Abstract: A 34-year-old male patient was referred for primary percutaneous coronary intervention for ST-segment elevation myocardial infarction with cardiogenic shock and was found to have embolic left coronary artery occlusion and subsegmental pulmonary artery emboli as a consequence of venous thrombosis to trauma to the thigh in the presence of a patent foramen ovale.
J INVASIVE CARDIOL 2013;25(3):162-164
Key words: STEMI, PFO closure
A 34-year-old male patient was referred to our hospital for primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (MI) with cardiogenic shock. He had been healthy with an unremarkable past medical history. Family history of premature death and cardiovascular disease was negative. The patient had suffered an apple-size bruise of the left thigh during a soccer match the day before. After getting up in the morning, he experienced severe chest tightness associated with worsening shortness of breath at rest and rapidly progressing diaphoresis. Cardiogenic shock developed rapidly. He received endotracheal intubation and high-dose catecholinergic support by a medical rescue team at home. He was flown by helicopter to our catheterization laboratory within 90 minutes of symptom onset. The electrocardiogram revealed extensive ST-segment elevation in leads V1-V6, I, and aVL (Figure 1). Left ventriculography showed markedly impaired systolic function with anterosepto-apical akinesia and severe ischemic mitral regurgitation. Coronary angiography performed under manual cardiac massage demonstrated complete thrombotic occlusion of the left anterior descending (LAD) coronary artery, the left circumflex (LCX) coronary artery, and a large intermediate branch (Figure 2). The right coronary artery was normal. Thrombus aspiration from the left coronary artery was performed with a manual suction device followed by several balloon dilatations for further thrombus fragmentation and administration of a weight-adjusted intravenous abciximab bolus, heparin, and acetylsalicylic acid. Patency of all 3 branches was achieved (Figure 2), but flow could only be re-established after percutaneous insertion of a left ventricular assist device (TandemHeart; CardiacAssist, Inc) via transseptal puncture. Transesophageal echocardiography (TEE), performed to exclude papillary muscle rupture as a cause for severe mitral regurgitation, depicted a patent foramen ovale (PFO) with spontaneous bidirectional shunt (Figure 3). No work-up for a hypercoagulable state was performed. The following night, the treatment was discontinued due to brain death. Autopsy demonstrated wall injury of the left femoral vein at the site of trauma with a fresh thrombus, bilateral subsegmental pulmonary artery emboli, and a large PFO (Figure 4).
Paradoxical embolism, typically through a PFO, is entertained in the differential diagnosis of acute myocardial infarction.1-8 It is generally only considered in the realm of otherwise normal coronaries although the presence of coronary artery disease is entirely independent of this mechanism. The detection of thrombus in the venous system or right atrium should not be considered a prerequisite for this diagnosis, as non-detectable small clots are common culprits. The direct detection of thrombus within a PFO being rare,9-11 the diagnosis of paradoxical embolism is usually assumptive. A strong association between the presence of a PFO and the risk for paradoxical embolism has been confirmed in several studies.12-16 More than a decade ago, a seminal report identified the PFO as an independent predictor of mortality and stroke in 139 patients with clinically significant pulmonary embolism.17 A field study confirmed this later without, however, pinpointing the PFO as culprit.18 It proved a striking incidence of stroke and myocardial infarction simultaneously with documented clinically apparent deep vein thrombosis or pulmonary embolism. This tragic case report documents the paradoxical embolism triad: venous thrombosis, right-to-left shunt, and multiple pulmonary and systemic arterial emboli. Non-surgical closure of PFO has been demonstrated feasible19,20 and safe.21
The case should cause reconsideration of the current Food and Drug Administration restriction regarding indication for PFO closure to patients with a recurrent event despite medical treatment.22
Acknowledgment. Martina Kuster, MD, Institute of Pathology, Bern University Hospital, Switzerland.
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From the Swiss Cardiovascular Center, Department of Cardiology; Bern University Hospital, Bern, Switzerland.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Meier holds a research grant from St Jude Medical. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted July 18, 2012, provisional acceptance given August 8, 2012, final version accepted August 10, 2012.
Address for correspondence: Bernhard Meier, MD, Chairman of Cardiology, Swiss Cardiovascular Center Bern, Bern University Hospital, 3010 Bern, Switzerland. Email: firstname.lastname@example.org