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Case Report

To Close or Not To Close? PFO, Sex and Cerebrovascular Events

Toby Ferguson, MD, Lauren H. Sansing, MD, Howard Herrmann, MD, Brett Cucchiara, MD
December 2006
The precise role of patent foramen ovale (PFO) in causing stroke remains controversial. Clinical factors felt to support a diagnosis of paradoxical embolization through a PFO include presence of concurrent deep vein thrombosis (DVT) and onset of symptoms with a Valsalva maneuver.1 Regarding the latter, sexual activity may be an often unrecognized Valsalva equivalent. The occurrence of stroke during sexual intercourse, therefore, may have important etiologic implications. We describe two cases of cerebrovascular events associated with sexual activity and strongly suggestive of paradoxical embolization through a PFO. Case Presentations Case 1. A 55-year-old male developed sudden vertigo, nausea, and gait imbalance at orgasm. His symptoms slowly improved over a period of 6 hours. Upon presentation to the emergency room 8 hours later, his neurologic exam was normal. A computed tomography (CT) scan revealed an old right thalamic stroke, but no acute changes. CT angiography showed normal cervical and cerebral vessels. Transesophageal echocardiography (TEE) demonstrated an atrial septal aneurysm and PFO with interatrial shunt during Valsalva. No evidence of an underlying hypercoagulable state was found. His medical history was notable for a stroke 4 years prior that occurred as he disembarked from a plane following a trans-Atlantic airline flight. Magnetic resonance imaging (MRI) at that time demonstrated an acute right thalamic infarction with normal cervical and cerebral vessels. TEE demonstrated an atrial-septal aneurysm and PFO. A diagnosis of probable paradoxical embolization was made, and daily aspirin was prescribed. Given his prior history and new symptoms consistent with posterior circulation transischemic attack (TIA), a diagnosis of recurrent paradoxical embolization was made. He subsequently underwent endovascular closure of his PFO and was prescribed daily aspirin. Case 2. A 30-year-old female presented to the emergency room after the acute onset of expressive aphasia and right-sided numbness during sexual intercourse. Immediately preceding symptom onset, she had an involuntary guttural utterance. On examination, she had right-sided numbness and weakness and expressive aphasia which fluctuated over the next 6 hours. MRI revealed a small left insular cortex infarction and normal cervical and cerebral vessels. TEE demonstrated a small PFO with interatrial shunt during Valsalva only. Hypercoagulability testing was unrevealing. Her D–dimer level was 2,086 ng/ml (normal: Discussion The connection between PFO and stroke remains controversial. Several factors support an association, including anecdotal cases where thrombus has been visualized spanning a PFO, an increased prevalence of PFO in young stroke patients compared to controls, and an increased incidence of pelvic DVT visualized by MRI in young patients with cryptogenic stroke.2–4 In contrast, roughly 25% of normal, healthy volunteers have a PFO on TEE. Most patients with PFO and stroke are not found to have a DVT on routine evaluation, and the risk of recurrent stroke in young patients with PFO is not increased compared to those without PFO.5–7 Undeniably, in many patients with PFO and cryptogenic stroke, the PFO is an “innocent bystander”. In such cases, other mechanisms of cerebral ischemia may be operative such as a hypercoagulable or inflammatory state that is difficult to definitively diagnose. The decision about whether to implicate a PFO in causing stroke in an individual patient is therefore usually fraught with uncertainty. In this respect, two particular features may provide support for PFO-mediated stroke. First, identification of coexistent DVT at the time of presentation obviously raises the likelihood of paradoxical embolization. The second feature is the onset of the cerebrovascular event with a Valsalva maneuver. Previous authors have considered this a critical defining feature of PFO-related stroke, although this is not universally accepted.1,5 During the Valsalva maneuver, the pressure in the right atrium exceeds that in the left atrium, causing shunting of blood flow from right to left in the presence of a PFO, and increasing the probability of paradoxical embolization. Sexual activity, encompassing both orgasm and vocalizations, represents a Valsalva equivalent. A prior study described 4 cases of young patients with ischemic stroke occurring during sexual intercourse.8 In each of these cases, PFO was a common factor, and no other etiology was identified. However, none of these cases had additional clinical features or diagnostic test results to strengthen the contention that paradoxical embolizaton had occurred. In contrast, we describe 2 patients who suffered cerebrovascular events during sexual intercourse in which further evidence supporting paradoxical embolization was present. Case 1 had a history of prior stroke immediately after a prolonged airplane flight, a well-described risk factor for venous thrombosis. Case 2 had an extremely elevated D-dimer level suggestive of DVT. These observations emphasize the importance of a careful and complete history of the events preceding stroke onset. Patients may well be reluctant to volunteer details of sexual activity precipitating stroke unless explicitly asked. It is quite possible that this association is therefore under-recognized. While optimal management of PFO in stroke patients remains unclear,9 we believe that the occurrence of stroke during sexual activity in a patient with PFO strongly implicates paradoxical embolization, and may support more aggressive therapies to prevent stroke recurrence such as endovascular PFO closure.
References 1. Bogousslavsky J, Garazi S, Jeanrenaud X, et al. Stroke recurrence in patients with patent foramen ovale: The Lausanne Study. Lausanne Stroke with Paradoxal Embolism Study Group. Neurology 1996;46:1301–1305. 2. Claver E, Larrousse E, Bernal E, et al. Giant thrombus trapped in foramen ovale with pulmonary embolus and stroke. J Am Soc Echocardiogr 2004;17:916–918. 3. Cramer SC, Rordorf G, Maki JH, et al. Increased pelvic vein thrombi in cryptogenic stroke: Results of the Paradoxical Emboli from Large Veins in Ischemic Stroke (PELVIS) study. Stroke 2004;35:46–50. 4. Overell JR, Bone I, Lees KR. Interatrial septal abnormalities and stroke: A meta-analysis of case-control studies. Neurology 2000;55:1172–1179. 5. Lamy C, Giannesini C, Zuber M, et al. Clinical and imaging findings in cryptogenic stroke patients with and without patent foramen ovale: The PFO-ASA Study. Atrial Septal Aneurysm. Stroke 2002;33:706–711. 6. Mas JL, Arquizan C, Lamy C, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001;345:1740–1746. 7. Meissner I, Whisnant JP, Khandheria BK, et al. Prevalence of potential risk factors for stroke assessed by transesophageal echocardiography and carotid ultrasonography: The SPARC study. Stroke Prevention: Assessment of Risk in a Community. Mayo Clin Proc 1999;74:862–869. 8. Becker K, Skalabrin E, Hallam D, Gill E. Ischemic stroke during sexual intercourse: A report of 4 cases in persons with patent foramen ovale. Arch Neurol 2004;61:1114–1116. 9. Messe SR, Silverman IE, Kizer JR, et al. Practice parameter: Recurrent stroke with patent foramen ovale and atrial septal aneurysm: Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2004;62:1042–1050.

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