eMedicine Specialties > Cardiology > Valvular Heart Disease

Tricuspid Regurgitation

Mary C Mancini, MD, PhD, Professor, Department of Surgery, Louisiana State University Health Sciences Center

Updated: Jul 29, 2008

Introduction

Background

Tricuspid regurgitation may result from structural alterations of any one or all of the components of the tricuspid valve apparatus. Components include the leaflets, chordae tendinea, annulus, and papillary muscles or adjacent right ventricular (RV) muscle. The lesion may be classified as primary when it is caused by an intrinsic abnormality of the valve apparatus or as secondary when it is caused by RV dilatation.

Pathophysiology

The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetent nature of the valve can result from primary structural abnormalities of the leaflets and chordae or from secondary myocardial dysfunction and dilatation.¹

Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. When due to the latter, it generally occurs in combination with tricuspid stenosis. Ebstein anomaly is the most common congenital form of tricuspid regurgitation.

In tricuspid regurgitation, chronic right ventricular volume overload results in right-sided congestive heart failure (CHF) manifested by hepatic congestion, peripheral edema, and ascites. For more on heart failure, see Medscape's Heart Failure Resource Center.

Frequency

United States

Incidence of tricuspid regurgitation appears to be 0.9%.

International

Incidence of tricuspid regurgitation appears to be less than 1%.

Mortality/Morbidity

The morbidity and mortality of the disease process are secondary to the underlying cause. In rheumatic disease, mortality rates with treatment are less than 3%. In Ebstein anomaly, mortality depends upon the severity of the valvular deformity and the feasibility of correction. Mortality rates with correction are approximately 10%. Tricuspid regurgitation resulting from myocardial dysfunction or dilatation has a mortality of up to 50% at 5 years.

Race

No race predilection is apparent.

Sex

No sex predilection is apparent.

Age

Ebstein anomaly can be detected at birth and during early childhood. In patients older than 15 years, the most common form of tricuspid regurgitation is rheumatic valvular disease. In the adult population, other predisposing factors, including carcinoid, bacterial endocarditis, and CHF, takes precedence.

Clinical

History

The patient with tricuspid regurgitation presents with the signs and symptoms of right-sided heart failure. The spectrum of presenting symptoms is dependent upon whether the condition is secondary to left ventricular (LV) dysfunction. If it is, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea accompany ascites and peripheral edema as common presenting complaints. Exercise intolerance may also be observed. The patient rarely reports angina, which may be present in the absence of coronary artery disease secondary to RV overload and strain.²

These patients must be questioned regarding intravenous drug use, history of rheumatic fever, and febrile episodes because bacterial endocarditis is a common cause of tricuspid valvular disease.

Physical

S₃ gallop is present, and the following physical findings may be found:

• Jugular venous distention with a prominent V wave: When present, a pansystolic murmur is heard along the lower left sternal border with inspiratory accentuation.
• Diminished peripheral pulse volume secondary to impaired forward blood flow: Patients with this sign may have relative hypotension secondary to therapeutic interventions used to decrease volume overload.
• Pulmonary rales if the tricuspid regurgitation is associated with LV dysfunction or mitral stenosis
• RV heave and S ₄ gallop that increases with inspiration
• Ascites
• Peripheral edema
• Cachexia and jaundice
• Atrial fibrillation (For more information on atrial fibrillation, see Medscape's Atrial Fibrillation Resource Center.)
• A high-pitched pansystolic murmur (loudest in the fourth intercostal space in the parasternal region). The murmur is usually augmented during inspiration and is reduced in intensity and duration in the standing position and during a Valsalva maneuver. A short, early diastolic flow rumble may be present due to increased flow across the tricuspid valve.

Causes

Pure tricuspid regurgitation can be caused by at least 10 conditions.

Rheumatic heart disease

• Tricuspid regurgitation secondary to rheumatic involvement is usually associated with mitral and aortic valve pathology.¹
• The valve develops diffuse fibrous thickening without commisural fusion, fused chordae, or calcific deposits. Occasionally, the chordae may be mildly thickened by fibrous tissue.
• Rheumatic disease is the most common cause of pure tricuspid regurgitation due to deformation of the leaflets.

Endocarditis

• This is an important cause of tricuspid regurgitation. Precipitating factors that can contribute to infection of the valve include alcoholism, intravenous drug use, neoplasms, infected indwelling catheters, extensive burns, and immune deficiency disease.
• The clinical presentation is often that of pneumonia from septic pulmonary emboli rather than CHF. Heart murmurs are frequently absent and blood cultures may be negative. Annular abscesses are not uncommon.

Ebstein anomaly 

• This entity is a congenital malformation of the tricuspid valve characterized by apical displacement of the annular insertion of the septal and posterior leaflets and atrialization of a portion of the ventricular myocardium.
• Prognosis for these patients depends upon the degree of apical displacement of the tricuspid annulus and the severity of the regurgitation.³

Prolapse (floppy, redundant)  

• The incidence of floppy tricuspid valve varies from 0.3-3.2%.
• The lesion appears to be associated with prolapse of the mitral valve and uncommonly occurs in an isolated fashion.
• Histological examination of the floppy tricuspid valve shows alterations on the valve spongiosa. 

Carcinoid  

• Pure tricuspid regurgitation can occur as part of the carcinoid heart syndrome.
• Fibrous white plaques form on the ventricular aspect of the tricuspid valve and endocardium, causing the valve to adhere to the RV wall.
• Proper coaptation of the leaflets does not occur during systole, resulting in tricuspid regurgitation.⁴

Papillary muscle dysfunction 

• Papillary muscle dysfunction may result from necrosis (secondary to myocardial infarction), fibrosis, or infiltrative processes.
• Although dysfunction secondary to myocardial infarction is less common than occurs with the mitral valve, the underlying cause must be determined in order to plan treatment. 

Trauma

• Trauma to the right ventricle may damage the structures of the tricuspid valve, resulting in insufficiency of the structure.⁵
• More commonly it is associated with stab wounds or projectile destruction of the valve. 

Connective-tissue diseases

• Patients with Marfan syndrome or other connective-tissue diseases (eg, osteogenesis imperfecta, Ehlers-Danlos syndrome) may have tricuspid regurgitation.
• Typically, dysfunction of other valves is also observed in the same patient.
• The etiology of the regurgitation can be attributed to a floppy tricuspid valve and a mildly dilated tricuspid valve annulus.

Medications

• Medications that act via serotoninergic pathways may cause valvular lesions similar to those observed with carcinoid.
• Medications used to treat migraine (eg, methysergide), Parkinson disease (eg, pergolide), and obesity (eg, fenfluramine) have been associated with tricuspid regurgitation.

Anatomically normal tricuspid valve

• A common etiology of tricuspid regurgitation is dilatation of the RV cavity.
• The valve structures are normal; however, because of enlargement of the cavity and dilatation of the annulus, proper coaptation of the leaflets is not possible.
• Causes of the dilatation include mitral stenosis, pulmonic stenosis or regurgitation, pulmonary hypertension, dilated cardiomyopathy, and RV failure.

Differential Diagnoses

Other Problems to Be Considered

Marfan syndrome
Inborn errors of collagen formation

Workup

Laboratory Studies

Chemistry findings in patients with tricuspid regurgitation may show abnormal liver function and hyperbilirubinemia secondary to liver congestion.

Imaging Studies

• Chest radiography
  • Marked cardiomegaly is evident.
  • Evidence of elevated right atrial pressure may include distention of the azygous vein and pleural effusions.
  • Ascites with diaphragmatic elevation may be present.
  • Pulmonary arterial and venous hypertension is common.
• Echocardiography
  • The right ventricle is dilated.
  • Paradoxical motion of the ventricular septum is observed and is similar to that found in an atrial septal defect.
  • Extremely useful in determining whether the incompetent nature of the valve is from primary structural abnormalities of the leaflets and chordae or from secondary myocardial dysfunction and dilatation.
  • Prolapse of the tricuspid valve, endocarditis, rheumatic heart disease, or Ebstein anomaly may be evident.
  • Doppler techniques are used to visualize the regurgitant flow. These techniques are useful to directly visualize regurgitant jets, measure the flow velocities of the regurgitant jets, and accurately estimate right ventricular systolic pressure.
  • Color flow Doppler echocardiography is a mainstay for evaluating tricuspid regurgitation. In trivial-to-mild tricuspid regurgitation, the jet is central and narrow. In moderate-to-severe pulmonic regurgitation, the width of the jet increases, as does the penetration of the jet into the right atrium.
  • Using pulsed wave and continuous wave Doppler, right ventricular and pulmonary arterial systolic pressure can be estimated (using continuous wave Doppler) by measuring the peak regurgitant flow velocity across the tricuspid valve, converting it to a pressure gradient (by use of the modified Bernoulli equation), and then adding the gradient to an estimate of the right atrial pressure.^6,7,8

Other Tests

Electrocardiography: Findings are usually nonspecific. Incomplete right bundle-branch block, Q waves in lead V1, and atrial fibrillation are found.

Procedures

Cardiac catheterization: Right atrial pressure and RV end-diastolic pressure are elevated. A rise or no change in right atrial pressure on deep inspiration is characteristic of tricuspid regurgitation. The use of angiography in this setting is controversial.

Treatment

Medical Care

For patients in whom tricuspid regurgitation is secondary to left-sided heart failure, treatment centers on adequate control of fluid overload and failure symptoms (eg, diuretic therapy).

Surgical Care

Surgical intervention is indicated when structural deformity of the valve (eg, Ebstein anomaly) exists, when the valve is destroyed by bacterial endocarditis, or when ventricular dilatation is severe and uncontrolled with medical therapy.

• Tricuspid regurgitation associated with mitral valve disease and pulmonary hypertension
  • Patients with mild tricuspid regurgitation do not require intervention.
  • As pulmonary vascular pressures fall with successful mitral valve therapy, the tricuspid regurgitation tends to disappear.
  • Severe regurgitation has been successfully treated with tricuspid annuloplasty.
• Organic disease of the tricuspid valve: Corrective measures for organic disease of the tricuspid valve usually involve valve replacement. Because of the increased incidence of mechanical prosthetic valve thrombosis in this low-flow position, a bioprosthetic valve is preferable. 
• Tricuspid valve endocarditis
  • Total excision of the tricuspid valve without immediate replacement is recommended. The diseased valvular tissue is excised to eradicate the endocarditis, and antibiotic treatment is continued. Most patients tolerate loss of the tricuspid valve well for years.
  • If right heart failure symptoms persist despite medical management and the infections have been controlled, an artificial valve can be inserted.
• Ebstein anomaly: If this anomaly produces symptomatic tricuspid regurgitation, then tricuspid valve repair or replacement is indicated.^9,10,11,1,12

Medication

The medical therapy used in the treatment of tricuspid regurgitation is directed toward the control of CHF that is causing or contributing to the problem.

Diuretics

Are used to control the fluid overload associated with the process.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to the 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/dose increments until a satisfactory effect is achieved.

Dosing

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; 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

Contraindications

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

Precautions

Pregnancy

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

Precautions

Avoid dehydration and depletion of potassium and other electrolytes

Cardiac glycosides

These drugs (primarily digoxin) are used to control atrial fibrillation and to increase myocardial contractility.

Digoxin (Lanoxin)

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.

Dosing

Adult

0.125-0.375 mg PO qd

Pediatric

Digitalization in infants and children not generally recommended; suggested doses are as follows:
TDD:
Premature infants: 0.02-0.03 mg/kg if tablet; 0.015-0.025 mg/kg if capsule, IV, or IM in divided doses
Full-term infants: 0.025-0.035 mg/kg if tablet; 0.02-0.03 mg/kg if capsule, IV, or IM in divided doses
1-24 months: 0.035-0.06 mg/kg if tablet; 0.03-0.05 mg/kg if capsule IV, or IM in divided doses
2-5 years: 0.03-0.04 mg/kg if tablet; 0.025-0.035 mg/kg if capsule, IV, or IM in divided doses
5-10 years: 0.02-0.035 mg/kg if tablet; 0.015-0.030 mg/kg if capsule, IV, or IM in divided doses
>10 years: 0.01-0.015 mg/kg if tablet; 0.008-0.012 mg/kg if capsule, IV, or IM in divided doses
May accomplish digitalization by giving one half TDD in first dose followed by 2 doses that are one fourth TDD given at 8-12h intervals
Maintenance dose:
Premature infants: 0.005-0.0075 mg/kg if tablet; 0.004-0.006 mg/kg if capsule, IV, or IM divided q12h
Full-term infants: 0.006-0.010 mg/kg if tablet; 0.005-0.008 mg/kg if capsule, IV, or IM divided q12h
1-24 months: 0.010-0.015 mg/kg if tablet; 0.0075-0.012 mg/kg if capsule IV, or IM divided q12h
2-5 years: 0.0075-0.010 mg/kg if tablet; 0.006-0.009 mg/kg if capsule, IV, or IM divided q12h
5-10 years: 0.005-0.010 mg/kg if tablet; 0.004-0.008 mg/kg if capsule, IV, or IM divided q12h
>10 years: 0.0025-0.005 mg/kg if tablet; 0.002-0.003 mg/kg if capsule, IV, or IM qd or divided q12h

Interactions

IV calcium may produce arrhythmias in digitalized patients; 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, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Contraindications

Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome

Precautions

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; 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; adjust dose in renal impairment; highly toxic (overdoses can be fatal)

Angiotensin-converting enzyme (ACE) inhibitors

Are used to provide afterload reduction, thereby decreasing the volume load on the right ventricle.

Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Dosing

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

Not established

Interactions

NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; the hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics

Contraindications

Documented hypersensitivity; renal impairment

Precautions

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF

Anticoagulants

Are used to prevent thrombosis and embolization from the prosthetic valve used in the treatment of tricuspid regurgitation.

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 international normalized ratio (INR) in the range of 2-3.

Dosing

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; adjust dose according to desired INR

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects include oral antibiotics, capecitabine, 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

Contraindications

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

Precautions

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

Follow-up

Further Inpatient Care

Inpatient care of patients with tricuspid regurgitation requires control of the following:

• Heart failure
• Treatment of any infectious process that may have affected the valve
• Control of arrhythmias that may be present (For related information, see Medscape's Cardiac Rhythm Management Resource Center.)

Anticoagulation is generally in order if atrial fibrillation is present or valve replacement has been undertaken. The international normalized ratio (INR) should be maintained between 3.0-4.0 following valve replacement, because of the associated low flow state.

Further Outpatient Care

Patients should be carefully monitored for control of any heart failure. Repeat echocardiography is indicated at 6-month intervals for patients in whom the valve has been removed. Annual echocardiography should be considered in patients whose valve has been replaced.

Inpatient & Outpatient Medications

Digitalis, diuretics (including potassium-sparing agents), ACE inhibitors, and anticoagulants are all indicated in the care of these patients. Antiarrhythmics are added as needed to control atrial fibrillation.

Deterrence/Prevention

Prevention of tricuspid regurgitation from bacterial endocarditis can be undertaken by securing good dental care and avoiding the use of illicit drugs, particularly by the intravenous route.

Complications

Complications of tricuspid regurgitation include cardiac cirrhosis, ascites, thrombus formation, and embolization. Complications of operative intervention can include heart block, arrhythmias, thrombosis of the prosthetic valve, and infection.

Prognosis

Prognosis in these patients is generally good. If the cause of the regurgitation is infection, removal of the valve generally cures the problem, provided that the inciting cause is removed (eg, poor dentition, illicit drug use). For patients with accompanying pulmonary hypertension or cardiac dilatation, the prognosis is directly associated with the prognosis for these problems.

Patient Education

Patients should be instructed to reduce their intake of salt. Elevation of the head of the bed may improve symptoms of shortness of breath. Careful instruction in the use of anticoagulants must be given.

Miscellaneous

Medicolegal Pitfalls

• Failure to accurately diagnose and treat tricuspid regurgitation
• Failure to adequately monitor patients for symptoms of heart failure
• Failure to adequately educate patients about tricuspid regurgitation and its management

References

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Keywords

tricuspid regurgitation, tricuspid valve, leaflets, chordae tendinea, annulus, papillary muscles, adjacent right ventricular muscle, intrinsic abnormality of the valve apparatus, tricuspid insufficiency, Ebstein's anomaly, Ebstein anomaly, tricuspid stenosis, chronic right atrial overload, right-sided congestive heart failure, CHF, hepatic congestion, peripheral edema, ascites, hypoxemia, cyanosis, polycythemia, rheumatic valvular disease, carcinoid, bacterial endocarditis, Marfan syndrome, osteogenesis imperfecta, Ehlers-Danlos syndrome, porcine heterograft, rheumatic heart disease, endocarditis, papillary muscle dysfunction, connective-tissue disease, dilatation of the right ventricular cavity, mitral stenosis, pulmonic stenosis, pulmonary hypertension, dilated cardiomyopathy, right ventricular failure, left-sided heart failure, organic disease of the tricuspid valve, mitral valve disease, pulmonary hypertension, tricuspid valve endocarditis

Contributor Information and Disclosures

Author

Mary C Mancini, MD, PhD, Professor, Department of Surgery, Louisiana State University Health Sciences Center
Mary C Mancini, MD, PhD is a member of the following medical societies: American Heart Association, American Medical Association, American Thoracic Society, Association for Academic Surgery, Association for Surgical Education, International College of Surgeons, International Society for Heart and Lung Transplantation, New York Academy of Sciences, Phi Beta Kappa, and Southern Thoracic Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

Martin Keane, MD, FACC, FAHA, Associate Professor, Cardiovascular Medicine Division, Department of Medicine, University of Pennsylvania School of Medicine
Martin Keane, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Echocardiography, Pennsylvania Medical Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Ronald J Oudiz, MD, Director of Pulmonary Hypertension, Associate Professor, Department of Medicine, Division of Cardiology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA
Ronald J Oudiz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria

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

Richard A Lange, MD, E Cowles Andrus Professor of Cardiology, Professor of Medicine, Johns Hopkins University School of Medicine
Richard A Lange, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Frank Sheridan, MD to the development and writing of this article.

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