British Journal of Radiology (2007) 80, e64-e66
© 2007 British Institute of Radiology
doi: 10.1259/bjr/54677520
Search your heart for a cause of syncope!
Ch C Fessas, MRCS(Eng), BSc(Hons)
E K Mayer, MRCS(Eng), BSc(Hons)
and
C D Fessas, MD, FACC, FESC
Nicosia Heart Institute, 22 Heras St. and Archbishop Makarios Avenue, 1061 Nicosia, Cyprus
Correspondence: Mr Christian C Fessas, Nicosia Heart Institute, 22 Heras St. and Archbishop Makarios Avenue, 1061 Nicosia, Cyprus. E-mail: plastic_surgeon{at}hotmail.com.
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Abstract
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A 66-year-old female presented to casualty with recurrent syncopal episodes and a history of ischaemic heart disease. Initial investigations did not provide a definitive diagnosis. Subsequent CT scanning identified a giant pseudoaneurysm of the left anterior descending coronary artery, which is the largest reported to date. We include a short discussion on current literature surrounding coronary artery pseudoaneurysmal disease.
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Case report
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A 66-year-old lady presented to a local casualty department following a blackout. There was no preceding chest pain, shortness of breath or palpitations. She had recently been experiencing intermittent dizzy spells and loss of balance. Observations, examination and repeated ECGs were all unremarkable. A chest radiograph demonstrated a left midzone shadow (Figure 1
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Significant past medical history included investigations for chest pain 2 years previously. Echocardiography at that time revealed a 5.5 cm aortic arch aneurysm with significant aortic valve disease, but angiography failed to demonstrate significant coronary artery disease. She underwent aortic hemi-arch resection and tube grafting, with aortic valve replacement. Aortic root size at the end of surgery was 4.2 cm. She made a good recovery post-operatively and had been well until this recent episode.
Other history included hypertension. There was a strong family history of ischaemic heart disease. Drug history included warfarin and anti-hypertensives.
The patient was discharged from the casualty department with no further follow up.
A few days later the patient represented with further blackouts. Again there was no complaint of chest pain, shortness of breath or palpitations. Blood pressure was 150/105 mmHg and equal in both upper limbs; there was no radio-femoral delay. Cardiovascular examination was unremarkable. Repeated ECGs, however, now showed evidence of an evolving anteroseptal myocardial infarction. Chest radiography demonstrated that the midzone shadow previously seen had expanded considerably (Figure 2).
Abnormal blood results were as follows: CK 2476 U (<142 U), CK-MB 134 u l–1 (<25 u l–1), LDH 1520 (207–414) and Troponin T positive. D-Dimer was raised at 950 ng ml–1 (<250 ng ml–1).
Differential diagnoses included anterior myocardial infarction, pulmonary embolism and aortic dissection.
Transthoracic echocardiography demonstrated an ejection fraction of 32% with global hypokinesis. The aortic root measured 4.32 cm, and confirmed the presence of the aortic prosthetic valve (velocity 1.98 m s–1), with no evidence of valvular dysfunction.
Spiral CT of the thorax showed a large pseudoaneurysm involving the origin of the left anterior descending artery, measuring 8.6 x 6.1 cm (Figure 3). The calcification within the wall of the aneurysm indicated a chronic process, although variations in blood flow were suggestive of an unstable condition.
The patient was managed conservatively due to her not being a candidate for surgery. She unfortunately died 6 weeks later.
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Discussion
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An aneurysm describes the localized dilatation of a thinned, but intact, vessel wall, which exceeds at least 1.5 times the diameter of adjacent normal segments. A pseudoaneurysm implies a breach in the vessel wall, delineated only by adventitial tissue or visceral pericardium, and is thus a spontaneous event.
Aneurysms of the native coronary arteries can be congenital or develop secondary to underlying pathology such as connective tissue disorders. They are well documented in the literature and have a reported incidence of 1–5%, increasing to 2–10% following coronary artery interventions [1, 2].
The distinction between true coronary aneurysms and pseudoaneurysms is purely anatomical, but has historically caused diagnostic difficulties at angiography. The true incidence of pseudoaneurysms therefore remains poorly defined. The increasing use of and expertise in intravascular ultrasound has increased our diagnostic potential. Early studies suggest that 4% of aneurysms diagnosed angiographically are in fact pseudoaneurysms [3].
Pseudoaneurysms typically result from catheter based coronary intervention, but have also been described following blunt chest trauma and in association with cardiac tumours [4, 5]. There are a few reported incidents of spontaneous pseudoaneurysm formation with as yet unidentified aetiology [6].
Patients with pseudoaneurysms can remain asymptomatic or present with varying symptoms, including chest pain, shortness of breath, palpitations and pre-syncopal/syncopal episodes. Secondary complications of pseudoaneurysm formation include distal embolisation, vessel thrombosis, spontaneous rupture and fistula formation.
The low incidence of spontaneous aneurysms means that experience in treatment originates from those arising following coronary interventions. Whereas aneurysms can be treated conservatively, similar management for pseudoaneurysms often has an unfavourable outcome [7]. The differentiation of aneurysms and pseudoaneurysms is therefore important with obvious therapeutic and prognostic implications. Bypass grafting with aneurysm resection, coil embolisation and intravascular stenting have all been described for pseudoaneurysms, but there is no current standardized treatment [8–10].
In the described case report an exact aetiology remains unclear. The differential diagnoses of the radiological appearances on initial plain chest radiography include left atrial enlargement or left ventricular aneurysm; on CT a coronary artery fistula, aortic root aneurysm, aortic root abscess with secondary haemorrhage or true aneurysm of the left anterior descending coronary artery could be considered. The presence of calcification within the wall of the pseudoaneurysm implies a chronic process, although the variations in blood flow within the aneurysm suggest an unstable condition. Given this patient's complex cardiac history, a delayed presentation secondary to either angiographical or surgical intervention cannot be excluded. It is our feeling however that in view of this patient's presentation a spontaneous coronary artery dissection with pseudoaneurysm formation is most likely. With the CT findings of a giant pseudoaneurysm measured at 8.6 cm x 6.1 cm we believe this to be the largest reported to date.
Received for publication July 24, 2005.
Revision received February 15, 2006.
Accepted for publication March 28, 2006.
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References
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- Swaye PS, Fisher LD, Litwin P, et al. Aneurysmal coronary artery disease. Circulation 1983;67:134–8.[Abstract/Free Full Text]
- Slota PA, Fischman DL, Savage MP, et al. Frequency and outcome of development of coronary artery aneurysm after intracoronary stent placement and angioplasty. Am J Cardiol 1997;79:1104–6.[CrossRef][Medline]
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- Schobel WA, Voelker W, Haase KK, et al. Occurrence of a saccular pseudoaneurysm formation two weeks after perforation of the left anterior descending coronary artery during balloon angioplasty in acute myocardial infarction. Cathet Cardiovasc Interv 1999;47:341–6.[CrossRef][Medline]
- Dorros G, Jain A, Kumar K. Management of coronary artery rupture: covered stent or microcoil embolisation. Cathet Cardiovasc Interv 1995;36:148–54.
- Strozzi M, Ernst A, Banfic L. Obliteration of a left main coronary artery aneurysm with a PTFE-coated stent. J Invasive Cardiol 2002;14:280–1.[Medline]
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Abstract
Case report
