Title: Dynamic (4D) CT perfusion offers simultaneous functional and anatomical

insights into pulmonary embolism resolution.

Abstract:

Objective: Resolution and long-term functional effects of pulmonary emboli are

unpredictable. This study was carried out to assess persisting vascular bed perfusion

abnormalities and resolution of arterial thrombus in patients with recent pulmonary

embolism (PE).

Methods and materials: 26 patients were prospectively evaluated by dynamic (4D)

contrast enhanced CT perfusion dynamic pulmonary CT perfusion. Intermittent

volume imaging was performed every 1.5-1.7 seconds during breath-hold using and

perfusion values were calculated by maximum-slope technique. Thrombus load

(modified Miller score; MMS) and ventricular diameter were determined. Perfusion

maps were visually scored and correlated with residual endoluminal filling defects.

Results: The mean initial thrombus load was 13.1±4.6 MMS (3-16), and 1.2±2.1

MMS (0-8) at follow up. From the 24 CTPs with diagnostic quality perfusion studies,

normal perfusion was observed in 7 (29%), and mildly-severely abnormal in 17

(71%). In 15 patients with no residual thrombus on follow up CTPA, normal

perfusion was observed in 6, and abnormal perfusion in 9. Perfusion was abnormal in

all patients with residual thrombus on follow up CTPA. Pulmonary perfusion changes

were classified as reduced (n=4), delayed (systemic circulation pattern; n=5), and

absent (no-flow; n=5).

The right ventricle was dilated in 12/25 (48%) at presentation, and normal in all 26

follow up scans. Weak correlation was found between initial ventricular dilatation

and perfusion abnormality at follow up (r=0.15).

Conclusions: Most patients had substantial perfusion abnormality at 3-6 months post

PE. Abnormal perfusion patterns were frequently observed in patients and in regions

with no corresponding evidence of residual thrombus on CTPA. Some defects exhibit

delayed, presumed systemic, enhancement (which we have termed ‘stunned’ lung).

CT perfusion provides combined anatomical and functional information about PE

resolution.

Introduction

Pulmonary embolism (PE) is common in the Western world with an estimated

incidence of approximately 3 in 1000 population per year [1] These patients are at

increased risk of recurrent thromboembolic episodes and secondary pulmonary

hypertension with a reported first year mortality of 5-6% [2,3]. Anticoagulants are

the main recognised treatment for PE [1], but are associated with risk of

haemorrhage resulting in morbidity and mortality [4].

Despite being a common disease many aspects of the natural course of the condition

are poorly understood. It is recognised that pulmonary emboli resolve in an

inconsistent manner. The reported rate of PE resolution on computed tomography

pulmonary angiography (CTPA) varies from 40-57% in early follow ups (within 2

weeks following the acute episode), to 77-81%, after 3months of the initial PE

diagnosis [5,6].

Despite significant improvements, exclusion of pulmonary embolism by CTPA is still

restricted by its insensitivity to small, subsegmental emboli [7,8]. The speed of

resolution of clots and extent of residual perfusion defects in different patient groups

remains to be clarified. How the clot burden and rate of clot resolution relate to

persisting micro-vascular perfusion abnormalities is also unclear. Clarification of

these issues may help in risk stratification (eg. risk of subsequent pulmonary

hypertension), and in guiding treatment strategies. The aim of this study was to use

dynamic (4D) computed tomography perfusion studies (CTP) to characterise

pulmonary perfusion abnormalities and residual thrombus load in patients with

previous pulmonary embolism and to compare the finding with the thrombus load and

right heart features as measured on the presentation conventional CTPA studies. The

study hypothesis was that CTP would be superior to CTPA in the diagnosis of

residual thromboembolic disease in patients recovering from a recent episode of PE.

Methods and material:

Patients:

Following institutional approval, 26 adult patients with history of an acute PE,

confirmed on CTPA (n=25) and perfusion scintigraphy (n=1) were prospectively

recruited. Written informed consent was obtained in all cases. Perfusion CT (CTP)

studies were performed 3-6 months following the initial PE episode. Exclusion

criteria included pregnancy, inability to undergo computed tomography (CT)

scanning, renal failure (serum creatinine >250 µmol/L or estimated glomerular

filtration rate <25 mL/min), previous recruitment to the study, known contrast

allergy, unable to give informed consent, and background parenchymal lung disease

as other potential causes of perfusion changes (emphysema, fibrosis). Patients

received anti-coagulation according to local guidelines following an episode of acute

PE (Warfarin Sodium for 6 months following the episode of PE, and for lifetime in

recurrent PE). Age and gender were recorded. Patient’s body size was classified by

measuring the maximum lateral thoracic width (LTW) on AP scout films at the

cardiac-diaphragm interface (at the level of liver) [9,10]. Based on the average LTW in

our cohort, patient size was graded thin, medium, and large, when the LTW was <32cm,

32-38cm, and >38cm, respectively [10].

Image acquisition and reconstruction:

The CTP scans were performed during a single breath-hold at deep inspiration.

Shallow abdominal breathing was permitted at the end stage of acquisition in patients

who were unable to hold their breath for the entire perfusion CT data acquisition.

All CT scans were performed on a 320-multidetector computed tomography scanner

(Aquilion ONE, Toshiba Medical Systems, Nasushiobara, Japan). Low dose scout

imaging was performed to localise the thoracic structures. Intermittent volume

imaging was performed every 1.5-1.7 seconds (11-12 volumes in total) with 3

seconds delay after the start of intravenous contrast injection. Scans were performed

with 16 cm z-axis coverage (320 x 0.5-mm collimation) with the lowest section at the

level of the diaphragm, 100 kVp, 0.5s rotation, and fixed tube current 100 mA (tube

current-time product 50 mAs). Variable tube current protocol (mA boost) was used in

one patient to reduce image noise in the pulmonary arteries. This included boosting

tube current (200mAs) in 3 volumes timed with the peak of the PA enhancement, and

standard current (100mA) for the rest of 8 volumes. Toshiba’s iterative

reconstruction algorithm (Adaptive Iterative Dose Reduction 3D; AIDR-3D, strong)

was used to reconstruct 0.5mm sections from the raw data (Toshiba Medical Systems,

Nasushiobara, Japan).

A dual-head power injector (Stellant CT Injection Systems, MEDRAD, Warrendale,

USA) was used for bolus injection of 70 mL iodinated contrast agent (Iomeron 400,

Bracco SPA, Milan, Italy; 400mg/mL) via a 16G antecubital vein catheter (Vasofix,

Braun, Melsungen, Germany) at a rate of 9 mL/sec, followed by 20 mL of saline

solution at the same rate.

Post processing of dynamic contrast enhanced perfusion CT Images:

Non-rigid registration of the contrast-enhanced studies was performed using a

dedicated commercial workstation to reduce the effect of motion (Vitrea FX v6.3,

Vital Images, Minnesota, USA). For the qualitative evaluation of the perfusion,

parametric maps of perfusion were produced using the same workstation using the

Dual Input Lung Perfusion software by maximum slope method (Vitrea FX v6.3,

Vital Images, Minnetonka, USA). Regions of interest (ROIs; 5 mm diameter) were

placed in the main pulmonary artery and descending aorta to define the pulmonary

and systemic arterial input functions. Same size ROI was placed in the left atrium and

the peak enhancement time point was used to differentiate pulmonary circulation

from systemic/bronchial circulation [9]. Regions of interest were drawn in the normal

lung parenchyma away from main vascular branches, chest wall/mediastinal

structures, and dependent/atelectatic lung changes. Computation of parametric

perfusion maps was performed using the same workstation (Body Perfusion, (Vitrea

FX v6.3, Vital Images, Minnetonka, USA). The perfusion analysis range was set

from -300 HU to -1000 HU to restrict the perfusion analysis to lung parenchyma and

to exclude major vessels and the soft tissues/bones. Pulmonary blood flow (PBF;

mL/mg/min) was calculated as the maximum slope of tissue enhancement curve

divided by the maximum arterial enhancement [12]. Parametric 512 × 512 matrix

colour-coded maps of the pulmonary flow (PF) and systemic arterial flow (AF), and

pulmonary index (PI=PF/PF+AF) were generated automatically [13].

Analysis of CT pulmonary angiography (CTPA) data:

The CTPA from the acute PE presentation episode and the follow up CTPA from the

dynamic contrast enhanced perfusion study were evaluated in consensus by two

thoracic radiologists (SM and EJVB) who were blinded to patients’ details. From the

11 CT volumes, the angiogram(s) with visually densest contrast within the pulmonary

artery were used to identify residual intravascular thromboembolic material.

Overall image quality of each CTPA was rated on a 4-point scale (1: non-diagnostic;

2, fair image quality; 3: good image quality; and 4: excellent image quality). Causes

for the compromised image quality were recorded (eg. motion, image noise, beam

hardening).

Two thoracic radiologists (EJVB & JTM) objectively assessed in consensus the

pulmonary arterial obstruction using the Modified Miller Scoring system (MMS) on

both the initial CTPA and on the angiogram from the perfusion scan [14]. The

modified Miller Score (MMS) is a score of thrombus load that was originally

proposed by Miller et al. for conventional angiography and adapted for CTPA scan

[14]. The right pulmonary artery was assigned nine segmental arteries (three to the

upper lobe, two to the middle lobe, and four to the lower lobe), whereas the left

pulmonary artery was assigned seven segmental arteries (two to the upper lobe, two

to the lingula, and three to the lower lobe). Each occluded segmental pulmonary

artery that is given a score of 1. Any more proximal occlusion scores the number of

segmental branches distal to the occlusion thereby giving a MMS of 0 (no thrombus)

to 16 (thrombus in all segmental arteries or saddle embolism) [14].

Diameter of the right ventricle (RV) and left ventricle (LV) was measured on the

axial sections in the basal segment at the level of mitral valve. The RV was defined as

dilated when the RV/LV ratio was >1.

Analysis of perfusion data:

Parametric perfusion maps were objectively assessed in consensus by 2 thoracic

radiologist with expertise in CTP studies (SM & EJVB). Four patterns of pulmonary

perfusion were identified on parametric maps and were confirmed by examination of

the time-density curves in the regions of interest. The perfusion patterns were

classified as: normal perfusion, reduced perfusion (reduced enhancement slope with

delayed peak compared to normal lung; Fig. 1), systemic perfusion (delayed peak

enhancement that is synchronised with the aortic enhancement peak), and absent

(only image noise observed, no real enhancement).

The two radiologists objectively scored lobar perfusion. The agreed score was to

reflect the volume of lung in each lobe. Compared to the modified Miller’s score, the

upper lobes were assigned lower scores compared to the lower lobes since the 16cm

detector area did not cover the apices of the upper lobes in any patient. Each of the

upper lobes, right lower lobe, left lower lobe, middle lobe and the lingual were

assigned, 3, 4, 3, 2 and 1 score (total of 16 score). An objective perfusion index (OPI)

was calculated as total scored perfusion divided by 16. The lung perfusion was then

graded as: severely abnormal (OPI <0.6), moderately abnormal (OPI 0.6-0.8), mildly

abnormal (OPI >0.8), and normal (OPI =1).

Statistical analysis:

All results were expressed as mean ± standard deviation (SD) unless indicated

otherwise. Correlations between the presence of RV dilatation at presentation and

perfusion abnormality in follow up was performed using Pearson’s correlation and

expressed as r2 values. SPSS for Windows (v10.0.1) was used for all statistical

analysis.

Results:

Twenty-six consecutive patients with recent PE and a mean age of 61 (±16.5 years;

range 23-86) were recruited (male/female=16/10). The average lower thoracic

diameter was 38cm (±4.7; 30-50). Based on the lower thoracic diameter

measurements, 3, 10, and 13 patients were classified as small, medium, and large,

respectively. The average time interval between the initial CTPA (when the diagnosis

of acute PE was made) and the follow up CTP was 22 ±16 weeks.

In 3 patients, the initial CTPA had to be repeated due to poor contrast timing and

hence sub-optimal enhancement of the pulmonary arteries. The mean total dose

length product (DLP) of the initial CTPA (including the repeat scans) and the CTP

was 724±328 and 615±159 mGy·cm, respectively. The DLP for the mA boost

protocol in a borderline large patient (LTW) was 690 mGy·cm. The estimated

effective doses for the CTPA and CTP studies were 10.1±4.6 and 8.6±2.2 mSv,

respectively (conversion factor=0.014 mSv/mGy.cm). The entire lung was covered in

the standard CTPA whilst the 16cm field of view coverage did not cover the whole

upper lobe in any patient.

The quality of pulmonary angiography on the initial CTPA was rated “excellent” in

22 cases, and “good” in 3. This does not take into account that the initial CTPA in 3

patients was non-diagnostic and had to be repeated. The quality of CT pulmonary

angiogram in the CTP series was rated as “excellent” in 12, “good” in 7, “sub-optimal

but diagnostic” in 4, and non-diagnostic in 3 cases. The causes for sub-optimal

quality of the angiograms were excessive noise in 3, beam hardening in 3, and motion

in 1 case. Excessive noise and beam hardening was almost exclusively seen in larger

patients (mean LTW 39.5cm ±4). The mA boost in a patient with LTW of 37cm

resulted in excellent improvement of the quality of pulmonary angiogram, when

compared to standard mA.

The pulmonary arterial obstruction, as evaluated by the Modified Miller Scoring

system (MMS) was 13.1±4.6 (3-16) in the initial CTPA, and 1.2±2.1 (0-8) in the

angiogram from the CTP series. From the 25 diagnostic follow up CTPA, MMS was

reported as 0 in 16 patients (64%), 1-3 in 7 patients (28%), and 7-8 in 2 patients (8%)

(Fig. 2).

In 4 patients there was CT evidence of ischemic lung injury (peripheral wedge-shape

consolidation in the territory of thrombosed arteries). All the changes resolved on

follow up examination and no scaring seen.

Perfusion analysis was non-diagnostic in 2 patients, sub-optimal but diagnostic in 6

patients, and good in 18. The common causes for quality compromises were the effect

of motion on calculated perfusion values (n=7), excessive image noise (n=3), and

beam hardening (n=1). Significant image noise and beam hardening in a very large

patient with LTW of over 50cm, and significant motion that was not corrected by

image registration accounted for the non-diagnostic perfusion studies.

Figure 2 shows the percentage of patients with residual thromboembolic by

pulmonary arterial obstructive score and CT perfusion abnormality at follow up.

From the 24 patients with diagnostic CTP, normal perfusion was observed in 7 (29%)

patients (OPI=1), 10 (42%) had mild perfusion abnormalities (OPI= 0.8-0.99), 5

(20%) had moderate perfusion abnormalities (OPI=0.6-0.79), and 2 (8%) had severe

perfusion abnormalities (OPI <0.6) (Fig. 2). Perfusion was normal in 6 patients, but

abnormal in 9 patients with normal follow up CTPA. In 2 patients who had

significant residual thromboembolic material in the post treatment CT, there

was a discrepancy between the abnormalities on CTPA and CTP in both patients.

One patient with significant residual thromboembolic material (MMS=8) had severe

perfusion abnormalities (OPI=0.56), whereas the other patient with significant

residual thromboembolic material (MMS=7) showed only mild perfusion

abnormalities. In contrast, in another patient with severe perfusion abnormalities

(OPI=0.58), only mild residual thromboembolic material (MMS=2) was observed.

Figures 3-4 show examples of patients with various levels of PE resolution on CTPA

at follow up, and inconsistent level of perfusion resolution on CTP. There was weak

correlation between the MMS at presentation and perfusion abnormality at follow up

(r=0.11; Pearson's Product-Moment Correlation).

Regional pulmonary perfusion abnormalities patterns were classified as reduced

perfusion in 4 patients, significantly delayed/from systemic circulation in 5 patients,

and absent (no-flow) in 5 patients. The lung parenchyma appeared normal in areas

with delayed perfusion (termed ‘stunned’ lung). Figure 5 shows an example of

abnormally delayed pulmonary perfusion in a patient with previous PE.

Right ventricular was dilated in 12/25 (48%) on the initial CTPA, and normal in all

26 follow up scans. There was weak correlation between the presence of RV

dilatation at presentation and perfusion abnormality at follow up (r=0.15; Pearson's

Product-Moment Correlation).

During the clinical follow up period (mean 33 months; 20-54 months), 7 patients

returned with recurrent symptoms. Further investigation confirmed pulmonary

thromboembolic disease or DVT in 5 (19%): 1 new PE, 3 residual thromboembolic

material, and 2 new DVTs. All these patients had mild to moderate perfusion

abnormality on CTP. None of patients with normal CTP had recurrent presentation

during the follow up period.

Discussion

Resolution of PE is reported to be variable, ranging from 32-48% in earlier studies

[13-18] , depending on the modality used (eg. CTPA or ventilation/perfusion

scintigraphy) and the timing of the follow up (6 weeks-10.5 months) [19]. It is not

clear to what degree the reported variation was due to the limitations of imaging

techniques used in these studies. More recent studies reported a higher

resolution rate on CTPA of 81%-100% within one month from the acute episode

[20,21]. Compared to other non-invasive imaging modalities, our study shows that

dynamic (4D) CT perfusion provides comprehensive assessment of the proximal clot

burden, pulmonary perfusion, cardiac chambers, and lung parenchyma in a single

imaging episode. Combined, the above information may potentially provide a strong

tool in the evaluation of clinical outcome and treatment guidance.

As indicated earlier, previous perfusion scintigraphy studies demonstrated persistent

perfusion abnormalities even after a year and follow up scintigraphy at the

completion of the anticoagulation was recommended [22,23]. A weakness of the

scintigraphy is that it does not differentiate between new and persisting perfusion

abnormalities and as a result, a persisting perfusion defects can be misinterpreted as fresh

pulmonary embolism which may lead to unnecessary treatment and hospitalisation

[23,24]. This clearly shows the advantage of the CTP as the angiographic data embedded

in the dynamic series would differentiate acute from resolving or persistent PE.

Currently, CTPA is the standard technique for the diagnosis of acute PE. However, a

study of 1193 patients demonstrated an inconsistent relationship between clot burden

and mortality [25]. Another study only showed a relationship between proximal clot

burden and clinical deterioration [2]. These results may be partly explained by the

insensitivity of CTPA in the diagnosis of small, subsegmental emboli [7,8].

Furthermore, CTPA underestimates distal obstructive burden as shown in our results,,

which may further explain an unreliable relationship between clot burden, mortality

and clinical deterioration [2,25]. Our study demonstrated recurrence only in patients

with abnormal CTP which demonstrates the clinical relevance of the findings on CT

perfusion. Adequately powered cohorts with longer follow-up are necessary to

evaluate the sensitivity and specificity of CTP studies in the estimation of clinical

outcome.

CTP has the advantage of CTPA that it can compensate for limited spatial resolution

by incorporating dynamic information of blood flow. Previous studies showed

different patterns of vascular remodelling following pulmonary arterial obstruction

[26]. In 1847, Virchow reported that the bronchial circulation could proliferate and

sustain lung tissue distal to a pulmonary embolism [27]. An experimental model of

chronic arterial obstruction showed that at 4 months, new bronchial vessels encircled

pulmonary arteries, veins and airways, and in some instances, bronchial vessels

branched out into the parenchyma and joined with capillaries [28]. In addition to

bronchial neovascularization, intercostal arteries may participate in the

neovascularisation of the ischemic lung [29]. Overall, systemic blood flow to the lung

may increase by as much as 30% of the original pulmonary blood flow [30]. Our

hypothesis is that this mechanism accounts for the delayed perfusion pattern which

we have observed in some of these 3-6 month post PE follow up scans.

Previous imaging studies demonstrated alternative pulmonary perfusion mainly in

patients with chronic thromboembolic disorders. A study of dual energy first pass

pulmonary perfusion in 20 patients with chronic thromboembolic pulmonary

hypertension demonstrated residual perfusion in 64% of lobes with apparently

completely occluded vessels where it was suggested that the blood supply was

maintained via systemic collaterals [31]. Another dual phase dual energy study of

acute and chronic thromboembolic disorders reported late iodine enhancement

indicating systemic pulmonary supply in chronic, but not in acute thromboembolic

disease [32]. Moreover, a study of patients with chronic thromboembolic pulmonary

hypertension also demonstrated systemic supply with dilated bronchial arteries that

returned to normal after thromboendarterectomy [33].

There is evidence that understanding the pattern of perfusion has prognostic value.

Kauczor et al reported that dilated bronchial arteries on CT were a significant

predictor for survival after pulmonary thromboendarterectomy [34]. Thus, bronchial

perfusion may have a protective role in pulmonary thromboembolic disease [35].

Other experimental studies reported another protective mechanism by the reflux of

left atrial blood through the pulmonary veins to gas-exchanging tissue after

pulmonary artery ligation [36]. To our knowledge, our study is the first imaging study

to observe the systemic circulation in patients recovering from acute PE. No

associated significant bronchial dilatation was observed. In the corresponding

segments, no CT evidence of parenchymal injury/scarring was observed indicating

that alternative perfusion routes may play a protective role in these patients.

Dynamic CTP exposes patients to ionising radiation. In this study, the overall

radiation dose of the CTP was comparable to standard CTPA. Further studies,

demonstrated that by using iterative imaging reconstruction, significant radiation dose

reduction of up to four folds in smaller patients, and up to 2 fold in the medium/large

size patients can be achieved whilst diagnostic perfusion studies are achieved [10]. In

larger patients, to achieve a diagnostic CTPA, tube current modulation at the peak PA

enhancement reduces image noise and beam hardening effect.

In this cohort, one perfusion study was non-diagnostic due to excessive motion that

could not be corrected by non-rigid registration. Future improvements in registration

techniques may allow CTP in patients with poor breath hold.

We demonstrated that right heart size was not a good indicator of recovery from

obstructive consequences of an acute PE. This is not surprising since with normal

RV, 50-75% of the pulmonary vasculature must be obstructed before RV failure can

be seen [37-39]. Moreover, in the acute state, other factors such as the vasoreactive

substances released in response to the event and the baseline cardiopulmonary status

also play a role in development of RV failure [40].

There are a few technical considerations. Whilst the duration of the dynamic scan in

this protocol was sufficient to determine pulmonary and early systemic perfusion, it

may not be long enough to identify very late systemic perfusion or the full contrast

wash-out. We used a maximum slope technique to estimate perfusion, the technique

does not rely on the wash-out phenomenon. To obtain adequate vascular and tissue

opacification, 70mLs of contrast was administered. This large volume might have

potentially violated the assumption of bolus characteristics that is a prerequisite for

accurate perfusion measurements. To get the shortest and densest peak enhancement,

contrast has to be delivered directly in the pulmonary arteries, but this will not be

feasible in routine clinical practice. We used a large bore venous catheter and a high

injection rate to reduce the length of the bolus delivery. Examination of the

pulmonary artery time-density curves in all cases demonstrated a fast up-slope of

density and a relatively short peak pulmonary artery enhancement.

This study had several potential shortfalls. Firstly, CTP was only performed in the

follow-up period and not at presentation and therefore the degree of perfusion

recovery could not be assessed. Secondly the accuracy of CTP in diagnosis of

pulmonary perfusion abnormalities could not be validated by the reference technique

(catheter pulmonary angiogram) due to the invasive nature of the angiographic

procedure.

Finally, larger cohorts with long-term follow-up will be necessary to highlight the

prognostic value of CTP in patients with acute PE.

Conclusion: This study suggests a role for CTP in follow up of patients with acute

PE, enabling quantification of pulmonary arterial bed obstruction in combination with

systemic revascularisation. Phenotyping of these patients using residual thrombus

load and perfusion characterisation may allow stratification of patients at risk of long-

term complications and recurrence of PE to guide treatments options. Moreover, CTP

can differentiate new PE from persistent thromboembolic changes in patients with

recurrent symptoms.

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Figure legends:

Fig. 1. Time density curves in normal (A) and abnormally perfused (B) lung

parenchyma, 3 months after an acute pulmonary embolism episode.

Peak enhancement is reduced and delayed in the regions with abnormal

perfusion (B), when compared to well perfused lung. Regions of interests in the

normal and abnormal lungs were selected from same lobes.

Fig. 2. Percentage of patients with residual thromboembolic (A) or

perfusion abnormality (B) during on the follow up CTPA or CTP.

The graph shows whist the CTPA was reported normal in 64% of patients, only

29% had a normal CTP. The data also demonstrates that a considerable number

of patients with moderate or severe perfusion abnormality did not demonstrate

equally high modified miller score.

CTPA: CT pulmonary angiogram; CTP: CT pulmonary perfusion study.

Fig. 3. Inconsistent resolution of obstructive pulmonary embolism (PE).

A. 74 year old female presented with saddle pulmonary embolus (arrows;

modified miller’s score=16). Follow up CT pulmonary angiography and

perfusion (coronal view) demonstrated full resolution of PE (B) and normal

perfusion (C).

D: 79 year old female patient presented with multiple pulmonary embolus

(arrows; modified miller’s score =16). Follow up CT pulmonary angiography

demonstrated full resolution of PE (E) but multilobar abnormal perfusion (F;

arrows).

Fig. 4. Matched and miss-matched CTPA / CTP findings in a 76 years old

female 3 months after an acute pulmonary embolism.

Fig. A demonstrates near occlusive thrombi in the segmental branches of the

upper lobes (red and yellow arrows). The angiogram and CT performed 3

months later only demonstrates very small volume of residual webs in the right

upper lobe PA branches (red arrow), but no residual disease in the left upper

lobe branches (yellow arrow; Fig. B).

In the parametric map, black/dark blue, yellow/green, and red colour codes

represent low, moderate, and high pulmonary blood flow. CTP demonstrates

residual perfusion abnormality in the lateral segment of the right upper lobe

corresponding to the visualised webs (Fig. C; arrow). There is also significant

perfusion abnormality in the left upper lobe despite apparent revascularisation

(Fig. D; arrow). Arrowhead shows false perfusion deficit secondary to beam

hardening from the dense contrast in the superior vena cava (SVC).

CTPA: CT pulmonary angiogram; CTP: CT pulmonary perfusion study.

Fig. 5. Pulmonary CT perfusion maps of a 43 year old female 3 months

following an episode of acute pulmonary embolism. A: pulmonary arterial

perfusion map; B: systemic arterial perfusion map; C: maximum intensity

projection (MIP) of the CT pulmonary angiogram.

In the parametric map, black/dark blue, yellow/green, and red colour codes

represent low, moderate, and high pulmonary blood flow. Images demonstrate

an under-perfused segment in the left upper lobe that is later perfused by

systemic circulation (bronchial arteries). MIP images demonstrated only

enhancement from the pulmonary veins and not the pulmonary artery branches.

There was no evidence of parenchymal lung abnormality (termed ‘stunned’

lung).

Role of the Funding Source’ Role of the Funding Source:

Chest, Heart, Stroke, Scotland provided funding support to conduct this study. It

did not interfere with study design, analysis, or presentation of the data.