Structural Heart Disease

Cryptogenic Stroke with Patent Foramen Ovale and May-Thurner Syndrome

Frank Amico, DO, Harit Desai, DO, Vincent Varghese, DO, and Jon C. George, MD, Division of Interventional Cardiology and Endovascular Medicine, Deborah Heart and Lung Center, Browns Mills, New Jersey

Frank Amico, DO, Harit Desai, DO, Vincent Varghese, DO, and Jon C. George, MD, Division of Interventional Cardiology and Endovascular Medicine, Deborah Heart and Lung Center, Browns Mills, New Jersey

Disclosures: Dr. Amico, Dr. Desai, and Dr. Varghese report no conflicts of interest regarding the content herein. Dr. George reports he is a consultant for Boston Scientific, Covidien, and Gore. The authors can be contacted via Dr. Jon George at georgej@deborah.org.

Case

A 53-year-old female with a past medical history of hypertension, dyslipidemia, asthma, and previous transient ischemic attack (TIA) was transferred to our institution following an embolic cerebrovascular accident (CVA) requiring systemic thrombolytic therapy. The patient underwent transesophageal echocardiogram (TEE), which detected a 12 mm patent foramen ovale (PFO) with right-to-left shunt (Figure 1). Given her initial clinical presentation of an acute CVA and prior history of TIA, a treatment plan for percutaneous PFO closure regarding secondary stroke prevention was initiated. 

She was brought to the cardiac catheterization lab where bilateral femoral venous access was obtained, and an AcuNav (Siemens) intracardiac echocardiography (ICE) catheter was inserted through the left common femoral vein, but halted by significant resistance in the left common iliac vein. Selective venogram of the left common iliac vein confirmed a subtotal thrombotic occlusion at the inferior vena cava (IVC) junction consistent with May-Thurner syndrome. A Glidewire (Terumo) with a support catheter was advanced to cross the subtotal occlusion into the IVC and a caval venogram performed to confirm intraluminal position.  

The ICE catheter was positioned in the right atrium for visualization of the interatrial septum and PFO. A multipurpose catheter with a soft, angled Glidewire was used to cross the PFO. The multipurpose catheter was then advanced into the left atrium, and chamber position confirmed via contrast injection (Figure 2). A 25 mm Helex septal occluder device (W.L. Gore) was selected for percutaneous closure, positioned via delivery sheath, and successfully deployed under echocardiographic and fluoroscopic guidance (Figure 3), with minimal residual flow by color Doppler (Figure 4). 

Next, the May-Thurner syndrome with left common iliac vein compression was addressed. Balloon angioplasty with a 12 x 20 mm balloon (Boston Scientific) was performed at nominal pressures, followed by deployment of a self-expanding 14 x 40 mm self-expanding nitinol stent (Covidien). Final venogram confirmed excellent result with brisk venous return. The patient tolerated the procedure without complication. Transthoracic echocardiogram performed 24 hours post-procedure demonstrated excellent device placement and stability. She was eventually discharged on dual antiplatelet therapy for three months. 

Discussion

A PFO occurs when the septum primum and septum secundum fail to fuse together, resulting in a communication between the right and left atria. With an incidence, in one autopsy study, of 27.3%, it has been linked to cryptogenic stroke.1 The presence of a PFO with an atrial septal aneurysm confers an increased risk of cryptogenic stroke.2 The precise relationship between a PFO and cryptogenic stroke is not exactly clear; however, paradoxical embolism appears to be a plausible mechanism. The diagnosis of PFO is established by the use of microbubbles. These microbubbles demonstrate an interatrial communication with right-to-left transit within 3 to 4 cardiac cycles of right atrial opacification. 

As documented in the study by Lamy et al, patients with a PFO are younger and less likely to have traditional risk factors for stroke (hypertension, hypercholesterolemia, smoking) than those without a PFO.3 Patients less than 55 years old had a higher association between PFO and cryptogenic stroke versus patients older than 55 years old. It is estimated that the annual rates of recurrent stroke among patients with PFO range from 1.5% to 12%, and depend on the characteristics of the population.4 In a systematic review of non-randomized studies of transcatheter closure versus medical therapy for PFO, the one-year rate of recurrent neurological thromboembolism was 0% to 4.9% with transcatheter intervention and 3.8% to 12.0% with medical therapy. The rate of major and minor complications associated with device closure was 1.5% and 7.9%, respectively.5

Three randomized, controlled trials comparing device closure against medical therapy for stroke recurrence have all failed to show a significant difference in secondary stroke prevention.6,7,8 However, a post-hoc analysis of the RESPECT trial demonstrated a reduction in stroke recurrence in device closure patients with a PFO and associated atrial septal aneurysm. Additionally, medically treated patients had substantially larger recurrent strokes in comparison to the device closure patients. Further study is ongoing regarding PFO closure and cryptogenic stroke; however, careful patient selection, such as younger patients with PFO and atrial septal aneurysm, may benefit the most from device closure. 

May-Thurner syndrome is caused by compression of the left common iliac vein between the overlying right common iliac artery and the underlying vertebral body.9 This can result in left iliofemoral deep vein thrombosis or chronic venous insufficiency. As in our case, the left common iliac vein was affected with thrombotic stenosis, which likely caused paradoxical embolism and stroke. Definitive therapy was performed with stent angioplasty of the left common iliac vein and device closure of the PFO.

References

 

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