CASE REPORT

A thrombus in transit through a patent foramen ovale Uzoma N. Ibebuogu, MD, FACC; Rami N. Khouzam, MD, FACC, FACP, FASNC, FASE, FSCAI; Gyanendra Sharma, MD, FACC; John W. Thornton, FACC; Roshanak Robati, MS; David Silverman, MD

ABSTRACT Patent foramen ovale (PFO) is a congenital heart defect that may first be diagnosed in adulthood and has a prevalence of 25% to 30%. Although many patients with PFO are asymptomatic and do not require treatment, paradoxical embolism can cause stroke or myocardial infarction. The authors report an unusual case of PFO with a transversing thrombus in an 80-year-old man. The patient’s initial presentation appeared clinically as acute coronary syndrome, but he was subsequently diagnosed with a massive thrombus in transit via a PFO and pulmonary embolus leading to right-sided heart failure. Keywords: patent foramen ovale, thrombus, pulmonary embolus, congenital heart defect, interatrial shunt, hemodynamic abnormalities FIGURE 1. Upper esophageal TEE (72 degrees) showing a

trapped and transversing thrombus (arrows) through the PFO

Patent foramen ovale (PFO) is a congenital heart defect with a prevalence of 25% to 30% that may first be diagnosed in adulthood. Most patients with PFO are asymptomatic, and the usual but rare associations include cryptogenic stroke, migraine, vascular headache, decompression sickness, and air embolism. Although PFO is common, an interatrial shunt with coexisting hemodynamic abnormalities is rare. This article describes an unusual case of a trapped thrombus in transit via a PFO in a patient who presented with severe shortness of breath and pulmonary embolism (PE). CASE An 80-year-old man with hypertension, diabetes, and coronary artery disease presented to the ED after two episodes of nausea and vomiting associated with shortness At the University of Tennessee Health Science Center in Memphis, Uzoma N. Ibebuogu is an assistant professor and Rami N. Khouzam is an associate professor. At Georgia Regents University in Augusta, Gyanendra Sharma and John W. Thornton practice in the Division of Cardiology, Roshanak Robati practices in the School of Medicine, and David Silverman practices in the Department of Medicine. The authors have disclosed no potential conflicts of interest, financial or otherwise. DOI: 10.1097/01.JAA.0000446233.16049.01 Copyright © 2014 American Academy of Physician Assistants

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of breath and diaphoresis. He reported no chest pain or palpitations. Physical examination revealed an elevated BP (141/95 mm Hg), tachycardia, tachypnea, and clear lung fields. His Spo2 was 86% on room air, and he had elevated cardiac enzymes (troponin I of 5.6 ng/mL [normal value, less than 0.05 ng/mL], creatine kinase [CK] of 473 IU/L [normal range, 60 to 174 IU/L], and CK-MB of 38.6 IU/L or 8.1% of CK [normal range, less than 5%]). Electrocardiography showed normal sinus rhythm, left axis deviation, diffuse nonspecific ST-segment and T-wave abnormalities, and an S1Q3T3 pattern. The S1Q3T3 pattern, a deep S in lead I and Q-wave and T-wave inversion in lead III, usually indicates acute cor pulmonale, and specifically PE. Anticoagulation, statin, beta-blocker, and aspirin therapy were initiated for suspected acute coronary syndrome. In view of the patient’s clinical presentation and elevated cardiac biomarkers, a transthoracic echocardiogram (TTE) was performed. This showed an ejection fraction of 55%, moderately dilated right atrial and ventricular cavities, right ventricular volume and pressure overload with a right ventricular systolic pressure of 61.5 mm Hg, a moderately dilated right atrial cavity, and a tubular echogenic mobile structure visualized in both atria and transversing a PFO. A subsequent transesophageal echocardiography (TEE) Volume 27 • Number 10 • October 2014

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A thrombus in transit through a patent foramen ovale

Key points PFO is a congenital heart defect that may first be diagnosed in adulthood. Many patients with PFO are asymptomatic and do not require treatment, but paradoxical embolism can cause stroke or myocardial infarction. A right-to-left shunt through a PFO is an independent predictor of adverse outcome in patients with major PE. Options for preventing paradoxical embolism in patients with PFO include medical therapy with anticoagulation or antiplatelet therapy and surgical or percutaneous closure. Fibrinolytics are not used because the clot may break off and embolize distally.

(Figures 1 and 2) confirmed a PFO with predominantly right-to-left shunting and a large tubular thrombus trapped in the PFO. A thrombus was also visualized in the right pulmonary artery. Doppler ultrasound of the lower extremity revealed an acute occlusive thrombus of the right distal popliteal vein. Initially, clinicians considered performing cardiac catheterization because of the patient’s elevated cardiac biomarkers and history of coronary artery disease. However, this intervention was put on hold because of the presence of the large thrombus and PE that most likely explained the rise in the patient’s cardiac biomarkers. Due to a large thrombus burden in the left atrium and risk of paradoxical embolism leading to a stroke, urgent cardiothoracic surgery was performed. A thrombus was removed surgically from the right atrium, left atrium, left ventricle (Figure 3), and inferior vena cava and the PFO was closed. The patient also had placement of a right ventricular assist device (VAD) because of intraoperative acute right ventricular failure. Postoperatively, the patient

FIGURE 2. Mid-esophageal TEE (0 degrees) showing the trans-

versing thrombus (arrow) through the PFO prolapsing through the mitral valve (MV) JAAPA Journal of the American Academy of Physician Assistants

was hypoxemic while on mechanical ventilation, and required volume expansion and afterload reducers as well as pressure support to maintain hemodynamic stability. The VAD was removed on postoperative day 5. A repeat TTE showed normal left ventricular function, proximal and mid-right ventricular akinesis with apical sparing consistent with cor pulmonale (McConnell sign), improved apical motion, and a severely dilated right atrial cavity. The patient’s clinical condition subsequently deteriorated, and he died about 3 weeks after presentation. DISCUSSION Usually, the mere presence of PFO is not clinically significant and patients are asymptomatic requiring no treatment. However, paradoxical embolism in a patient with a PFO can cause stroke or myocardial infarction (MI) and adverse clinical outcomes. MI is considered an indication for surgical closure of the PFO. Previous studies have shown that a right-to-left shunt through a PFO is an independent predictor of adverse outcome in patients with major PE, carrying twice the risk of death when compared with patients without evidence of a right-to-left atrial shunt.1 The death of our patient reflects this observed increase in mortality. In an autopsy study of 965 normal hearts, the prevalence of PFO declined progressively with age, while the size of PFO increased progressively with age, with a mean diameter of 5.8 mm in patients older than 90 years.2 The reason for this is not known, but may explain the late presentation of paradoxical embolus in the older age group. In our patient, an initial assessment of acute coronary syndrome was made based on his symptoms, elevated cardiac biomarkers, and history of coronary artery disease. Clinical evaluation with echocardiography led to the diagnosis of acute PE and a thrombus trapped in a PFO. Interestingly, our patient did not have a stroke despite a large thrombus burden. Doppler ultrasonography confirmed deep venous thrombosis of the lower extremity as the primary source of the thrombus. The patient’s elevated cardiac biomarkers probably were due to the PE. Serum troponin I is elevated in about 30% of patients with a moderate-to-large PE, and the presumed mechanism is acute right heart overload, which was present in our patient.3 MI due to a paradoxical intracoronary embolus, which has been reported in previous case reports, cannot be excluded in our patient in the absence of a cardiac catheterization; however, this scenario seems less likely. The therapeutic options for the secondary prevention of paradoxical embolism in patients with PFO include medical therapy with anticoagulation or antiplatelet therapy and surgical or percutaneous closure. Fibrinolytics are not considered in this scenario as the clot may break off and embolize distally. Although the efficacy of PFO closure on the rate of recurrent paradoxical embolism has not been established, the choice of medical versus surgical therapy depends on several factors, such as size of the PFO, recurrent www.JAAPA.com

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CASE REPORT

paradoxical embolism, and failed preventive medical therapy for thromboembolism. In a nonrandomized comparison between percutaneous PFO closure and medical therapy, patients undergoing percutaneous closure had a significantly lower incidence of death or recurrent embolic events when compared with patients treated medically.4 The optimal therapy for patients with a PFO has not been established by randomized controlled trials. Recent guidelines from the American Heart Association/American Stroke Association (AHA/ASA) concluded that evidence

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was insufficient to evaluate the efficacy of PFO closure compared to medical therapy.5 In patients with PFO alone, antiplatelet therapy is recommended instead of anticoagulation, unless anticoagulation is indicated for other causes.6 For patients with a PFO and ischemic stroke or transient ischemic attack, antiplatelet therapy is reasonable to prevent a recurrent event. Warfarin is reasonable for high-risk patients who have other indications for oral anticoagulation, such as patients with an underlying hypercoagulable state or evidence of venous thrombosis.6

Volume 27 • Number 10 • October 2014

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A thrombus in transit through a patent foramen ovale

Our patient underwent emergent thoracotomy for thrombectomy and surgical PFO closure due to the large thrombus straddling his PFO and the obvious risk of a massive paradoxical embolic event. Previous studies were based on anecdotal evidence that cerebrovascular ischemic event in patients with a PFO resulted from paradoxical embolism, and necessitated secondary prevention with closure or anticoagulation. However, the documented presence of a trapped thrombus in the PFO in our patient clearly showed that the PFO is a potential source of paradoxical embolus in cases of cerebrovascular ischemic events. This case illustrates a possible indication for a primarily surgical approach in the management of a PFO. Unfortunately our patient died of a large PE and irreversible right heart failure, but did not have a stroke. When stroke appears imminent, a surgical strategy may be crucial to prevent it. In the absence of randomized controlled trials, a firm conclusion cannot be drawn from a single case. However, such a strategy seems to be an attractive and reasonable option. A prospective, randomized trial is needed to compare primary surgical closure in clinical scenarios such as this one with initial conservative medical management

FIGURE 3. PFO thrombus removed during surgery

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with anticoagulation followed by percutaneous closure of PFO after thrombus resolution. In summary, our case demonstrates an unusual case of a massive transversing thrombus in transit via a PFO and PE leading to right-sided heart failure and eventually death in an older patient. Review of the guidelines and current literature about medical therapy (antiplatelets and anticoagulation), PFO closure, and surgical procedures is emphasized. An imminent need for surgical intervention in such patients, in the form of embolectomy and patch repair, may be necessary. JAAPA REFERENCES 1. Konstantinides S, Geibel A, Kasper W, et al. Patent foramen ovale is an important predictor of adverse outcome in patients with major pulmonary embolism. Circulation. 1998;97(19): 1946-1951. 2. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984; 59(1):17-20. 3. Meyer T, Binder L, Hruska N, et al. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction. J Am Coll Cardiol. 2000;36(5):1632-1636. 4. Windecker S, Wahl A, Nedeltchev K, et al. Comparison of medical treatment with percutaneous closure of patent foramen ovale in patients with cryptogenic stroke. J Am Coll Cardiol. 2004;44(4):750-758. 5. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Stroke. 2006; 37(2):577-617. 6. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Circulation. 2006;113(10):e409-e449.

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A thrombus in transit through a patent foramen ovale.

Patent foramen ovale (PFO) is a congenital heart defect that may first be diagnosed in adulthood and has a prevalence of 25% to 30%. Although many pat...
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