European Journal of Echocardiography 2008 9(1):60-62; doi:10.1016/j.euje.2006.08.015
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2006. For permissions please email: journals.permissions@oxfordjournals.org.
Ventricular septal rupture following abciximab infusion
Jayanth R. Arnold*,
Jonathan Timperley,
Andrew R.J. Mitchell,
Stephen Westaby and
Oliver Ormerod
Department of Cardiology, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK
Received 27 July 2006; accepted after revision 29 August 2006; online publish-ahead-of-print 11 October 2006.
* Corresponding author. Tel: + 44 01865 228934; fax: +44 01865 220585. E-mail address: ranjitarnold{at}yahoo.co.uk
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Abstract
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Ventricular septal rupture is a rare complication of myocardial
infarction. Despite a significant reduction in its incidence
with reperfusion therapy, thrombolysis has been implicated in
the pathogenesis of septal rupture. There is little information
regarding the impact of glycoprotein IIb–IIIa receptor
blockers on ventricular septal rupture. We report a case of
rupture of the ventricular septum occurring after treatment
with the glycoprotein IIb–IIIa receptor blocker abciximab,
in the absence of thrombolysis.
Keywords: Ventricular septal defect; Abciximab; Myocardial infarction; Surgical repair
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Case report
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A 55-year old man presented with a 4-h history of chest pain.
He had no history of ischaemic heart disease, was hypertensive
and smoked cigarettes. Four years previously, he had suffered
a spontaneous intracerebral haemorrhage with a full recovery.
The ECG was consistent with an infero-posterior myocardial infarction
(MI). Transthoracic echocardiography revealed infero-posterior
hypokinesia. He was treated with clopidogrel 300 mg, aspirin
300 mg and intravenous heparin 5000 IU. In view of his prior
cerebral haemorrhage, the patient was transferred for coronary
angiography. Prior to angiography the patient received a weight
adjusted bolus of abciximab (17 mg). Coronary angiography revealed
thrombus in the mid-portion of the dominant right coronary artery
(
Figure 1) and a normal left coronary circulation (
Figure 2).
A single drug-eluting stent was deployed successfully. Heparin
6000 IU was administered intravenously and an abciximab infusion
commenced (0.51 mg per hour for 12 h). At the end of the procedure
he developed complete heart block and profound hypotension,
requiring temporary pacing and an intra-aortic balloon pump.
Following this, the patient had multiple episodes of haemodynamically
poorly tolerated VT. The patient remained hypotensive, oliguric
and in pulmonary oedema despite inotropic and vasodilator therapy.
Transthoracic echocardiography revealed a non-dilated left ventricle
with infero-posterior akinesia, a dilated right heart with impaired
ventricular function. There was a large ventricular septal defect
(VSD) in the mid-inferior septum (
Figure 3) with severe
left to right shunting (
Figure 4). In view of the patient's
condition, he was referred for immediate cardiac surgery. His
pre-operative risk using the logistic EuroSCORE was 87%. Surgery
was performed under cardio-pulmonary bypass, involving right
ventriculotomy through the infarcted tissue and closure of the
large, necrotic defect with a bovine pericardial patch. After
a 2-week admission to intensive care, he made a good recovery.
In view of the extensive myocardial injury and VT, the patient
received an implantable cardioverter-defibrillator prior to
discharge. At 3 month follow-up he remained well and free of
angina.
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Discussion
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A VSD is a recognised but infrequent complication of ST-elevation
MI in current cardiological practice, with a reported incidence
of 1–3% without reperfusion therapy, typically occurring
in inferior or more frequently, anteroseptal MIs.
1 Recognised
risk factors include advanced age, female sex, hypertension,
the absence of preceding angina or MI and angiographic total
occlusion of the infarct-related artery.
1 Initial therapy includes
haemodynamic support with inotropes, vasodilators and an intra-aortic
balloon pump. The mortality rate is nearly 100% with medical
management and 50% with surgery. Surgery is ideally delayed
3-6 weeks post MI to allow healing of potentially friable tissue.
With the advent of reperfusion therapy, the overall incidence
of VSD has declined from 1 to 3% in the pre-thrombolytic era
to 0.2%.
1 A significant reduction in septal and free wall rupture
has been observed both with thrombolysis and percutaneous coronary
intervention. Underlying mechanisms include the restoration
of vessel patency leading to myocardial salvage and prevention
of infarct expansion. However, the overall reduction in septal
rupture with thrombolysis may be partially offset by an increased
incidence of early rupture.
2 It has also been suggested that
late thrombolysis (>12 h after symptom onset) may increase
the risk of VSD. Although the impact of reperfusion therapy
on subsequent septal rupture has been assessed, there is little
information regarding the use of glycoprotein IIb–IIIa
receptor blockers. The use of these agents in non-ST elevation
MI is well attested and a recent meta-analysis of 11 randomised
trials involving 27, 115 patients with ST-elevation MI demonstrated
a significant mortality benefit of adjunctive abciximab in patients
treated with primary angioplasty but not in those receiving
thrombolysis.
3 Abciximab was also associated with an increased
risk of major bleeding complications with thrombolysis but not
with angioplasty. However, there were no specific data on its
impact on septal rupture. To date, there are three case reports
of mechanical complications in the literature (septal rupture,
pulmonary artery rupture and free wall rupture) occurring in
patients treated with glycoprotein IIb–IIIa receptor blockers.
4–6 However, in all three cases the outcome was confounded by the
concomitant use of thrombolytic agents. This is the first case
report of septal rupture occurring with a glycoprotein IIb–IIIa
receptor blocker in the absence of thrombolysis. It may be hypothesized
that these agents accelerate the occurrence of early rupture
as a result of increased myocardial haemorrhage. In this case,
there was a temporal correlation between the start of the infusion
and the onset of haemodynamic instability, which may itself
have coincided with septal rupture.
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References
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- Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med (2002) 347:1426–32.[Free Full Text]
- Rhydwen GR, Charman S, Schofield PM. Influence of thrombolytic therapy on the patterns of ventricular septal rupture after acute myocardial infarction. Postgrad Med J (2002) 78:408–12.[Abstract/Free Full Text]
- De Luca G, Suryapranata H, Stone GW, Antoniucci D, Tcheng JE, Neumann FJ, et al. Abciximab as adjunctive therapy to reperfusion in acute ST-segment elevation myocardial infarction: a meta-analysis of randomized trials. JAMA (2005) 293:1759–65.[Abstract/Free Full Text]
- Balachandran KP, Oldroyd KG. Free wall rupture following rescue angioplasty and intravenous abciximab for failed thrombolysis. Scott Med J (2001) 46:87–8.[Web of Science][Medline]
- Chadow HL, Gaba MK, Safi A, Afflu E, Feit A. Rescue PTCA complicated by pulmonary artery rupture after tPA and abciximab. Catheter Cardiovasc Interv (1999) 46:89–91.[CrossRef][Web of Science][Medline]
- Altunkeser BB, Ozdemir K, Ozdemir A, Gok H. A subacute left ventricular free wall rupture after thrombolytic and glycoprotein IIb/IIIa inhibitor treatment: an overlooked finding of left ventriculography. Jpn Heart J (2002) 43:289–93.[CrossRef][Medline]
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