Copyright © 2006, The European Society of Cardiology
Paradoxical coronary emboli following a long-haul airline flight
aDepartment of Cardiology, Hillingdon Hospital, Pield Heath Road, Uxbridge, Midddlesex UB8 3NN, UK
bDepartment of Cardiology, Harefield Hospital, Harefield, Middlesex, UK
Received 19 January 2006; received in revised form 24 March 2006; accepted after revision 14 April 2006.
simon.dubrey{at}thh.nhs.uk
* Corresponding author. Tel.: +44 1895 279255; fax: +44 1895 256509.
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Abstract |
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A 33-year-old man presented with an acute myocardial infarction (MI) after a recent long-haul flight. Angiography revealed thrombus in the right and circumflex coronary artery but no underlying atherosclerosis. Echocardiography revealed the presence of an atrial septal defect (ASD). In view of the recent flight, the presence of an ASD and occlusive thrombi in two coronary arteries, it was considered that the pathophysiological cause was paradoxical embolisation. Transcutaneous device closure of the ASD was implemented to prevent further catastrophic paradoxical embolic events.
Keywords: Paradoxical embolism; Myocardial infarction; Atrial septal defect; Airline flight
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Case report |
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A 33-year-old man presented with severe retrosternal chest pain. An ECG showed ST-segment elevation in the inferolateral leads. He had started smoking 6months prior to this event. Substance misuse was denied.
Treatment was commenced with oxygen, aspirin, clopidogrel, morphine, heparin and immediate referral for primary coronary angioplasty (PTCA). Angiography showed a normal left main and left anterior descending (LAD), thrombus in the proximal right (RCA) (Fig. 1), with no flow in the distal posterior descending and thrombus in the circumflex coronary artery (Cx). A Diver C.E. (Invatec Inc.) clot extraction catheter was passed and thrombus was removed from the RCA and Cx. A bolus of intravenous abciximab (glycoprotein IIb/IIIa inhibitor) was administered. No underlying atheromatous disease was evident in the coronary arteries. Tests revealed a normal full blood count, renal, liver and thyroid function, a C-reactive protein of 51mg/L, total cholesterol of 3.41mmol/L, fasting blood glucose of 9.4mmol/L and HbA1c of 10.2%. Antithrombin III, protein C and S, prothrombin time, partial thromboplastin time, fibrinogen, homocysteine, cardiolipin antibodies and factor V Leiden were normal.
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Transthoracic echocardiography showed inferobasal hypokinesia but otherwise good left ventricular function (EF 55%) and no thrombus. Transoesophageal echocardiography (TOE) revealed a 1x1.4 cm secundum atrial septal defect (ASD) with left to right flow into an enlarged right atrium (RA) (Fig. 2). There was sluggish flow within the RA, and reduced right ventricular (RV) function and an akinetic RV free wall. A Doppler scan of the inferior vena cava, pelvic veins and lower limbs was normal. The patient underwent successful device closure of the ASD.
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Discussion |
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Myocardial infarction (MI) in the under-35 age group is due to coronary atherosclerosis in 75% of cases.1 Alternative mechanisms for infarction at this age include thrombophilia, polycythaemia, thrombocytosis, endocarditis, valvular disease, systemic diseases, coronary arteritis, trauma and cocaine.
Paradoxical embolisation of thrombus via an ASD or patent foramen ovale (PFO) is accepted as a possible aetiology of cryptogenic ischaemic stroke and peripheral vascular thrombotic occlusion. Paradoxical coronary embolisation causing acute MI with normal coronaries is less well recognised, but may account for 5–10% of such emboli.2
Our patient had two risk factors (smoking and new-onset diabetes) for atherosclerosis, but angiography only showed occlusive thrombi in the RCA and Cx coronaries. Even in the presence of atherosclerotic disease, it would be unusual to have simultaneous plaque rupture and arterial occlusion in two distinct coronary vessels. A thrombophilia screen proved to be negative; important because there is an increased prevalence of thrombophilia in young patients with MI and few conventional risk factors.3 The recent flight and an ASD raised the possibility of embolisation to the coronary arteries from a deep venous thrombosis. An embolic phenomenon would also be more consistent with the finding of thrombi in two sites. Doppler evaluation of the lower limb and pelvic veins did not reveal thrombus, which is reported in a significant proportion of patients with cryptogenic stroke and patent foramen ovale.4 A definitive diagnosis is made only on visualising an embolus in transit through an ASD or PFO.5
Management of coronary emboli comprises immediate reperfusion therapy (thrombolysis or percutaneous intervention) and prevention of recurrence. Acute MI due to emboli have been successfully treated using thrombus aspiration devices.6 Strategies for prevention of future paradoxical embolic events include lifelong oral anticoagulation and/or surgical or transcutaneous closure of ASDs or PFOs. There are no randomised controlled trials comparing oral anticoagulation with transcutaneous closure of ASDs and PFOs. Transcatheter PFO closure appears safe to protect against recurrent strokes in patients with cryptogenic stroke.7,8 Recurrence rates of neurologic events after surgical closure of PFOs are as high as 20% per year.8 At present, the only unequivocal indication for device closure of PFOs is recurrence of paradoxical embolic events despite therapeutic anticoagulation.9
Device closure of ASDs appears to have a low recurrence rate of further paradoxical embolic events and may avoid life-long anticoagulation. Our patient needed to fly back to India and we felt that device closure of the ASD was the most appropriate treatment to prevent further paradoxical embolic events.
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References |
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[Abstract/Free Full Text] - Kizer J.R., Devereux R.B. Patent foramen ovale in young adults with unexplained stroke. N Engl J Med (2005) 353:2361–2372.
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