eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Atrial Septal Defect, Patent Foramen Ovale: Treatment & Medication

Author: Barry A Love, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Assistant Professor, Division Pediatric Cardiology, Pediatrics and Medicine, Division of Pediatric Cardiology, Mount Sinai School of Medicine
Coauthor(s): Michael A Portman, MD, Research Director, Department of Pediatrics, Division of Cardiology, Associate Professor, Childrens' Hospital
Contributor Information and Disclosures

Updated: Mar 18, 2009

Treatment

Medical Care

  • A small left-to-right shunt associated with a patent foramen ovale (PFO) should not require treatment.
  • In patients who have experienced a stroke or transient ischemic attack, treatment with aspirin or warfarin appears to decrease the risk of a subsequent event; however, no evidence in adults suggests that warfarin is superior to aspirin.16

Surgical Care

  • In most instances, no therapy is needed for a patent foramen ovale. The simple presence of a patent foramen ovale in an infant, child, or adult is a normal finding. Asymptomatic patients do not require medication and should not consider patent foramen ovale closure.
  • Closure of a patent foramen ovale is indicated if right-to-left shunting is identified as a previous or potential source of paradoxical embolism. Closure should be performed in patients with a patent foramen ovale and history of stroke only after an extensive evaluation excludes other causes of the stroke or sources of emboli. Closure may also be indicated in patients who have recurrent symptoms of stroke while receiving warfarin. Patent foramen ovale closure may be indicated in preparation for neurosurgical procedures in the sitting position, which carry a high risk of paradoxical air embolism.17 Closure may also be indicated in divers, for whom a patent foramen ovale represents an increased risk for decompression illness.18 .
  • Transcatheter closure of a patent foramen ovale is controversial. In the setting of cryptogenic stroke and a patent foramen ovale, nonrandomized data show that transcatheter closure is effective in preventing recurrent strokes.19
    • In the United States, 2 closure devices, the Amplatzer PFO Occluder (AGA Medical Company; Golden Valley, MN) and the CardioSEAL device (NMT Medical; Boston, MA), were available under a special humanitarian device exemption (HDE) for patent foramen ovale closure; however, the HDE was withdrawn in 2006 because the number of device uses exceeded the 4000/year allowed by the US Food and Drug Administration under the HDE rules. Currently, no device is specifically approved for patent foramen ovale closure in the United States. Outside the United States, several closure devices are available including the Amplatzer PFO Occluder, the StarFlex PFO Occluder (NMT Medical; Boston, MA), the CardioSEAL device, and the Gore Helex Occluders (Gore Medical, Flagstaff, AZ). Transcatheter suture closure20 and radiofrequency closure21  are investigational; to date, the results have been disappointing.  
    • Ongoing randomized controlled trials are comparing medical therapy (warfarin or aspirin) with transcatheter device closure of patent foramen ovale in the prevention of stroke. Patients who have had one stroke with a patent foramen ovale may qualify for these trials. One of the difficulties in comparing therapies for secondary prevention of stroke in patients with a patent foramen ovale is the relatively low recurrence rate. In patients with stroke and a patent foramen ovale, the recurrence risk appears to be 1-3% per year.14 In patients with atrial septal aneurysm, the risk is somewhat higher at about 5% per year.14 Even so, this relatively low recurrence risk means that randomized trials need to enroll large numbers of patients and observe them for many years to establish a benefit (or at least noninferiority) to medical therapy.
    • In the United States, off-label use of transcatheter closure devices is common in situations in which patients have a patent foramen ovale and have had a single stroke and do not wish to enter a randomized trial. Although the American Academy of Neurology has discouraged this type of an approach and encourages participation in randomized controlled trials,22 evidence of nonrandomized trials is sufficient for many to proceed with this approach. The Amplatzer Septal Occluder (AGA Medical Company; Golden Valley, MN), approved for closure of atrial septal defects, and the CardioSEAL device, approved for closure of muscular ventricular septal defects, are both used off-label for transcatheter patent foramen ovale closure in the United States.
  • In patients with orthodeoxia-platypnea secondary to a patent foramen ovale, patent foramen ovale closure is curative and normalizes the arterial oxygen saturation.
  • Surgical closure of a foramen ovale has largely been supplanted by the availability of safe and effective transcatheter closure methods. The safety and effectiveness of surgical foramen ovale closure has not been systematically compared with medical therapy or transcatheter device closure.

Consultations

  • Consultation with a pediatric cardiologist for evaluation of associated congenital heart defects and assessment of degree of left-to-right or right-to-left shunting may be indicated.
  • Consultation with a neurologist in patients with suspected stroke is indicated.

Activity

  • Activity is not restricted. However, scuba diving at depths greater than 35 ft increases the risk of decompression illness. Patent foramen ovale closure is therefore recommended for divers who descend to depths greater than 35 ft.18

Medication

Anticoagulants

These agents are used to prevent recurrent or ongoing thromboembolic occlusion. Systemic anticoagulation may be indicated for patients with patent foramen ovale (PFO) and history of stroke or those at a significantly increased risk for paradoxical embolus.


Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor dose to maintain an INR in the range of 2-3.

Adult

5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR

Pediatric

Administer weight-based dose of 0.05-0.34 mg/kg/d PO qd; adjust dose according to desired INR

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, PO contraceptives, and sucralfate
Medications that may increase anticoagulant effects of warfarin include PO antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen and sulindac

Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Antiplatelets

Aspirin, at doses of 3-5 mg/kg daily, acts as an antiplatelet agent and appears to reduce the risk of recurrent stroke in patients with cryptogenic stroke and patent foramen ovale.


Aspirin (Anacin, Bayer)

Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Hydrolyzed rapidly in plasma, and elimination follows zero-order pharmacokinetics.
Irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate). Platelet inhibition lasts for the life of the cell (approximately 10 d). May be used in low doses to inhibit platelet aggregation and to improve complications of venous stases and thrombosis. Indicated to prevent recurrent ischemic stroke.

Adult

81 mg or 325 mg PO qd

Pediatric

3-5 mg/kg PO qd

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of the association of aspirin with Reye syndrome, do not use in children (<16 y) with viral infections

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia or history of blood coagulation defects or those taking anticoagulants

More on Atrial Septal Defect, Patent Foramen Ovale

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Treatment & Medication: Atrial Septal Defect, Patent Foramen Ovale
Follow-up: Atrial Septal Defect, Patent Foramen Ovale
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References
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References

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Further Reading

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Keywords

atrial septal defect, patent foramen ovale, ASD PFO, interatrial communication, congenital heart defect, left-to-right shunting, right-to-left shunting, incompetent valve of the fossa ovalis, right atrial enlargement, left atrial enlargement, paradoxical embolism, mitral valve stenosis, mitral valve regurgitation, patent ductus arteriosus, ventricular septal defect, tricuspid valve stenosis, right ventricular hypoplasia, tricuspid atresia, total anomalous pulmonary venous return, migraine headaches, deep venous thrombosis, hypoplastic left-sided heart syndrome, stroke, transient ischemic attacks

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Contributor Information and Disclosures

Author

Barry A Love, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Assistant Professor, Division Pediatric Cardiology, Pediatrics and Medicine, Division of Pediatric Cardiology, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Michael A Portman, MD, Research Director, Department of Pediatrics, Division of Cardiology, Associate Professor, Childrens' Hospital
Michael A Portman, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Physiological Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Paul M Seib, MD, Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children's Hospital
Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Alvin J Chin, MD, Professor of Pediatrics, Division of Cardiology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine
Alvin J Chin, MD is a member of the following medical societies: American Association for the Advancement of Science and American Heart Association
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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