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  1. 1. Case report Jean-Michel Juliard MD Cardiology department Hôpital Bichat Paris
  2. 2. Medical history <ul><li>Male patient: born March 25, 1943 </li></ul><ul><li>1985: bilateral leg venous thrombosis following orthopedic surgery </li></ul><ul><li>Medical therapy for hypertension: labetalol </li></ul><ul><li>December 27-31, 2001: taken to the intensive care unit of a community hospital near Paris for severe bilateral pulmonary infection; treated with oxygen and antibiotics. </li></ul>
  3. 3. Case presentation <ul><li>Saturday, January 19, 2002: the patient was suddenly awoken at 6 AM by a painful left arm, and experienced the following symptoms: </li></ul><ul><ul><li>Lipothymia associated with ataxia during a few minutes </li></ul></ul><ul><ul><li>Continuous chest pain in the precordium area </li></ul></ul><ul><ul><li>Shortness of breath, which started with his pulmonary infection in December 2001 </li></ul></ul><ul><li>On the same day, the patient is transferred to our cardiac surgery department since aortic dissection is suspected. </li></ul>
  4. 4. Examination upon arrival in the cardiac surgery unit <ul><li>Blood pressure: 95/55 mm Hg </li></ul><ul><li>Heart rate 110 bpm </li></ul><ul><li>Oxygen arterial saturation 91% despite 15 liters nasal airflow </li></ul><ul><li>Left upper limb hemiparesis and radial pulsations are over </li></ul><ul><li>No cardiac insufficiency </li></ul><ul><li>No symptoms of deep venous thrombosis </li></ul>
  5. 5. ECG at the community hospital emergency room: 07h18 Ongoing acute inferior wall infarction
  6. 6. ECG upon admission in the cardiac surgery department: 11h51 Q waves in leads II, III, and aVF 5 hours and 51 minutes after onset of chest pain
  7. 7. Transthoracic echocardiography at bedside <ul><li>Left ventricular (LV) function is well preserved except for a slight inferior wall hypokinesia </li></ul><ul><li>No LV thrombus formation </li></ul><ul><li>Aortic root is not enlarged; no intimal flap is identified </li></ul><ul><li>Right ventricle: global enlargement and hypokinesia; systolic pulmonary artery pressure is estimated at 60 mm Hg </li></ul><ul><li>No abnormality on mitral and aortic valves </li></ul><ul><li>No pericardial effusion </li></ul>
  8. 8. Transesophageal echocardiography <ul><li>The diagnosis of aortic dissection is excluded </li></ul><ul><li>No atherosclerotic plaque on the aortic arch </li></ul><ul><li>Consistent data with transthoracic echocardiography to assess left and right ventricular function </li></ul><ul><li>A patent foramen ovale (PFO) associated with atrial septal aneurysm (ASA) is identified </li></ul>
  9. 9. Pulmonary helical computed tomography on January19, 2002 The arrows indicate bilateral thrombus formation
  10. 10. Diagnosis – summary <ul><li>The diagnosis of aortic dissection has been ruled out </li></ul><ul><li>We are facing a patient with three major problems: </li></ul><ul><ul><li>Massive bilateral pulmonary embolism </li></ul></ul><ul><ul><li>Subacute ischemia of the left upper limb with no critical situation </li></ul></ul><ul><ul><li>Acute inferior wall infarction, uncomplicated </li></ul></ul><ul><li>The patient is transferred from the cardiac surgery unit to the coronary care unit </li></ul>
  11. 11. Comments <ul><li>We have to treat both venous and arterial thrombosis at the same time, ie, antithrombin agents are mandatory. </li></ul><ul><li>Besides heparin, aspirin must be given especially at the acute phase of myocardial infarction. </li></ul><ul><li>Fibrinolytic agents could have been suggested, either for massive pulmonary embolism with right ventricular dysfunction or for the acute myocardial infarction. </li></ul><ul><ul><li>At this time we are very late, >6 hours after symptom onset, past the time window where fibrinolysis is beneficial. </li></ul></ul><ul><ul><li>The next slide shows that it would not have been the right treatment. </li></ul></ul>
  12. 12. Clinical outcome <ul><li>Favorable outcome regarding the subacute ischemia of the left upper limb without need for surgical intervention. </li></ul><ul><li>Uncomplicated left inferior wall myocardial infarction (CPK 350, troponin 8); delayed coronary angiogram on February, 04, 2002: no abnormalities. </li></ul><ul><li>No recurrent pulmonary embolism; venous Doppler identified right deep popliteal venous thrombus formation. </li></ul><ul><li>Cerebral magnetic resonance imaging (February, 6,2002): recent cerebral infarction (left cerebellum hemisphere) associated with old infarctions in another territories (brain hemispheres). </li></ul><ul><ul><li>What should have been the risk of fibrinolysis? </li></ul></ul>
  13. 13. Cerebral magnetic resonance imaging Without gadolinium With gadolinium Recent cerebellum infarction Enhancement with gadolinium injection
  14. 14. Physiopathology <ul><li>Paradoxical embolism due to : </li></ul><ul><ul><li>Antiphospholipid antibodies: 40 GPL U, no other coagulation abnormalities (protein C, protein S, antithrombin III …) </li></ul></ul><ul><ul><li>Thrombus migrations from the right to the left side of the heart through the patent foramen ovale </li></ul></ul>
  15. 15. PFO associated with ASA
  16. 16. Numerous devices are available for percutaneous PFO closures CARD I A AMPLATZER ® STAR-Flex ® INTRASEPT ®
  17. 17. Left atrium Right atrium We selected the device manufactured by Cardia
  18. 18. Echocardiographic control after implantation Left atrium Right atrium Device
  19. 19. Further investigations <ul><li>Prostatic hypertrophy despite normal prostatic markers; 10 prostatic biopsies performed on December 3, 2002 and 7 out of 10 show prostatic carcinoma. </li></ul><ul><li>April 23, 2003, overall surgical prostatectomy is successfully performed with no sequela. </li></ul><ul><li>November 2005: </li></ul><ul><ul><li>The patient is in good shape; he received medications for hypertension and diabetes. </li></ul></ul><ul><ul><li>He had no recurrent thrombotic events since PFO closure associated with anticoagulant therapy (INR target 2.5). </li></ul></ul><ul><ul><li>Prostatic markers are undetectable. </li></ul></ul><ul><ul><li>Antiphospholipid antibodies are still slightly elevated (33 GPL U). </li></ul></ul>
  20. 20. Conclusions <ul><li>Case report relating acute thrombotic events in different territories, arterial and venous. </li></ul><ul><li>Favored by: </li></ul><ul><ul><li>At the venous level: elevation of antiphospholipid antibodies (associated with prostatic carcinoma) different from primary antiphospholipid syndrome. </li></ul></ul><ul><ul><li>At the arterial level, paradoxical embolisms facilitated by the patent foramen ovale. </li></ul></ul><ul><li>Discussion about the optimal antithrombotic treatment and the benefit of PFO closure in such complex situations. </li></ul>
  21. 21. Our PFO closure indications in our institution <ul><li>Cryptogenic stroke in young patients (60 years) with PFO associated with ASA. </li></ul><ul><li>Recent stroke with previous strokes identified on cerebral imaging with PFO ± ASA. </li></ul><ul><li>Recurrent stroke despite aspirin therapy. </li></ul><ul><li>PFO associated with paradoxical embolism (our case report). </li></ul><ul><li>The other indications must be taken individually: </li></ul><ul><ul><li>Decompression sickness in divers </li></ul></ul><ul><ul><li>Platypnea-orthodeoxia syndrome </li></ul></ul><ul><ul><li>Migraine headache with aura </li></ul></ul><ul><ul><li>Pulmonary hypoxemia when PFO can cause or worsen hypoxemia </li></ul></ul>
  22. 22. Future of PFO closure <ul><li>Randomized studies comparing PFO closure and medical treatment are ongoing (RESPECT, CARDIA STAR, CLOSURE I). </li></ul><ul><li>PFO closure using intracardiac echocardiography (avoiding general anesthesia) appears safe and feasible. </li></ul><ul><li>New techniques with biological devices or even no device (PFO closure using radiofrequency) are still under evaluation. </li></ul>
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