DOI:10.2214/AJR.07.3715
AJR 2008; 191:1072-1076
© American Roentgen Ray Society
CT Angiography Findings of the Left Atrium and Right Ventricle in Patients with Massive Pulmonary Embolism
Iclal Ocak1 and
Carl Fuhrman
1 Both authors: Department of Radiology, Thoracic Imaging Division, University
of Pittsburgh Medical Center, 200 Lothrop St., Pittsburgh, PA 15213.
Received January 23, 2008;
accepted after revision April 23, 2008.
Address correspondence to I. Ocak
(ocaki{at}upmc.edu).
Abstract
OBJECTIVE. The purpose of this study was to show the imaging
findings of the left atrium and right ventricle on CT angiography in patients
with massive pulmonary embolism.
CONCLUSION. Massive pulmonary embolism can cause abrupt acute
pulmonary arterial hypertension, right ventricular dysfunction, and decrease
in left ventricular preload. Patients with these findings on CT angiography
can have a poorer prognosis than those without these imaging findings.
Consequently, recognizing anatomic changes such as right ventricular dilation
or septal bowing, decrease in size of left atrium and pulmonary veins (a
manifestation of decreased pulmonary venous return) would be useful for risk
stratification at the time of massive pulmonary embolism.
Keywords: left atrium • massive pulmonary embolism • right ventricular dysfunction
Introduction
Pulmonary embolism is the third most common cardiovascular dis ease in the
United States [1]. Massive
pulmonary embolism traditionally has been defined as a 
50% obstruction of
the pulmonary vasculature or occlusion of diameter of two or more lobar
arteries [2]. Mortality rates
can be as high as 31% to 58% when shock is present
[3]. If unsuspected, 70% of
patients will die of massive pulmonary embolism. Approximately 65% of the
patients will die within 1 hour, and 92.9% will die within the first 2.5 hours
of presentation with massive pulmonary embolism. Classically, massive
pulmonary embolism results from migration of a venous thrombus through the
right atrium and right ventricle with thrombus lodgment in the major branches
of the pulmonary artery. Right ventricular dysfunction (RVD) will occur as a
direct consequence of the acute obstruction of the major branches of the
pulmonary artery [4].
Right ventricular size and motion abnormalities after massive pulmonary
embolism have been described on echocardiography and CT. Given the promising
results found with echocardiography, several investigators have attempted to
determine prognosis from findings at CT. Authors of several retrospective
studies have suggested that right-sided heart strain and embolic burden at CT
are prognostic findings [5,
6].
The purpose of this study was to show the imaging findings of the left
atrium and right ventricle on CT angiography in patients with massive
pulmonary embolism and also to measure the volume changes within the right
ventricle and left atrium and the diameter changes within the pulmonary veins
before and after massive pulmonary embolism. Even though CT findings of right
heart strain are well described in the literature, to the best of our
knowledge this is the first study that describes imaging findings of the left
atrium, pulmonary veins, and right ventricle together before and after massive
pulmonary embolism [4,
6–10].
Materials and Methods
CT images were acquired using a 64-MDCT scanner (VCT, GE Healthcare), with
the following parameters: detector collimation, 0.625 mm; field of view, 33.7
cm; tube voltage, 120 kV; tube current range, 330–500 mAs. Bolus timing
was used for optimal opacification of pulmonary arteries. Whole-lung CT images
were obtained after administration of 100 mL of ioversol (Optiray 350,
Mallinckrodt Imaging [350 mg I/mL]) through the antecubital vein at a flow
rate of 4 mL/s using a power mechanical injector. Helically acquired axial
images were reconstructed in 1.25-mm-thick axial reconstructions by using
soft-tissue and lung reconstruction algorithms.
The CT data sets were transferred and post-processed at the Advantage 4.3
workstation (GE Healthcare). Image analysis was performed using volume
rendering in addition to transverse source images. The volumes of the left
atrium and right ventricle were measured before and after the massive
pulmonary embolism on the workstation. The volumes of the left atrium and
right ventricle and the diameters of the right and left superior and inferior
pulmonary veins were com pared quanti tatively before and after massive
pulmonary embolism.
Statistical analyses were made using Microsoft Excel 2006. The paired
Student's t test was used to compare differences. A level of
p 
0.05 was considered significant.
Results
There were two women and one man in our study. All of the patients had more
than 50% embolic burden on one of the major branches of the pulmonary artery
(Table 1). After the massive
pulmonary embolism, increased volume of the right ventricle and decreased
volume of the left atrium were observed
(Table 2). Occlusion of the
pulmonary arteries by massive pulmonary embolism resulted in dilatation of the
right atrium, right ventricle, and superior vena cava (Fig.
1A,
1B,
1C,
1D,
1E,
1F). Contrast-enhanced axial CT
scans also showed decreased size of the left atrial appendage, left atrium,
and pulmonary veins (Fig. 2A,
2B). There were decreased
diameters of the right or left superior and inferior pulmonary veins with
massive pulmonary embolism, compared with the images without massive pulmonary
embolism (Table 3).
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Fig. 1A —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT volume-rendered images of whole heart show change in volume of left
atrium during massive pulmonary embolism (A) and after treatment of
massive pulmonary embolism (B).
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Fig. 1B —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT volume-rendered images of whole heart show change in volume of left
atrium during massive pulmonary embolism (A) and after treatment of
massive pulmonary embolism (B).
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Fig. 1C —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT images show decreased size of left atrium and superior pulmonary
veins before treatment for massive pulmonary embolism (C) compared with
images after treatment of massive pulmonary embolism (D).
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Fig. 1D —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT images show decreased size of left atrium and superior pulmonary
veins before treatment for massive pulmonary embolism (C) compared with
images after treatment of massive pulmonary embolism (D).
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Fig. 1E —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT images show large right ventricle and compressed left ventricle
before treatment for massive pulmonary embolism (E) compared with
normal size of right and left ventricles after massive pulmonary embolism
(F).
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Fig. 1F —Imaging findings of heart in 24-year-old woman during large
pulmonary artery embolism and after treatment. Transverse contrast-enhanced
chest CT images show large right ventricle and compressed left ventricle
before treatment for massive pulmonary embolism (E) compared with
normal size of right and left ventricles after massive pulmonary embolism
(F).
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Fig. 2A —59-year-old woman with massive pulmonary embolism. Transverse
contrast-enhanced chest CT images at level of left atrium obtained before
treatment for massive pulmonary embolism (A) show enlargement of right
atrial appendage, superior vena cava, and small size of left atrial appendage
and left atrium compared with image after treatment of massive pulmonary
embolism (B).
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Fig. 2B —59-year-old woman with massive pulmonary embolism. Transverse
contrast-enhanced chest CT images at level of left atrium obtained before
treatment for massive pulmonary embolism (A) show enlargement of right
atrial appendage, superior vena cava, and small size of left atrial appendage
and left atrium compared with image after treatment of massive pulmonary
embolism (B).
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There was a statistically significant difference in the diameter change of
the pulmonary veins (p = 0.0002) and volume change of the left atrium
(p = 0.01) with and without massive pulmonary embolism. However,
there was no difference in the volume change of the right ventricle with and
without massive pulmonary embolism (p = 0.2). Transthoracic
echocardiography confirmed moderate right ventricular hypokinesis and
dilatation in the two patients, suggestive of a hemodynamically significant
massive pulmonary embolism (Table
1).
Discussion
Massive pulmonary embolism is a fatal cardiovascular disorder. Mortality is
caused in part by pressure overload of the right ventricle secondary to acute
pulmonary arterial hypertension caused by the massive pulmonary embolism. This
initially results in right ventricular dysfunction, which may progress to
right ventricular failure and decreased output from the right ventricle
[5]. This contributes to
decreased venous return to the left atrium from the portions of the lung
involved with massive pulmonary embolism and results in underfilling of the
left atrium and left ventricle. The dilated and dysfunctional right ventricle
also displaces the interventricular septum toward the left and can compress
the left ventricle. Hence, left ventricular preload is, in addition, impaired
by decreased left ventricular distensibility as a consequence of a leftward
shift of the interventricular septum and of pericardial restraint, both of
which are related to the degree of right ventricular dilatation
[2]. Finally, all of these
changes result in acute decreased cardiac output, with resultant hypotension
and shock that characterize the clinical findings in massive pulmonary
embolism [3,
8]. Hypotensive shock is
associated with a threefold to sevenfold increase in mortality. The presence
of hypotensive shock in patients with acute massive pulmonary embolism
represents a failure of the available compensatory mechanisms to sustain
tissue perfusion.
Right Ventricular Dysfunction
Kasper et al. [11] found
that the presence of right ventricular afterload stress detected by
echocardiography is a major determinant of short-term prognosis in patients
with clinically suspected acute pulmonary embolism. They showed that 1-year
mortality from massive pulmonary embolism was 13% in patients with right
ventricular afterload stress at presentation compared with 1.3% in those
without.
Fang et al. [12] studied
serial echocardiographic changes recorded before and after anticoagulant
therapy administered to two patients with acute pulmonary embolism. Dilatation
of the right ventricle, abnormal motion of the interventricular septum, and
mild tricuspid regurgitation were noted in both patients. Echocardiograms
obtained after the patients received anticoagulant therapy revealed
normalization of the echocardiography parameters in both patients. The
reversal of the right ventricular strain pattern revealed by an echocardiogram
occurred as a result of the regression of pulmonary hypertension after
anticoagulant therapy [12].
Accordingly in this study, CT performed after the patients had received
anticoagulant therapy revealed normalization of the CT parameters in all
patients. Anatomic changes such as right ventricular dilation and displacement
of the interventricular septum completely resolved after anticoagulant
therapy.
Lim et al. [10] compared
the accuracy of CT with echocardiography in the detection of RVD in 14
patients with acute massive pulmonary embolism. In their study, correlated
with echocardiography, CT for RVD detection had a sensitivity of 91.6% and a
specificity of 100%. He et al.
[13] compared the sensitivity
and specificity of CT and echocardiog raphy in detecting RVD. The extent of
pulmonary vascular obstruction was graded using the CT clot burden scoring
system. They used obstruction of 30% of the pulmonary vascular bed as a
reasonable, conservative reference standard. This degree of pulmonary vascular
obstruction was chosen as the reference standard based on the work of van der
Meer et al. [5] and Ribeiro et
al. [14] who described a loss
of perfusion of greater than 30% of the lung as best separating patients with
and without right ventricular dysfunction. Reports of echo cardiography
examinations were review ed when available. The sensitivity and specificity of
CT and echocardiography in revealing right heart dysfunction were calculated
and compared using pulmonary vascular obstruction of 30% as the reference
standard.
The sensitivity and specificity of CT and echocardiography in revealing RVD
were found to be 81% versus 56% and 47% versus 42%, respectively. A
significant difference between the mean clot burdens of patients with and
without RVD on CT was found
[14]. In our two cases, there
was good correlation of CT and transthoracic echocardiography findings in
terms of the right ventricular dilatation and bowing of the interventricular
septum. One of the cases had no trans thoracic echocardiography.
Decreased Left Atrium Volume and Pulmonary Vein Diameters
In all cases, reductions in the volume of the left atrium and diameter of
the pulmonary veins were observed compared with CT before massive pulmonary
embolism or after the treatment of massive pulmonary embolism. Underfilling of
the left atrium could be caused by the mechanisms, which include decreased
preload, decreased afterload, and pericardial strain. Imaging findings of the
left atrium and pulmonary veins after massive pulmonary embolism have not been
shown in the literature. Such underfilling may be an important predictor of
massive pulmonary embolism and an indicator of significantly reduced venous
return to the left heart. CT evaluation of the left atrium, left atrial
appendage, and pulmonary veins in addition to the right ventricular chamber
and interventricular septum analysis might reflect the degree of hemodynamic
compromise in patients with acute massive pulmonary embolism.
One limitation of this study was that CT examinations were performed
without ECG-gating. Measurement of the volume of the heart chamber during a
consistent point in the cardiac cycle was not possible in non-ECG-gated CT
scanning. However qualitative comparison is still possible in terms of these
findings, which may be an important predictor
[13] of decreased left heart
function related to impaired venous return. Prospective pulmonary embolism
management studies will be needed to investigate whether left atrial size and
pulmonary vein diameter measurements on CT should guide treatment decisions in
combination with other established risk assessment tools.
References
- Stein PD, Hull RD, Ghali WA, et al. Tracking the uptake of
evidence: two decades of hospital practice trends for diagnosing deep vein
thrombosis and pulmonary embolism. Arch Intern Med2003; 163:1213
–1219[Abstract/Free Full Text]
- Wood KE. Major pulmonary embolism: review of a pathophysiologic
approach to the golden hour of hemodynamically significant pulmonary embolism.
Chest 2002; 121:877
–905[CrossRef][Medline]
- Wood KE. The presence of shock defines the threshold to initiate
thrombolytic therapy in patients with pulmonary embolism. Intensive
Care Med 2002; 28:1537
–1546[CrossRef][Medline]
- Santos Martínez LE, Uriona Villarroel JE, Exaire
Rodríguez JE, et al. Massive pulmonary embolism, thrombus in transit,
and right ventricular dysfunction [in Spanish]. Arch Cardiol
Mex 2007; 77:44
–53[Medline]
- van der Meer RW, Pattynama PMT, van Strijen MJL, et al. Right
ventricular dysfunction and pulmonary obstruction index at helical CT:
prediction of clinical outcome during 3-month follow-up in patients with acute
pulmonary embolism. Radiology 2005;235
: 798–803[Abstract/Free Full Text]
- Schoepf UJ, Kucher N, Kipfmueller F, Quiroz R, Costello P,
Goldhaber SZ. Right ventricular enlargement on chest computed tomography: a
predictor of early death in acute pulmonary embolism.
Circulation 2004;110
:3276
–3280[Abstract/Free Full Text]
- Araoz PA, Gotway MB, Harrington JR, Harmsen WS, Mandrekar JN.
Pulmonary embolism: prognostic CT findings. Radiology2007; 242:889
–897[Abstract/Free Full Text]
- Araoz PA, Gotway MB, Trowbridge RL, et al. Helical CT pulmonary
angiography predictors of in-hospital morbidity and mortality in patients with
acute pulmonary embolism. J Thorac Imaging2003; 18:207
–216[CrossRef][Medline]
- Chung T, Emmett L, Mansberg R, Peters M, Kritharides L. Natural
history of right ventricular dysfunction after acute pulmonary embolism.
J Am Soc Echocardiogr 2007;20
: 885–894[CrossRef][Medline]
- Lim KE, Chan CY, Chu PH, Hsu YY, Hsu WC. Right ventricular
dysfunction secondary to acute massive pulmonary embolism detected by helical
computed tomography pulmonary angiography. Clin
Imaging 2005; 29:16
–21[CrossRef][Medline]
- Kasper W, Konstantinides S, Geibel A, Tiede N, Krause T, Just H.
Prognostic significance of right ventricular afterload stress detected by
echocardiography in patients with clinically suspected pulmonary embolism.
Heart 1997; 77:346
–349[Abstract/Free Full Text]
- Fang BR, Chiang CW, Lee YS. Echocardiographic detection of
reversible right ventricular strain in patients with acute pulmonary embolism:
report of 2 cases. Cardiology 1996;87
: 279–282[Medline]
- He H, Stein MW, Zalta B, Haramati LB. Computed tomography
evaluation of right heart dysfunction in patients with acute pulmonary
embolism. J Comput Assist Tomogr 2006;30
: 262–266[CrossRef][Medline]
- Ribeiro A, Lindmarker P, Johnsson H, Juhlin-Dannfelt A, Jorfeldt L.
Pulmonary embolism: a follow-up study of the relation between the degree of
right ventricle overload and the extent of perfusion defects. J
Intern Med 1999; 245:601
–610[CrossRef][Medline]
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Abstract
Introduction
