eMedicine Specialties > Cardiology > Congenital Heart Disease in the Adult

Eisenmenger Syndrome: Treatment & Medication

Author: Mikhael F El-Chami, MD, Fellow, Department of Cardiology, Emory University School of Medicine
Coauthor(s): Charles D Searles Jr, MD, Assistant Professor of Medicine, Division of Cardiology, Emory University School of Medicine; Consulting Staff, Division of Cardiology, Director of Stress Echo Laboratory, Grady Memorial Hospital
Contributor Information and Disclosures

Updated: Jun 5, 2008

Treatment

Medical Care

  • Fluid balance and climate control
    • Avoid sudden fluid shifts or dehydration, which may increase right-to-left shunting.
    • Avoid very hot or humid conditions, which may exacerbate vasodilation, causing syncope and increased right-to-left shunting.
  • Oxygen therapy
    • The use of oxygen supplementation is controversial.
    • Oxygen therapy has been shown to have no impact on exercise capacity and survival in adult patients with Eisenmenger syndrome.2,3
    • Some patients might benefit from nocturnal supplementation, although it is most useful as a bridge to heart-lung transplant.
    • Air travel appears to be safe as long as the airplanes are adequately pressurized. Supplemental oxygen during commercial air travel is often recommended, but limited data exist regarding this issue.4
  • Pulmonary vasodilator therapy
    • The pathophysiology of pulmonary hypertension in patients with Eisenmenger syndrome is somewhat similar to that of idiopathic pulmonary arterial hypertension (IPAH); both are associated with a neurohormonal imbalance of endogenous pulmonary vasodilators and vasoconstrictors. This imbalance leads to vascular remodeling, intimal fibrosis, and increased pulmonary vascular resistance (PVR). Therefore, in the management of patients with Eisenmenger syndrome, use of pulmonary vasodilating agents that have been shown to be useful in the management of patients with IPAH is conceptually appealing. Recent data support this use.
    • Long-term prostacyclin therapy was shown to improve hemodynamics (decrease in mean PA pressure, improvement in cardiac index, and decrease in PVR) and quality of life in patients with congenital heart disease and PAH.5 Another study evaluated epoprostenol infusion in adolescents with congenital heart disease and Eisenmenger physiology showing improved oxygenation (from 69% to 85%) and improvement in a 6-minute walk test distance (from 48 yd to 375 yd).6
    • Bosentan, an endothelin receptor antagonist, was the second vasodilator to be evaluated in patients with Eisenmenger syndrome. In a small retrospective study of 9 patients with congenital heart disease and Eisenmenger syndrome, bosentan therapy resulted in improved oxygen saturation (from 79% to 88%) and improved New York Heart Association (NYHA) class.7 A larger, multicenter, prospective study by Schulze-Neick et al tested the same hypothesis. In this study, bosentan titrated to 125 mg orally bid was associated with improvement in 6-minute walk test distance (362 m to 434 m), improvement in NYHA class (3.1 to 2.4), and a decrease in systolic PA pressure (111 mm Hg to 106 mm Hg).8

      A multicenter, prospective, double-blind, placebo-controlled study (the BREATH-5 study) tested the effect of bosenten titrated to 125 mg bid in 54 patients with Eisenmenger syndrome. Bosentan reduced the mean pulmonary arterial pressure and improved exercise capacity and World Health Organization (WHO) class.9 A longer follow-up of the BREATH-5 population (up to 40 wk) showed that bosentan remained safe and had a positive impact on patients with Eisenmenger syndrome.10   
    • A retrospective study that examined the outcomes of patients with Eisenmenger syndrome who were treated with pulmonary vasodilators versus those who were not showed that treatment with prostacyclin analogues and/or endothelin receptor antagonists delayed the need for transplantation.11
    • Sildenafil is another vasodilatory agent originally used for erectile dysfunction but recently approved for IPAH. Studies suggest that sildenafil is safe and effective in patients with Eisenmenger syndrome. In a randomized, placebo-controlled study of 20 patients with PAH (10 patients with Eisenmenger syndrome and 10 with IPAH), sildenafil improved NYHA class, 6-minute walk test distance, and exercise duration. Furthermore, sildenafil therapy resulted in a decrease in systolic PA pressure from 98 mm Hg to 78 mm Hg. The effects of the drug were similar for the 2 patient populations in this study.12

      In a study by Chau et al, sildenafil improved hemodynamics and symptoms in patients with pulmonary hypertension secondary to Eisenmenger syndrome and a similar group of patients with idiopathic arterial hypertension.13
    • In a study from India, another phosphodiesterase inhibitor (tadalafil) was shown to be safe and effective in 16 symptomatic patients with Eisenmenger syndrome. Tadalafil improved oxygen saturation (84% to 89% at 12 wk), and the mean WHO class (2.31 to 1.25).14
    • In summary, vasodilator therapy improves symptoms in patients with Eisenmenger syndrome and should be used routinely in the management of this patient population. However, a single medical therapy has not been consistently shown to reduce mortality in patients with Eisenmenger syndrome.
  • Anticoagulation: Silversides et al reported that the incidence of proximal pulmonary artery thrombus in this patient population was 21%.15 This study raised the issue of anticoagulation in Eisenmenger patients. These patients are at increased risk of bleeding; hence, the use of anticoagulation is still not routinely recommended.
  • Contraception, pregnancy, and genetic counseling
    • Avoid pregnancy. Tubal ligation is strongly recommended in women with Eisenmenger syndrome.
    • If patients refuse tubal ligation, hormone therapy (controlled release levonorgestrel or norethindrone and ethinyl estradiol preparations) is preferred over intrauterine devices, which can cause significant menorrhagia and potentially increase the risk of endocarditis.
    • The fetal mortality rate is approximately 25%, and the maternal mortality rate exceeds 50%.
    • Therapeutic abortion is recommended for women in the early stages of pregnancy.
    • The risk of congenital heart defects in offspring is approximately 10% and sometimes higher, depending on the primary natural cardiac defect.
    • Fetal echocardiography is recommended for pregnant patients or siblings.
  • For resuscitation in the event of massive acute bleeding, replace losses with fresh frozen plasma, cryoprecipitate, and platelets.
  • Endocarditis
    • Patients with Eisenmenger syndrome are at very high risk for endocarditis. Endocarditis prophylaxis should be emphasized and patients should be given repeat instructions about this issue. For standard general prophylaxis for dental, oral, respiratory tract, esophageal, genitourinary, and other gastrointestinal procedures, refer to the American Heart Association recommendations for the prevention of bacterial endocarditis.16
    • Infective endocarditis prophylaxis (nonchemotherapeutic)
      • Encourage good oral hygiene (soft-bristle toothbrushing twice a day, mouthwash or hydrogen peroxide rinses, soft conical rubber gum stimulator, semiannual dental visits).
      • Skin care advice should include using a nonabrasive cleanser and avoidance of squeezing skin.
      • Nail biting should be avoided.
  • Right heart failure is often present in patients with Eisenmenger syndrome, but limited treatment options are available for this complication. Typically, digoxin and diuretics have been used. Diuretics, specifically loop diuretics, are used for symptomatic relief of congestion. However, diuretics should be used cautiously in these patients given their preload-dependent state.
  • Erythrocytosis
    • Erythrocytosis is almost always present in patients with Eisenmenger syndrome. This could result in symptoms of hyperviscosity that include visual disturbances, fatigue, headache dizziness, and paresthesias. Routine phlebotomy is not usually recommended for this condition, except in the presence of hyperviscosity symptoms. Before initiating phlebotomy, dehydration must be ruled out since it can falsely increase the hematocrit level. Furthermore, phlebotomy should always be performed with concomitant fluid replacement.
    • Repeated phlebotomy can result in iron deficiency anemia. Patients with an iron deficiency have apparent normal hematocrit level and low mean corpuscular volume (MCV). The iron deficient erythrocytes are less deformable than normal erythrocytes, and this lack of deformability can worsen hyperviscosity.17
    • To manage erythrocytosis, first rule out dehydration. Then, if the patient has symptoms of hyperviscosity and the hematocrit level is greater than 65%, venesect 250-500 mL of blood and replace with an equivalent volume of isotonic sodium chloride (or 5% dextrose if in heart failure).
  • Thrombotic and bleeding complications
    • Eisenmenger syndrome patients are prone to thrombotic events as part of their hyperviscosity. At the same time, they are susceptible to bleeding because their platelets are dysfunctional. Therefore, patients who have a hematocrit level greater than 65% and are undergoing noncardiac surgery should receive phlebotomy and concomitant fluid replacement in order to decrease the risk of thrombotic and bleeding events.18
  • Central nervous system (CNS) events can occur secondary to paradoxical embolus, CNS venous thrombosis, intracranial hemorrhage, or brain abscesses in the setting of endocarditis.18 Endocarditis prophylaxis, the use of air filters with all intravenous catheters during hospital admissions, and adequate management of hyperviscosity can help decrease these potentially fatal complications.

For more information, see Medscape CME activity, Eisenmenger's Syndrome: Pathophysiologic Insights and Pharmacologic Treatment Rationales.

Surgical Care

  • Heart-lung transplantation
    • Heart-lung transplantation is the procedure of choice if repair of the underlying cardiac defect is not possible.
    • It was performed successfully for the first time in 1981. Since then, the outcome has improved due to better immunosuppressive therapy, new antiviral agents, and improved patient selection.
    • Reported actuarial survival rates are 68% at 1 year, 43% at 5 years, and 23% at 10 years.
    • The main complications are infection, rejection, and obliterative bronchiolitis.
  • Bilateral lung transplantation
    • Repair of the underlying cardiac defect is required, but it is considered the preferable procedure if the cardiac defect is simple.
    • Bilateral lung transplantation is better than single-lung transplantation in terms of mortality, New York Heart Association functional class, cardiac output, and postoperative pulmonary edema.
  • Advantages over heart-lung grafting include no transplant coronary artery disease or cardiac rejection, and this approach may be considered an option in current times of donor organ shortage, although exact indications have yet to be defined.
  • Corrective surgery
    • Repair of the primary defect is contraindicated in the context of established severe pulmonary arterial hypertension. However, corrective surgery may be possible in certain cases if a significant degree of left-to-right shunting remains and if responsiveness of the pulmonary circulation to vasodilator therapy can be demonstrated.
    • Limitations include a transient dynamic right ventricular outflow tract obstruction, and exact indications for this approach have not yet been defined.

Consultations

  • Pediatric cardiologist (pediatric patients)
  • Adult cardiologist who specializes in adult congenital heart disease (adult patients)
  • Early input from heart-lung transplant team

Diet

  • Patients with right-sided congestive heart failure should avoid excessive sodium intake.
  • Sodium restriction must be balanced with the need to maintain intravascular volume.

Activity

  • Intense athletic activities carry the risk of sudden death.
  • Patients should not participate in competitive sports.
  • In certain patients, an exercise prescription can be individualized based on exercise testing that documents a level of activity that meets the following 3 criteria:
    1. Oxygen saturations remain greater than 80%.
    2. No symptomatic arrhythmias occur.
    3. No evidence of symptomatic ventricular dysfunction is present.

Medication

The medical treatment of Eisenmenger syndrome is directed toward improvement of symptoms related to heart failure and pulmonary hypertension and preventing and managing complications related to cyanotic congenital heart disease.

For more information, see Medscape CME activity, Eisenmenger's Syndrome: Pathophysiologic Insights and Pharmacologic Treatment Rationales.

Diuretics

These agents are useful to remove fluid and reduce preload and afterload in the treatment of heart failure.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which in turn results inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg per dose increments until a satisfactory effect is achieved.

Adult

20-80 mg/dose PO, increase in increments of 20-40 mg/dose at intervals of 6-8 h; maintenance dose is qd/bid
20-40 mg/dose IV/IM, may be repeated in 1-2 h as needed and increased by 20 mg/dose with each succeeding dose up to 1000 mg/d with a usual dosing interval of 6-12 h

Pediatric

Not established

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few mo of therapy and periodically thereafter

Cardiac glycosides

Positive inotropic and negative chronotropic effects are useful in the setting of left or right heart failure.


Digoxin (Lanoxin, Lanoxicaps)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system.
Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Adult

PO loading: 0.75-1.50 mg
PO maintenance: 0.125-0.500 mg qd
IV/IM loading: 0.5-1 mg
IV/IM maintenance: 0.125-0.500 mg qd

Pediatric

Not established

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Prostaglandins

These drugs can be effective in reversing reactive pulmonary vasoconstriction and can, therefore, lower pulmonary vascular resistance, decrease afterload, reduce the right ventricle, and reduce right-to-left shunting. In some patients, chronic prostacyclin analogue therapy (epoprostenol) can be of benefit, particularly as a bridge to heart-lung transplantation.


Epoprostenol (Flolan)

Strong vasodilator of all vascular beds. May decrease thrombogenesis and platelet clumping in the lungs by inhibiting platelet aggregation.
Continuous chronic infusion should be administered through a central venous catheter.

Adult

Initiate infusion at 4 ng/kg/min IV less than maximum tolerated infusion rate determined during acute dose ranging
If maximum tolerated infusion rate <5 ng/kg/min, start chronic infusion rate at one half maximum tolerated infusion rate

Pediatric

Not established

Coadministration with anticoagulants may increase bleeding risk due to shared effects on platelet aggregation

Documented hypersensitivity; hyaline membrane disease; dominant left-to-right shunt; respiratory distress syndrome; congestive heart failure due to severe left ventricular systolic dysfunction

Pregnancy

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

Precautions

Coadminister whenever possible with anticoagulants to reduce risk of thromboembolism

Vitamins

Recurrent phlebotomy for erythrocytosis can lead to microcytic anemia. Iron stores should be replaced if deficiency is symptomatic and hematocrit is <65%.


Iron sulfate (Feosol, Ferrous sulfate)

A nutritionally essential inorganic substance.

Adult

325 mg PO qd until hematocrit rises (usually 1 wk), then discontinue

Pediatric

Not established

Absorption is enhanced by ascorbic acid; interferes with tetracycline absorption; food and antacids impair absorption

Documented hypersensitivity; hemochromatosis; hemosiderosis

Pregnancy

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

Precautions

Gastrointestinal upset; iron toxicity is observed with ingestion of large amount and can be fatal, especially in children; parenteral (IV) administration may cause several reactions, including headaches, malaise, fever, generalized lymphadenopathy, arthralgia, and urticaria; can cause severe anaphylaxis; other reactions include phlebitis at infusion site

Anti-inflammatory medications

Indicated for symptomatic secondary gout.


Colchicine

Decreases leukocyte motility and phagocytosis in inflammatory responses.

Adult

Acute dose: 0.6 mg PO q2h until pain relieved or until diarrhea develops
Prophylactic dose: 0.6 mg PO qd or bid

Pediatric

Not established

Sympathomimetic agent toxicity and effect of CNS depressants are significantly increased with colchicine

Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias; dehydration; uric acid kidney stones; blood dyscrasia; age <2 y; pregnancy

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Risk of renal failure, hepatic failure, permanent hair loss, bone marrow suppression, numbness or tingling in hands and feet, disseminated intravascular coagulopathy, and decreased sperm count

Endothelin antagonists

These agents competitively bind to endothelin-1 (ET-1) receptors EtA and EtB in endothelium and vascular smooth muscle, inhibiting vessel constriction and elevation of blood pressure.


Bosentan (Tracleer)

Endothelin receptor antagonist indicated for the treatment of PAH in patients with WHO class III or IV symptoms to improve exercise ability and decrease rate of clinical worsening. Inhibits vessel constriction and elevation of blood pressure by competitively binding to ET-1 receptors EtA and EtB in endothelium and vascular smooth muscle. This leads to significant increase in cardiac index (CI) associated with significant reduction in pulmonary artery pressure, PVR, and mean right atrial pressure. Due to teratogenic potential, can only be prescribed through the Tracleer Access Program (1-866-228-3546).

Adult

<40 kg: 62.5 mg PO bid; not to exceed 125 mg/d
>40 kg: 62.5 mg PO bid for 4 wk initially, then increase to 125 mg PO bid

Pediatric

Not established; 62.5 mg PO bid recommended if <40 kg, or >12 years; not to exceed 125 mg/d

Toxicity may increase when administered concomitantly with inhibitors of isoenzymes CYP450 2C9 and CYP450 3A4 (eg, ketoconazole, erythromycin, fluoxetine, sertraline, amiodarone, and cyclosporine A); induces isoenzymes CYP450 2C9 and CYP450 3A4 causing decrease in plasma concentrations of drugs metabolized by these enzymes including glyburide as well as other hypoglycemics, cyclosporine A, hormonal contraceptives, simvastatin, and possibly other statins; hepatotoxicity increases with concomitant administration of glyburide

Documented hypersensitivity; coadministration with cyclosporine A or glyburide

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Causes at least 3-fold elevation of liver aminotransferases (ie, ALT, AST) in about 11% of patients; may elevate bilirubin (serum aminotransferase levels must be measured prior to initiation of treatment and then monthly); caution in patients with mildly impaired liver function (avoid in patients with moderate or severe liver impairment); not recommended while breastfeeding; monitor hemoglobin levels after 1 and 3 mo of treatment and every 3 mo thereafter; exclude pregnancy before initiating treatment and prevent thereafter by use of reliable contraception; headache and nasopharyngitis may occur


Ambrisentan (Letairis)

Endothelin receptor antagonist indicated for pulmonary arterial hypertension in patients with WHO class II or III symptoms. Improves exercise ability and decreases progression of clinical symptoms. Inhibits vessel constriction and elevation of blood pressure by competitively binding to endothelin-1 receptors ETA and ETB in endothelium and vascular smooth muscle. This leads to significant increase in cardiac index associated with significant reduction in pulmonary artery pressure, pulmonary vascular resistance, and mean right atrial pressure. Because of the risks of hepatic injury and teratogenic potential, only available through the Letairis Education and Access Program (LEAP). Prescribers and pharmacies must register with LEAP in order to prescribe and dispense. For more information, see http://www.letairis.com or call (866) 664-LEAP (5327).

Adult

5 mg PO qd initially; may increase to 10 mg PO qd if 5 mg/d tolerated; do not chew, crush, or split tab

Pediatric

Not established

Glycoprotein-P, OATP, UGTs (ie, 1A9S, 2B7S, 1A3S), CYP2C19, and CYP3A substrate; coadministration with CYP3A (eg, cyclosporine, atazanavir, clarithromycin, indinavir, itraconazole, ketoconazole, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin) or 2C19 inhibitors (eg, omeprazole) may decrease elimination and therefore increase serum levels; CYP3A and 2C19 inducers (eg, rifampin) may increase metabolism and therefore decrease serum levels

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Common adverse effects include peripheral edema, nasal congestion, sinusitis, and facial flushing; caution with mild hepatic impairment or history of moderate-to-severe hepatic impairment; hepatic injury may occur (monitor bilirubin, ALT, and AST values at baseline and then monthly); may use in women of childbearing potential only after negative pregnancy test result and must use 2 reliable methods of contraception (unless tubal sterilization or Copper T 380A or LNg 20 IUD inserted); may decrease hemoglobin and hematocrit values (monitor at baseline, 1 mo, and then periodically)

Phosphodiesterase (type 5) enzyme inhibitors

The antiproliferative effects of the phosphodiesterase type 5 pathway (PDE5), which regulates cyclic guanosine monophosphate hydrolysis, may be significant in the chronic treatment of pulmonary hypertension with PDE5 inhibitors such as sildenafil.


Sildenafil (Revatio)

Promotes selective smooth muscle relaxation in lung vasculature possibly by inhibiting PDE5. This results in subsequent reduction of blood pressure in pulmonary arteries and increase in cardiac output.

Adult

20 mg PO tid

Pediatric

Not established

Potentiates vasodilatory effect of NO resulting in potentially fatal drop in blood pressure; coadministration with ketoconazole, erythromycin, or cimetidine increases plasma sildenafil concentrations; coadministration with rifampin decreases plasma levels of sildenafil

Documented hypersensitivity; concurrent or intermittent using of organic nitrates in any form

Pregnancy

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

Precautions

Adverse effects include headaches (16%), flushing (10%), upset stomach (7%), nasal congestion (4%), and a blue haze at the periphery of vision (3%); adverse effects occur more often in men taking the 100 mg dose; serious adverse effects occur in patients with severe heart disease and those who are taking nitrates; rates of MI were 1.7 and 1.4 per 100 man-years for sildenafil and placebo groups

More on Eisenmenger Syndrome

Overview: Eisenmenger Syndrome
Differential Diagnoses & Workup: Eisenmenger Syndrome
Treatment & Medication: Eisenmenger Syndrome
Follow-up: Eisenmenger Syndrome
Multimedia: Eisenmenger Syndrome
References
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Further Reading

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Keywords

Eisenmenger complex, Eisenmenger defect, Eisenmenger disease, Eisenmenger tetralogy, exercise intolerance, cyanosis, heart failure, hemoptysis, ventricular septal defect, VSD, overriding aorta, congenital cardiac shunt defect, pulmonary hypertension, patent ductus arteriosus, PDA, large congenital cardiac left-to-right shunts, surgically created extracardiac left-to-right shunts, increased pulmonary blood flow, transposition of the great arteries, atrial septal defect, persistent truncus arteriosus, unrestricted pulmonary blood flow, common atrioventricular canal, Blalock-Taussig anastomosis, Waterston shunt, Potts shunt, chronic cyanotic heart disease, large nonrestrictive ventricular septal defect, nonrestrictive patent ductus arteriosus

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Contributor Information and Disclosures

Author

Mikhael F El-Chami, MD, Fellow, Department of Cardiology, Emory University School of Medicine
Mikhael F El-Chami, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Charles D Searles Jr, MD, Assistant Professor of Medicine, Division of Cardiology, Emory University School of Medicine; Consulting Staff, Division of Cardiology, Director of Stress Echo Laboratory, Grady Memorial Hospital
Charles D Searles Jr, MD is a member of the following medical societies: American Heart Association and Sigma Xi
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman of Medicine, Vice Dean for Clinical Affairs, Chairman, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Park W Willis IV, MD, Sarah Graham Distinguished Professor of Medicine and Pediatrics, University of North Carolina at Chapel Hill School of Medicine
Park W Willis IV, MD is a member of the following medical societies: American Society of Echocardiography
Disclosure: Nothing to disclose.

 
 
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