intravascular webs and steno-
sis with or without post-stenotic dilatation (Castañer et al.).
F . Return of an essentially normal perfusion pattern in
both lungs
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Systemic collaterals also take time to develop and are there-
fore not a feature of acute PE. Another useful clue to the
chronicity of the disease on CT is the presence of geographical
variation in lung parenchymal attenuation, termed as ‘mosaic
attenuation’.
It is possible to evaluate the cardiac chambers even on a
non-ECG gated CTPA. The diameter ratio of right to left
ventricle on transverse CT sections has the strongest predic-
tive value and most robust evidence base for adverse clinical
outcomes in acute PE.A RV/LV ratio ≥1.0 has been shown
to have a 2.5-fold risk for all-cause mortality and a fivefold
risk for PE–related mortality (Meinel at al.). On this study,
there is dilatation of the right ventricle, under-filled small left
ventricular cavity size (RV:LV>1.5) with flattening of inter-
ventricular septum.
The appearances of catheter pulmonary angiography
mirror that of CTPA with multifocal, predominantly central
filling defects bilaterally associated with large wedge shaped
perfusion defects. Similar bilateral wedge shaped segmental
mismatched perfusion defects are also seen on the VQ scin-
tigraphy. Unlike CTPA, it is difficult to differentiate acute
and chronic thromboembolic disease solely using
scintigraphy as both can produce similar defects. A baseline
VQ at presentation can be very useful to follow the tempo-
ral evolution of the disease but perfusion deficits can be
persistent for up to 12 months after the initial event and do
not necessarily equate to CTEPH (Nijkeuter etal.). Happily
in this case, the follow-up VQ shows complete resolution of
the perfusion defects, effectively excluding progression to
CTEPH.
A small proportion of patients labelled as acute PE at the
time of initial presentation actually have acute on chronic
thromboembolic disease (Guérin etal.). This is an important
distinction to make as they have very different therapeutic
options. Of the various imaging modalities, CTPA is the non-
invasive method of choice for differentiating the two condi-
tions, particularly in an emergency setting.
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Clinical Comments
Though this patient was initially referred for pulmonary
thromboendarterectomy surgery, there were a number of
considerations that supported a more conservative approach.
Available information does suggest that when cardiopulmo-
nary symptoms are presented for greater than 2 weeks at the
time of initial presentation, that there’s a higher likelihood
that some component of chronic thromboembolic disease
may be present. Though the presence of RV enlargement
and strain are concerning, this in itself is not a distinguishing
feature between an acute pulmonary embolic event versus
the presence of chronic thromboembolic disease. The absence
of RVH, the CT appearance of the thrombus, the absence of
pulmonary vascular changes that are associated with orga-
nized, recanalized thrombus as described by Dr. Gopalan,
and the absence of other findings that might suggest long-
time pulmonary arterial obstruction, such as bronchial arte-
rial collateral blood vessels—as was the situation in this
case—makes acute or subacute pulmonary emboli the most
likely diagnosis. The pulmonary hemodynamic profile as well
supported the diagnosis of a more acute pulmonary embolic
event. The classic findings of Sutton and colleagues in the
1970s established that with an acute PE, a modest rise in
pulmonary pressures are to be expected given the limitations
of a “unconditioned” RV presented with an abrupt rise in
vascular resistance. For those with chronic thromboembolic
disease, however, the right ventricle has been able to com-
pensate for the longstanding elevation in RV afterload, and
pulmonary pressures at presentation can be significantly
elevated.
Points ofEmphasis
With the availability of numerous interventional modalities to
treat acute and chronic thromboembolic disease, especially for
clinically decompensating patients, it becomes increasingly
important to be able to distinguish between clinical entities.
Chapter 16. Case 16: Acute Versus Chronic …
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Diagnosis
1. Acute pulmonary emboli with right heart strain.
Further Reading
Castañer E, Gallardo X, Ballesteros E, etal. CT diagnosis of chronic
pulmonary thromboembolism. Radiographics. 2009;29(1):31–50.
Eischer L, Eichinger S, Kyrle PA.The risk of recurrence in women
with venous thromboembolism while using estrogens: a prospec-
tive cohort study. J Thromb Haemost. 2014;12(5):635–40.
Guérin L, Couturaud F, Parent F, etal. Prevalence of chronic throm-
boembolic pulmonary hypertension after acute pulmonary embo-
lism. Prevalence of CTEPH after pulmonary embolism. Thromb
Haemost. 2014;112(3):598–605.
Meinel FG, Nance JW Jr, Schoepf UJ, Hoffmann VS, Thierfelder
KM, Costello P, Goldhaber SZ, Bamberg F. Predictive value of
computed tomography in acute pulmonary embolism: systematic
review and meta-analysis. Am J Med. 2015;128(7):747–59.
Nijkeuter M, Hovens MM, Davidson BL, Huisman MV.Resolution
of thromboemboli in patients with acute pulmonary embolism: a
systematic review. Chest. 2006;129:192–7.
Sutton GC, Hall RJC, Kerr IH.Clinical course and late prognosis of
treated subacute massive, acute minor, and chronic thromboem-
bolic disease. Br Heart J. 1977;39:1135–42.
Vinogradova Y, Coupland C, Hippisley-Cox J. Use of combined
oral contraceptives and risk of venous thromboembolism: nested
case-control studies using the QResearch and CPRD databases.
BMJ. 2015;350:h2135.
D. L. Zwicke et al.
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157© Springer Nature Switzerland AG 2020
W. R. Auger, D. Gopalan (eds.), Clinical Cases in Chronic
Thromboembolic Pulmonary Hypertension, Clinical Cases in
Cardiology, https://doi.org/10.1007/978-3-030-17366-1_17
Case Presentation
A 58 year-old Caucasian male with a history of DVT pre-
sented for evaluation of shortness of breath. At his initial
assessment, he reported a 2year history of progressive symp-
toms. He endorsed exertional dyspnea with walking more
than ¼ mile and noted shortness of breath when climbing one
Chapter 17
Case 17: Can Severe
Pulmonary Arterial
Pulmonary Hypertension
Mimic CTEPH?
JeanM.Elwing, DeepaGopalan, andWilliamR.Auger
J. M. Elwing (*)
Pulmonary Hypertension Program, Division of Pulmonary Critical
Care Medicine, University of Cincinnati College of Medicine,
Cincinnati, OH, USA
e-mail: jean.elwing@uc.edu
D. Gopalan
Department of Radiology, Imperial College Hospitals, London, UK
e-mail: d.gopalan@nhs.net
W. R. Auger
Lewis Katz School of Medicine, Temple University,
Philadelphia, PA, USA
e-mail: Bill.Auger@tuhs.temple.edu
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158
flight of stairs. He denied associated chest pain but did expe-
rience lightheadedness, dizziness and presyncope with activ-
ity. He also noted recent onset of lower extremity edema.
His past medical history was notable for controlled GERD,
anxiety, a DVT in 2010 on full dose anticoagulation, recurrent
superficial venous thrombosis, homozygous MTHFR C677T
mutation, OSA, controlled asthma, splenectomy after an auto-
mobile accident in 1968 and remote tobacco abuse. He denied
a history of connective tissue disease. He did not have known
prior pulmonary emboli or a family history of pulmonary
hypertension. Social history was notable for tobacco abuse,
quitting more than a decade prior to presentation. He denied
any previous stimulant or anorexigen use. He had no history
of illegal substance or alcohol abuse.
Examination was notable for blood pressure of
120/90mmHg, pulse of 72, and saturations of 98% on room air.
He was in no acute distress. Cardiopulmonary exam revealed
hepatojugular reflux without JVD at 45°. Cardiac auscultation
was notable for regular rate and rhythm with an accentuated
P2 but no appreciable murmurs. Lungs were clear to ausculta-
tion without bruits over posterior lung fields. 1+ bilateral lower
extremity edema was appreciated on extremity exam.
Laboratory and routine testing revealed hemoglobin of
15.2g/dL.Creatinine was mildly elevated at 1.26mg/dL with a
sodium level in the normal range at 142 mmol/L. BNP was
within acceptable limits at 84pg/mL.Liver functions were nor-
mal. EKG revealed sinus rhythm with septal T-wave changes
but no other significant abnormality. Radiographic evaluation
revealed a chest X-ray (Fig.
1 7. 1 ) with clear lung fields.
Because of significant symptoms, further assessment was
pursued. Echocardiogram was notable for normal systolic left
ventricular (LV) function with ejection fraction of 55%.
Right ventricle was mild to moderately dilated. Tricuspid
valve was moderate to severely regurgitant and pulmonary
pressures were estimated at 78mmHg.
His abnormal echocardiogram prompted further evalua-
tion of the etiology and severity of his elevated pulmonary
pressures. Additional laboratory assessment revealed normal
thyroid function and no significant abnormalities on autoim-
mune workup. Pulmonary function testing (Table 17. 1 ) did
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159
F . Chest X-ray with normal heart size and no significant
parenchymal abnormalities
T .
Pulmonary
function test without
signicant obstruction or
restriction. Diffusing
capacity was mildly
decreased
FEV1 (L) 2.96
FEV1% 89
FVC (L) 4.31
FVC% 92
FEV1/FVC (%) 69
TLC (L) 6.56
TLC% 98
RV 1.52
RV% 65
VC 5.04
VC% 1.08
DLCO (mL/
mmHgs)
19.5
DLCO % 78
Chapter 17. Case 17: Can Severe Pulmonary ....
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160
not reveal significant changes that could account for severity
of elevated pulmonary pressures.
Additional imaging was performed to assess for possibility
of pulmonary embolism as etiology of his progressive short-
ness of breath and echocardiographic findings. Ventilation
(Fig.1 7. 2 )/perfusion (Fig.1 7. 3 ) scanning was performed and
revealed bilateral patchy perfusion defects without signifi-
cant ventilation abnormalities.
Based on V/Q, there was concern for chronic thromboem-
bolic pulmonary hypertension (CTEPH). A more definitive
evaluation with CT pulmonary angiogram (CTPA) (Fig.1 7. 4 )
was therefore requested. CTPA revealed enlarged pulmonary
arteries but no evidence of significant parenchymal lung dis-
ease or pulmonary emboli.
Patient then proceeded to further assessment with right
heart catheterization (RHC) (Table 1 7. 2 ) and pulmonary
angiogram (Fig. 1 7. 5 ). RHC revealed moderately elevated
pulmonary pressures in a precapillary pattern without evi-
dence of acute or chronic thromboembolic disease on
angiography.
After completion of his assessment, he was reevaluated
and data reviewed. His workup was consistent with symptom-
atic precapillary pulmonary hypertension. Initial testing with
F . Xenon ventilation scanning with symmetric ventilation
and mild bilateral retention
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