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(2.856L/min). The RQ was 1.15. The anaerobic reserve (peak-
AT VO2) was 1.81, which was 63% of the predicted peak
VO2. VE peak (100.8L/min) reached 52% of the MVV mea-
sured just prior to exercise (194L/min). The oxygen satura-
tion during peak exercise was 92%, physiological VD/VT was
0.27, heart rate (179 BPM) was 104% of the predicted maxi-
mum heart rate and the BP was 144mmHg/90mmHg. The
O2 pulse at peak exercise was 19.6mL/beat mL/beat (438%
of the O2 pulse at rest and 109% of the predicted maximum
of 17.9 mL/beat). The O2 pulse increased continuously
throughout the point when the patient reached anaerobic
threshold and continued to increase even after the VO2
exceeded the predicted peak VO2. Summary of the CPET
results:
• This was a maximal exercise test.
• The patient reached >100% of maximal predicted oxygen
consumption, consistent with supra-normal aerobic exer-
cise capacity.
• Normal cardiac response to exercise, with no evidence of
impairment of heart rate or stroke volume reserve.
• There was no evidence of a ventilatory limitation.
• There was modest oxygen desaturation (nadir 92%), how-
ever, the SpO2 did not fall below 95% until a VO2 was
twofold the value at the onset of anaerobic threshold and
>100% of the maximal predicted VO2.
• The absence of significant ventilatory inefficiency at peak
workload as well as the absolute fall in the VE/VCO2
throughout exercise is consistent with relatively normal
pulmonary vascular recruitment with exertion.
Overall interpretation: The presence of a greater than nor-
mal aerobic exercise capacity, normal cardiac response to
exercise, and absence of significant ventilatory inefficiency
did not support the presence of objective exercise physiologic
limitation on the basis of chronic thromboembolic disease.
Follow-up 12 months after the initial surgical evaluation
revealed that the patient was engaged in high intensity exercise
programs, experiencing an overall improvement in his athletic
P. R. Forfia et al.
67
capabilities. His echocardiogram showed a normal sized right
atrium and right ventricle, with normal RV wall thickness and
normal RV systolic function; only trace tricuspid regurgitation.
The findings on lung scintigraphy were unchanged.
Radiographic Interpretation
The chest radiograph does not show any generic features of
pulmonary hypertension such as cardiomegaly or proximal
pulmonary artery dilatation. Allowing for the mild rotation,
the lungs and pleural spaces are clear.
There are bilateral segmental mismatched perfusion
defects on VQ scintigraphy with no significant change in the
appearances over a 6-month period after commencement of
anticoagulation. It is not surprising to see persistent scinti-
graphic perfusion defects following acute PE.Complete reso-
lution may not be achieved for almost up to a year after the
initial diagnosis. The reported residual obstruction rate on
VQ after institution of anticoagulation is variable. A systemic
analysis showed residual defects in more than 65% of
patients at 3months and 50% at 6months after which throm-
bus resolution reaches a plateau phase (Nijkeuter etal.). A
more recent study showed persistent defects in 30% of cases
after 6 months of anticoagulation and was associated with
higher incidence of symptoms, shorter distances covered in
the 6MWT and higher systolic pulmonary artery pressure
(Sanchez etal.). Since VQ cannot readily distinguish between
acute PE and CTEPH, it is necessary to perform another test,
usually CTPA to look for features of chronic thromboem-
bolic disease. Another VQ pitfall is that the radiolabeled
particles can potentially pass through partially obstructed
vessels and hence perfusion defects can underestimate the
severity of vascular obstruction and may not correlate with
pulmonary vascular resistance or mean pulmonary artery
pressure (Ryan etal.). Therefore, VQ cannot be relied upon
in the evaluation of disease morphology and operability
assessment.
Chapter 7. Case 7: It’s Not CTEPH, but It Is Chronic…
68
Catheter pulmonary angiography shows limited proximal
thromboembolic disease with a pouch defect in the origin of
the right upper lobe branch and lobar lingular occlusion.
There is also attenuation of anterior basal branch of the left
lower lobe from mid segmental level. The remaining vessels
are smooth with no intimal irregularity.
Clinical Comments
As noted by Dr. Gopalan, the presence of residual perfusion
defects following an acute pulmonary embolic event, despite
appropriate antithrombotic therapy, can be found in a consid-
erable number of patients. If these perfusion defects are in
the region of a previous acute thromboembolism, it likely
reflects organized thrombotic residua, or in more contempo-
rary terms, chronic thromboembolic disease (CTED).
Recognized within the spectrum of the “Post PE Syndrome”,
clinically relevant questions then need to address the extent
of CTED present and whether it is accompanied by cardio-
pulmonary symptoms, or associated with pulmonary hemo-
dynamic compromise (Fig.7. 4 ).
All patients after PE
All patients after PE
Reported symptoms of
reduced functional status
Persistent thrombi
Measurable limitations in
cardiopulmonary function
CTEPH
CTEPH
Post-PE syndrome
F . Post PE Syndrome: Klok et al. Blood Reviews 2014;
28:221
P. R. Forfia et al.
69
It is also speculated that the presence of chronic throm-
botic residua represents a precursor to CTEPH.There are
several unresolved issues, however, including whether there’s
a certain amount of CTED that will trigger the development
of the secondary small vessel (see Introduction), the patho-
physiologic mechanism responsible for this transition, and
the time course for these changes to occur. As a result, the
clinician is then faced with the difficult task of recommending
a treatment plan for patients such as presented here. Though
there was clearly operable chronic thromboembolic disease
in this case, this was not enough to proceed with a thrombo-
endarterectomy acknowledging that surgery is not risk free
(Chap. 11 and Taboada et al.). And the “prevention of
CTEPH” by removing the CTE lesions is speculative at best
in the absence of a well-defined natural history of this prob-
lem. Typically, surgery has been advocated in this particular
patient group if (1) they are symptomatic and are impaired
from a functional status perspective, or (2) if significant
physiologic derangement, such as elevated dead space venti-
lation or ventilatory inefficiency, can be documented.
Essentially, if there a problem that can be fixed and result in
a demonstrable improvement if a patient’s quality of life, an
endarterectomy or perhaps balloon pulmonary angioplasty
should be considered.
Point ofEmphasis
The presence of chronic thromboembolic disease by itself does
not necessarily warrant invasive intervention. The decision to
proceed with surgery or balloon pulmonary angioplasty
requires a careful assessment of the risks and anticipated ben-
efits for the patient undergoing such aggressive treatment.
Diagnosis
1. Chronic thromboembolic disease without pulmonary
hypertension at rest.
Chapter 7. Case 7: It’s Not CTEPH, but It Is Chronic…
70
Further Reading
Held M, Grün M, Holl R, et al. Cardiopulmonary exercise test-
ing to detect chronic thromboembolic pulmonary hyperten-
sion in patients with normal echocardiography. Respiration.
2014;87(5):379–87.
Klok FA, van der Hulle T, den Exter PL, Lankeit M, Huisman
MV, Konstantinides S. The post-PE syndrome: a new concept
for chronic complications of pulmonary embolism. Blood Rev.
2014;28:221–6.
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.
Ryan KL, Fedullo PF, Davis GB, Vasquez TE, Moser KM.Perfusion
scan findings understate the severity of angiographic and hemo-
dynamic compromise in chronic thromboembolic pulmonary
hypertension. Chest. 1988;93:1180–5.
Sanchez O, Helley D, Couchon S, etal. Perfusion defects after pul-
monary embolism: risk factors and clinical significance. J Thromb
Haemost. 2010;8(6):1248–55.
Taboada D, Pepke-Zaba J, Jenkins DP, Berman M, etal. Outcome of
pulmonary endarterectomy in symptomatic chronic thromboem-
bolic disease. Eur Respir J. 2014;44(6):1635–45.
P. R. Forfia et al.
71© 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_8
Case Presentation
A 33year-old female with a limited past medical history pre-
sented to the Pulmonary Vascular clinic with complaint of
dyspnea on exertion 2months after a diagnosis of large bilat-
eral pulmonary embolisms (PE) in the central pulmonary
arteries (Fig.8.1).
Chapter 8
Case 8: Another Case
ofCTED: Is Surgery
theWay?
ColleenMcEvoy, DeepaGopalan, andWilliamR.Auger
C. McEvoy (*)
Division of Pulmonary and Critical Care Medicine,
Washington University in St. Louis, St. Louis, MO, USA
e-mail: c.mcevoy@wustl.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
72
At the time of her acute pulmonary embolism, the echo-
cardiogram revealed LVEF 50%, RV hypokinesis, RV pres-
sure overload with PASP 40–45mmHg. She did not require
thrombolytic therapy. Troponins were negative. Lower
extremity duplex dopplers were negative for acute deep vein
thrombosis. She was placed on anticoagulation with enoxapa-
rin and bridged to rivaroxaban. The PE was thought to be
provoked from a long car trip. She complained of shortness of
breath carrying her children and groceries. She had difficulty
climbing stairs, though denied chest pain, lower extremity
edema and presyncope.
During her initial clinic evaluation, vital signs showed BP
115/82, heart rate 103, respiratory rate of 24, oxygen satura-
tion 96% on room air. Physical examination was unremark-
able. Laboratories were notable for BNP 5pg/mL, complete
blood count and comprehensive metabolic panel were within
normal limits. Imaging was significant for a V/Q scan (Fig.8.2)
with perfusion defects in left lower lobe, lingula and right
upper lobe.
Her echocardiogram showed normal LV and RV size and
systolic function, TAPSE 1.8cm. PASP 35mmHg, saline con-
trast study mildly positive for right to left shunt most consis-
tent with a patent foramen ovale (PFO). Six minute walk test
revealed a distance of 1050 ft and no desaturations with
concluding Borg Score of 2. Pulmonary function testing was
F . Selected images from computed tomography pulmonary
angiography at time of diagnosis of pulmonary embolism
C. McEvoy et al.
73
significant for reduced DLCO 44% predicted. Given that the
acute pulmonary embolism was only 2 months prior and the
echocardiogram did not show features of pulmonary hyper-
tension or right heart enlargement, the perfusion defects seen
on V/Q scan were felt to be due to her acute PE.Therefore,
the decision was made to continue anticoagulation and
repeat imaging 6 months after her acute pulmonary
embolism.
At the follow up appointment, 6months after acute PE,
the patient continued to complain of dyspnea on exertion
and impaired exercise tolerance. No signs of right heart
failure. Repeat VQ scan (Fig. 8.3) demonstrated multiple
perfusion defects, unchanged from prior scintigraphy.
CT angiogram of the chest (Fig.8.4) showed resolution of
larger more central filling defects within the pulmonary arter-
ies, now with residual linear appearing peripheral filling
defects consistent with pulmonary artery webs at the segmen-
tal level, particularly in the right lower lobe and left lower
lobe pulmonary arteries, mosaic attenuation and mild enlarge-
ment of the right ventricle. Repeat echocardiogram showed
F . Ventilation perfusion scintigraphy 2 months post-acute
pulmonary embolism
Chapter 8. Case 8: Another Case ofCTED: ...
74
upper normal RV size and mild RV hypokinesis (RV global
longitudinal strain −13.7%), PASP 25 mmHg, normal IVC
size.
Due to her young age, persistence of symptoms 6months
post acute PE, with chronic changes consistent with chronic
thromboembolic disease on CTA chest and V/Q scan, she was
referred to CTEPH Center for evaluation and consideration
of pulmonary thromboendarterectomy (PTE). A right heart
catheterization was performed to evaluate for chronic throm-
boembolic pulmonary hypertension (CTEPH). Resting pul-
monary hemodynamics: RA 10, PA 42/19 (mean 29), PCWP
14, thermodilution cardiac output 5.4 L/min, cardiac index
2.5L/min/m
2
, PVR 2.8 Wood Unit, PA saturation 64%. Using
weights, her upper extremities were exercised resulting in an
increase in her thermodilution cardiac output to 8.1L/min, PA
pressure was 72/30 (mean 49), PCWP 17. She was diagnosed
with chronic thromboembolic disease (CTED), characterized
by persistent pulmonary thromboembolic occlusion with mild
F . Ventilation perfusion scintigraphy 6months post-acute
pulmonary embolism
C. McEvoy et al.
75
a
b
F . (a–d) Selected images from computed tomography pul-
monary angiography 6months post-acute pulmonary embolism
Chapter 8. Case 8: Another Case ofCTED: ...