Substantive incidental cardiac findings revealed by non-cardiac CT examination of the thorax
Joint Division of Medical Imaging, Peter Munk Cardiac Centre, Toronto General Hospital, Toronto, Canada
M Durand, MB ChB, FCRad
(Diag)
N Paul, MD, MRCP, FRCR, FRCRC
Joint Division of Medical Imaging and Division of Cardiology, Peter Munk Cardiac Centre, Toronto General Hospital, Toronto, Canada
A Crean, MD, MRCP, FRCR
Limitations inherent in CT imaging of the thorax left the heart as an ill-defined and largely ignored area. The advent of multi-detector CT scanning and shortened imaging times has allowed clear identification of cardiac structures and pathology. Motion-free cardiac images require synchronisation of image acquisition with the cardiac cycle (cardiac ‘gating’ or ‘triggering’). However, significant information can be obtained from careful scrutiny of ungated chest CT images, which may then direct further imaging or investigation. We review 5 cases demonstrating interesting cardiac findings identified on non-cardiac scans.
S
Afr J Rad
2013;17(1):34-37. DOI:10.7196/SAJR.791
For years, the technological limitations inherent in CT imaging
of the thorax meant that the heart was an ill-defined and
largely ignored ‘space-filler’ between the lungs. With the
advent of multi-detector CT scanning (MDCT) in the late 1990s,
and shortened imaging times, it has now become possible to
clearly identify cardiac structures and pathology. Motion-free
cardiac images require synchronisation of image acquisition with
the cardiac cycle (cardiac ‘gating’ or ‘triggering’). However,
significant information can often be gleaned from careful
scrutiny of ungated chest CT images, which may then direct
further imaging or investigation.
In the following examples, we review 5 cases demonstrating interesting cardiac findings identified on non-cardiac scans.
Case 1
History
A 26-year-old woman presented to her referring physician with a history of abdominal pain, generalised swelling and bloating. Her facial swelling was reported to be worse in the mornings, with subsequent improvement during the course of the day. She volunteered a history of congenital rubella. On examination, no ascites, hepatomegaly or peripheral oedema was identified. Her blood results showed normal liver function with bilirubin 8 µmol/l, ALT 29 units/litre, AST 32 units/litre and ALP 92 units/litre. Her albumin, however, was slightly decreased at 26 g/l. An abdominal CT scan was ordered to assess her symptoms.
Imaging
Abdominal CT scan demonstrated a mildly enlarged liver with dilated hepatic veins, dilated inferior vena cava (Fig. 1a), and diffuse heterogeneous enhancement following administration of intravenous iodinated contrast medium (CM) (Fig. 1b) − all in keeping with hepatic venous congestion.
Limited images of the chest demonstrated
pericardial thickening and calcification adjacent to the right
ventricle (Fig. 1c). This raised the possibility of constrictive
pericarditis, and a cardiac MRI was requested. This demonstrated
small ventricles with relative bi-atrial enlargement (Fig. 1d).
The pericardial thickening seen on the CT scan was confirmed on
the MRI scan (Fig. 1d). The cine images demonstrated ‘septal
bounce’ in keeping with constrictive physiology. The patient had
invasive measurement of cardiac pressures which confirmed a
constrictive physiology.
Fig. 1. Axial post contrast-enhanced CT scans of the abdomen
in a 26-year-old woman with a history of abdominal pain,
generalised swelling and bloating. (a
)
CT scan
through the upper abdomen demonstrates dilated inferior vena
cava (arrow) and hepatic veins (arrow heads). (b) CT scan
through the upper liver demonstrates a mildly enlarged liver
with diffuse heterogeneous enhancement in keeping with hepatic
venous congestion. (c) Post contrast images through the lower
chest on abdominal CT scan demonstrate some pericardial
thickening with foci of pericardial calcification adjacent to
the basal right ventricle and atrio-ventricular groove
(arrow).(d) The four-chamber cine steady-state free precession
(SSFP) cardiac MRI image demonstrates biatrial enlargement
with small biventricular volumes. Pericardial thickening is
also noted adjacent to the atrio-ventricular groove (arrow).
Bilateral pleural effusions are also seen (LA = left atrium;
RA = right atrium).
Diagnosis
Pericardial thickening and calcification with a restrictive physiology was the diagnosis. The pericardial thickening and calcifications were most likely due to previous pericarditis. It is possible that the patient might have developed this as a consequence of her rubella infection,1 although it would be unusual for her to present with symptoms so long after a congenital infection. It is more probable that her presentation resulted from a recent episode of subclinical pericarditis that resulted in pericardial calcification.
Teaching point
The normal
pericardium measures less than 2 - 3 mm. Pericardial
thickening >4 mm together with clinical features of
predominantly right-sided cardiac failure are suggestive of
constrictive physiology. While CT can be particularly useful
in assessing pericardium thickness and calcifications, MRI is
used to distinguish between constrictive pericardial disease
and restrictive myocarditis.2 Septal bounce can be
demonstrated on free breathing cine MRI images in patients
with constrictive physiology, which distinguish it from
restrictive cardiomyopathy. Note, however, that although
pericardial constriction and restrictive cardiomyopathy are
very different pathologies, they give rise to a final common
physiological appearance of impaired diastolic ventricular
filling – so-called ‘restrictive filling pattern’ or
‘restrictive physiology’. Hence, even pericardial constriction presents with a restrictive physiology: a source of much
diagnostic confusion and a reason why CT and MRI are so
valuable.
Case 2
History
A 63-year-old man was referred to our department for follow-up after right upper and middle lobe lobectomy for lung cancer. Clinically, he was stable with no new symptoms. He volunteered a history of 3 myocardial infarctions after triple coronary bypass surgery in 1993.
Imaging
The transaxial images from thoracic MDCT
demonstrated an aneurysm in the proximal (Fig. 2a) and distal
aspects (Fig. 2b) of the saphenous venous graft to the right
coronary artery (RCA), with mural thrombi in both aneurysms.
Fig. 2. Post contrast-enhanced chest CT scan in a 63-year-old
man followed up post lobectomy for lung carcinoma. (a)
Transaxial
CT image at the level of the aortic valve demonstrates an
eccentric mural thombus within an aneurysm of the proximal
saphenous vein to right coronary artery graft (arrow) (Ao =
aortic root; LA = left atrium). (b) Transaxial CT image to the
left of the distal saphenous vein right coronary artery graft
demonstrates concentric mural thrombus within a second
aneurysm at the implantation site of the graft (arrow).
Diagnosis
Saphenous vein graft aneurysms were diagnosed. Although the distal aneurysm was closely related to the suture line, the proximal aneurysm was distal to the suture line. Both were felt to represent true aneurysms. Owing to the patient’s underlying medical conditions, it was decided to treat these aneurysms with percutaneous deployment of Amplatzer vascular plugs despite the associated risk of myocardial infarction.
Teaching point
Saphenous vein graft aneurysms are a rare complication of coronary bypass surgery and can be divided into true and pseudo-aneurysms. Pseudo-aneurysms are associated with technical complications at the suture line or infections. The distinction is academic as surgical resection and revascularisation are the preferred treatment for both.3
Case 3
History
A 67-year-old man was admitted to an outlying hospital with a late presentation of an anterior ST segment elevation myocardial infarction. At the time of admission, an attempted percutaneous coronary intervention was unsuccessful. Three days later, he was transferred to the ICU at our hospital with severe hypoxaemia and a clinical presentation suggestive of septic shock. A chest CT was requested to rule out pulmonary embolism or pneumonia.
Imaging
Thoracic MDCT demonstrated an area of
hypoperfusion in the inter-ventricular septum (Fig. 3a),
suggesting an area of infarction, and a muscular ventricular
septal defect (VSD) apical and inferior to this (Fig. 3b).
Bilateral basal atelectasis was noted with no evidence for
pulmonary embolism.
Fig. 3. Post contrast chest CT scan in a 67-year-old man
performed to rule out pulmonary embolism or pneumonia. (a)
Transaxial CT image at the level of the interventricular
septum demonstrates hypoperfusion of the mid-distal septum
(arrow) in comparison with the basal septum (*). (b)Transaxial
CT image at the level of the inferior septum demonstrates a
large defect in the muscular portion of the septum (arrow).
(LV = left ventricle; RV = right ventricle.)
Diagnosis
Postmyocardial infarction ventricular septal defect was diagnosed. The patient had a myocardial infarction involving the muscular portion of the inter-ventricular septum complicated by a VSD. Myocardial perfusion isotope studies and stress perfusion cardiac MRI are often used to determine the extent of myocardial ischaemia and scarring in patients with ischaemic heart disease. It is less well appreciated that myocardial infarction can also be seen on even ungated MDCT as a region of myocardial hypoperfusion.
Teaching point
Ventricular septal rupture after myocardial infarction is a rare complication with a reported incidence of 1 - 2%.4 Rupture occurs 3 - 5 days after the myocardial infarction and the patient presents with sudden deterioration, new onset cardiac murmur, congestive heart failure, and often in cardiogenic shock. Treatment is initial stabilisation with inotropes and often an intra-aortic balloon pump with subsequent surgical closure of the defect. There are, however, a few small case series reported in the literature where transcatheter closure of these defects has been successfully performed.5
Case 4
History
A 54-year-old man was referred for an abdominal CT for suspected cardiogenic liver cirrhosis. On examination, the patient had generalised oedema, and abdominal distention with mild ascites. The patient had had congenital valvular heart disease and had undergone several pulmonary valve surgeries since childhood. His pulmonary valve was replaced with a porcine root in 2002.
Imaging
The
abdominal images revealed chronic passive liver congestion
with features of hepatic cirrhosis. Venous phase axial images
through the lower chest demonstrated a filling defect in the
coronary sinus (Fig. 4).
Fig. 4. Venous phase transaxial image from a CT scan in a
54-year-old man demonstrates a filling defect in the
coronary sinus in keeping with a thrombus.
Diagnosis
Coronary sinus thrombosis was diagnosed. The patient had a coronary sinus thrombosis that was subsequently resected during surgical replacement of the mitral valve and down-sizing of the right atrium.
Teaching point
A few cases of primary coronary sinus thrombosis have been reported6 but coronary sinus thrombosis is mostly associated with previous invasive cardiac procedures such as central venous line placement, insertion of pacing wires, or coronary sinus catheterisation for ventricular lead placement during cardiac resynchronisation therapy.7 This patient had had several previous invasive cardiac procedures as well as a severely dilated right atrium, both predisposing to thrombosis formation.
Case 5
History
A 65-year-old man, under disease surveillance for metastatic gastric carcinoma, was sent for routine chest, abdomen and pelvis CT. The patient had completed one cycle of chemotherapy 18 months previously and was clinically well with no new symptoms.
Imaging
The venous phase chest CT demonstrated a
mass lesion in the inferior aspect of the right ventricle
(Fig. 5a). This was better appreciated on the sagittal
reconstructed images of the chest (Fig. 5b). Cardiac MRI was
performed to assess contrast enhancement of the lesion to
determine whether this was a thrombus or intracardiac mass.
The mass (Fig. 5c) demonstrated gadolinium enhancement on the
perfusion images (Figs 5d and e).
Fig. 5. Post contrast venous phase chest CT scan in a
65-year-old man with gastric carcinoma. (a) Transaxial
images demonstrate a filling defect (arrow) in the basal
right ventricle (LV = left ventricle). (b) Post
contrast-enhanced sagittal reconstructed image of the chest
demonstrates a filling defect in the basal right ventricle
(LV = left ventricle). (c) Cardiac MRI steady-state free
precession image obtained in a short axis orientation
demonstrates a mass lesion in the basal right ventricle
(arrow) (LV = left ventricle). (d) The right ventricular
mass demonstrates gadolinium enhancment during perfusion
imaging as demonstrated on (e) the enhancement curve display
on the right.
Diagnosis
Enhancing right atrial mass was diagnosed; the mass most probably represents a metastasis from the known gastric carcinoma.
Teaching point
Cardiac masses are uncommon but, when they do occur, a metastatic origin is by far the most common cause. MRI first-pass perfusion imaging with gadolinium is often used to distinguish between thrombus and masses. Conventionally, thrombus does not enhance with gadolinium; however, large chronic thrombi may occasionally have peripheral enhancement, making differentiation between mass and thrombus challenging.8 Typically, tumours demonstrate at the least partial uptake of gadolinium unless very avascular. The most common tumors metastasising to the heart are breast, kidney, oesophagus, lymphoma, leukaemia and melanoma.8
1. Fink C, Schaad UB, Stocker FP. Perikarditis als Komplikation von Roteln. [Pericarditis as a complication of rubella]. Schweizerische Medizinische Wochenschrift. 1987;117(1):28-32.
2. Wang ZJ, Reddy GP, Gotway MB, Yeh BM, Hetts SW, Higgins CB. CT and MR imaging of pericardial disease. Radiographics 2003;23 Spec No:S167-180.
3. Kalimi R, Palazzo RS, Graver LM. Giant aneurysm of saphenous vein graft to coronary artery compressing the right atrium. Ann Thorac Surg 1999;68(4):1433-7143. [http://dx.doi.org/10.1016/S0003-4975(99)00848-6]
4. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101(1):27-32. [http://dx.doi.org/10.1161/01.CIR.101.1.27]
5. Moreno N, Silva JC, Andrade A. Complicated transcatheter closure of postinfarction ventricular acute septal defect. J Invasive Cardiol 2011;23(10):E244-246.
6. Ramsaran EK, Sadigh M, Miller D. Sudden cardiac death due to primary coronary sinus thrombosis. South Med J 1996;89(5):531-533. [http://dx.doi.org/10.1097/00007611-199605000-00019]
7. Parmar RC, Kulkarni S, Nayar S, Shivaraman A. Coronary sinus thrombosis. J Postgrad Med 2002;48(4):312-313.
8. O’Donnell DH, Abbara S, Chaithiraphan V, et al. Cardiac tumors: optimal cardiac MR sequences and spectrum of imaging appearances. AJR 2009;193(2):377-387. [http://dx.doi.org/10.2214/AJR.08.1895]