Some patients with stroke cannot find the cause, especially young patients bring with the fight confusion, and now it is found that some of them are caused by foramen ovale non-occlusion.
Concept of patent foramen ovale
During fetal life, the lungs are unable to receive blood flow, and blood returning to the right atrium is shunted to the left atrium through an open foramen ovale; after birth, the foramen ovale closes spontaneously in about 75% of individuals, whereas in 25% of individuals, the foramen ovale is not closed. An unclosed foramen ovale is hemodynamically nonsensical interatrial traffic. Normally, the membrane of the foramen ovale blocks the left-to-right shunt, and when conditions exist that cause elevated right atrial pressure, the foramen ovale reopens, providing a conduit for singular emboli (e.g., paradoxical embolism, paradoxical embolism, paradoxical embolism). If a small embolus is present in the patient’s lower extremity, it can reach the right atrium with the blood circulation. When the patient exerts force (i.e., Valsalva maneuver, e.g., coughing, breath-holding), the unclosed foramen ovale opens and the embolus reaches the left atrium through the foramen ovale and subsequently the brain, forming a cerebral embolism, i.e., the paradoxical embolism described above.
The incidence of PFO in stroke patients is as high as 40-50%, and the detection rate in the general healthy population also reaches 20%. It is estimated that 30,000-60,000 stroke patients in the United States are caused by emboli passing through PFO each year. There is no such large-scale epidemiological survey in China, so it is difficult to estimate the incidence accurately in China.
With the development of cardiac ultrasound imaging, saline injection contrast imaging is able to show interatrial shunts, making the close relationship between cryptogenic stroke and PFO clearer.
Association of PFO with stroke and special occupations
There is a tendency for the foramen ovale to increase with age, possibly due to right atrial enlargement pulling on the foramen ovale. Special occupations, especially divers or diving enthusiasts, combined with PFO can lead to chimeric embolism, and the incidence of chimeric embolism is 4.5 times higher in those with decompression sickness combined with PFO than in those without PFO. Reports of TIA and chimeric embolism in divers and pilots have shown that these particular professions developed stroke symptoms such as limb numbness, hemiparesis, and vertigo after diving and flying, and that PFO was detected on ultrasonography, with a right-to-left shunt after Valsalva maneuver, and that these symptoms ceased after interventional treatment to seal the foramen ovale. Stroke can also occur in healthy adults with PFO, especially in patients with combined lower extremity thromboembolic disease.
Ancillary diagnostic methods for PFO
Transesophageal ultrasound (TEE) is the diagnostic method of choice for PFO and can clearly show the septal structures. Currently, intravenous acoustic contrast is mostly used, and patients are asked to cough or perform Valsalva maneuver to increase the right atrial pressure, which causes a right-to-left shunt and increases the sensitivity of the examination. The size of PFO is judged according to the number of shunted microbubbles: a small shunt of no more than 10 microbubbles, a large shunt of more than 10, and a large shunt further subdivided into shower type (more than 25 microbubbles).
Transthoracic ultrasound (TTE) color Doppler plus acoustic imaging is convenient, painless, and 100% specific, but less sensitive than TEE, which is about 80%. Therefore, a negative TTE cannot completely exclude the diagnosis of PFO, and a positive TEE can be avoided.
Transcranial Doppler ultrasound (TCD) combined with acoustic contrast is mostly used in patients with sensory abnormalities and neurological disease. TCD can detect contrast microbubbles from PFO in the cerebral circulation, leading to a presumed right-to-left shunt at the cardiac level.
Treatment of PFO Pharmacological treatment includes anticoagulation and antiplatelet agents Studies have shown that even with oral anticoagulation and antiplatelet agents such as warfarin and aspirin, the recurrence rate of cerebral ischemia is still as high as 8%.
Surgical treatment Surgical treatment is one of the effective means of treating PFO, but it is highly invasive and some patients still have recurrent stroke or TIA after surgery
There are several blockers used for PFO treatment, and clinical studies have shown that transcatheter blocking of PFO is a safe and effective non-surgical method.
Indications and contraindications for Amplatzer blocker intervention: one of the following is an indication
(1) Patients with PFO combined with cerebral embolism of unknown origin;
(2) PFO combined with unexplained TIA or cerebral ischemic lesion;
(3) PFO combined with extracranial thromboembolism of unknown cause;
(4) PFO combined with cerebral infarction caused by thrombosis of the venous system;
(5) Residual leak after surgical occlusion of PFO. Contraindications include.
(1) Any cerebral infarction for which other causes can be identified, such as cardiogenic, peripheral vascular system, vasculitis, hypercoagulable state;
(2) Contraindications to antiplatelet or anticoagulation therapy;
(3) Inferior vena cava or pelvic vein thrombosis resulting in complete vascular obstruction, systemic or local infection, sepsis, intracardiac thrombosis;
(4) Pregnancy.
It is now believed that stroke of unknown origin combined with PFO is a strong indication for blocker therapy, and early intervention in special occupations such as divers with concomitant PFO has the potential to prevent the occurrence of stroke.
Percutaneous PFO occlusion is easy to perform, with a high success rate and few complications. For patients with stroke of unknown cause, who also have a confirmed PFO with right-to-left shunt, interventional occlusion therapy should be used.