Case report. A 51-year-old female was admitted with complaints of the sudden onset of severe dyspnea, followed by precordial discomfort. The patient was obese. Admission blood pressure was 190/100 mmHg, with a heart rate of 102 b.p.m, arterial oxygen saturation of 92% on 10 l/min. supplemental oxygen, and respiratory rate of 26 /minute. There was jugular venous distension of 3 cm sitting upright. Pulmonary examination revealed bilateral basilar rales. The heart sounds were normal, with no murmurs, rubs or gallops. The prior medical history was notable only for systemic hypertension. She did not have a history of tobacco abuse. An electrocardiogram revealed sinus tachycardia, with 2 mm of ST-segment elevation in leads II, III, aVF, and 2 mm of ST-segment depression in leads I and aVL. The patient was treated with oral acetylsalicylic acid (325 mg), intravenous unfractionated heparin, and intravenous nitroglycerin. Within 60 minutes from symptom onset, the patient was transferred to the cardiac catheterization laboratory for primary percutaneous coronary angioplasty. Coronary angiography showed an irregular luminal defect, surrounded by contrast, in the distal right coronary artery (RCA) (Figure 1A – arrow). The other coronary arteries had no visible atherosclerotic disease. The occlusion was crossed with a guidewire and a 3 mm angioplasty balloon catheter. After one balloon inflation, there was no residual stenosis of the RCA (Figure 1B). The left ventricular end diastolic pressure was 25 mmHg. Left ventriculography demonstrated mild postero-basal hypokinesis, with a calculated ejection fraction of 65%. Despite resolution of chest pain, the patient remained dyspneic, and a right heart catheterization was then performed. The mean right atrial pressure was 24 mmHg, with a right ventricular pressure of 79/20 mmHg and a pulmonary artery pressure of 78/29 mmHg. Despite multiple attempts and repositioning of the pulmonary artery catheter, an adequate pulmonary capillary wedge pressure tracing could not be obtained. The right atrial blood oxygen saturation was 56%. The pulmonary artery blood oxygen saturation was 54%, with an arterial blood saturation of 90%. Given the lack of angiographic abnormalities throughout the coronary arterial tree, and the demonstration of a large thrombus in the distal RCA, the inferior wall myocardial infarction was thought to be the result of a direct (left-to-left) or paradoxical (right-to-left) embolism. The presence of severe pulmonary hypertension, signs of reduced cardiac output, decreased arterial oxygen saturation and persistent dyspnea, despite normal left ventricular systolic function, raised the suspicion of a concomitant pulmonary embolism. Computed tomographic pulmonary angiography demonstrated extensive bilateral, filling defects in the upper and lower lobar pulmonary arteries, consistent with pulmonary embolism (Figure 2A – arrows). A transthoracic echocardiographic exam revealed normal left and right ventricular size and systolic function, with an atrial septal aneurysm. A patent foramen ovale, with right-to-left shunting across the atrial septum during normal breathing, was noted after intravenous injection of agitated saline (Figure 2B – arrowheads). Thrombosis of the right posterior tibial vein was visualized on a lower extremities venous ultrasound. Studies for inherited prothrombotic states such as factor V Leiden and the prothrombin gene G20210A mutation, activity of protein C, protein S and antithrombin, homocysteine concentrations, and cardiolipin antibodies were obtained. With the exception of a slightly elevated homocysteine concentration of 12.4 micromol/l (normal Discussion. Paradoxical embolization represents the passage of embolic material from the venous to the systemic arterial circulation through a cardiac defect. It was first described in 1877 by Cohnheim, who hypothesized that a clot passing across a PFO was the likely cause of stroke and subsequent death in a young woman.1 The average prevalence of PFO in the general population was 26% on a pooled analysis of autopsy studies.2 The diagnosis of a PFO can be established using contrast echocardiography if, on a four-chamber view, microbubbles cross the atrial septum into the left atrium within three heart cycles after contrast opacification of the right atrium. While small clots, originating in the venous system, embolize to the lungs without any clinical consequence, occasionally, some will pass into the arterial circulation across a PFO. Paradoxical embolization to the brain or the heart may produce a stroke or myocardial infarction respectively. Conditions, which increase the right atrial pressure such as chronic obstructive pulmonary disease, sleep apnea, or pulmonary embolism, may facilitate paradoxical embolization through transient reversal of the normal interatrial pressure gradient. The incidence of paradoxical embolization to the coronary arteries is not well known. It is estimated that the coronary arteries are involved in less than 10% of all paradoxical emboli.3,4 Coronary paradoxical embolization has the clinical and electrocardiographic presentation of a typical myocardial infarction involving one or multiple epicardial coronary arteries. Occasionally, other organs, such as the brain or lungs, may also be involved. Coronary angiography may reveal segmental occlusion with the notable absence of significant atherosclerotic disease.5 In patients without evident risk factors for venous thromboembolism, the search for a prothrombotic state is indicated. Appropriate therapy needs to address both the acute thrombotic episode and the prevention of further clinical events. There is ongoing debate with regard to the indication, timing and modality of PFO closure in patients who present with stroke due to a paradoxical embolism. In a recent review, the only absolute indication for PFO closure was recurrent paradoxical embolism to the brain in the presence of a PFO associated with an atrial septal aneurysm.6 Paradoxical embolization to the coronary arteries is a rare occurrence, and there is no current evidence-based data to support the percutaneous or surgical closure of the PFO. Despite this lack of evidence, and due to the potential significant morbidity, consideration should be given to closure of a PFO in a patient presenting with coronary paradoxical embolization. Our patient had a lower extremity venous thrombosis, a hemodynamically significant pulmonary embolism, a myocardial infarction and evidence of a PFO with an atrial septal aneurysm. The patient has been continued on oral anticoagulation therapy and a repeat echocardiographic exam, performed 3 months after hospital discharge, revealed a return to normal estimated pulmonary systolic pressure but persistence of right-to-left shunting at the atrial level with Valsalva’s maneuvre. She is to continue with anticoagulant therapy. Closure of the PFO as definitive therapy is warranted should she have a recurrent embolic event.
1. Cohnheim J. Thrombose und Embolie: Vorlesung uber Allgemeine Pathologie. Berlin, Germany: Hirschwald; 1877;I:134. 2. Windecker S, Meier B. Patent foramen ovale and atrial septal aneurysm: When and how should they be treated. ACC Curr J Rev 2002;11:97‚Äì101. 3. Johnson, BI. Paradoxical embolism. J Clin Pathol 1951;4:316‚Äì322. 4. Loscalzo J. Paradoxical embolism: Clinical presentation, diagnostic strategies and therapeutic options. Am Heart J 1986;112:141‚Äì145. 5. Cheng TO. Paradoxical embolism: A diagnostic challenge and its diagnosis during life. Circulation 1976;53:565‚Äì568. 6. Meier B, Lock JE. Contemporary management of patent foramen ovale. Circulation 2003;107:5‚Äì9.