eMedicine Specialties > Cardiology > Valvular Heart Disease

Tricuspid Stenosis: Treatment & Medication

Author: Mary C Mancini, MD, PhD, Professor, Department of Surgery, Louisiana State University Health Sciences Center
Contributor Information and Disclosures

Updated: Jul 29, 2008

Treatment

Medical Care

In the treatment of tricuspid stenosis, medical care consists of assessment and treatment of the underlying cause of the valvular pathology.

  • Treat bacterial endocarditis with the appropriate antibiotics as determined by the sensitivity of the organisms cultured.
  • Medically address cardiac arrhythmias depending on their characterization.
  • Decreasing right atrial volume overload with diuresis and salt restriction helps decrease symptoms and improve hepatic function.

Surgical Care

Tricuspid stenosis remains a surgical disease and requires either commissurotomy or replacement of the valve if right heart failure or low cardiac output has resulted. Surgery is rarely performed solely on the tricuspid valve; it is usually performed in combination with mitral and/or aortic valve disease repair. (6)

  • With tricuspid valve replacement, the risk of thrombosis is significant and many surgeons advise warfarin therapy for either mechanical or bioprosthetic valve placement.
  • Percutaneous balloon valvuloplasty has been used successfully, as long as concomitant regurgitation is not significant.
  • The therapy chosen depends on the structure of the valve and the degree of deformity encountered.
  • When possible, excise intracavitary pathology, whether it be tumors or other structural abnormalities.
  • Redundant portions of the dilated right atrium can be excised during the same procedure for restoring the atrium back to normal size.

Consultations

  • Consultation with infectious disease specialists may be appropriate if the stenosis is secondary to an infectious process.
  • An endocrinologist may be of assistance if carcinoid syndrome or an inborn error of metabolism is the cause of the pathology.

Diet

  • No specific dietary restrictions are necessary before therapy.
  • Fluid and sodium restriction is prudent if signs of venous congestion are present.
  • If a valve replacement is undertaken and the patient must be anticoagulated, dietary instructions must be provided regarding those foods that interfere with anticoagulation and are rich in vitamin K.

Activity

  • Activity is usually self-limited by the patient because of easy fatigability secondary to oxygen deprivation.
  • Once the pathology has been corrected, no activity restrictions are necessary.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antiarrhythmic agents

Alter the electrophysiologic mechanisms responsible for arrhythmia.


Digoxin (Lanoxin)

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

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

Medications that may increase 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 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

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 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

Anticoagulants

Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.


Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Tailor dose to maintain an INR in the range of 2-3.

Adult

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

Pediatric

0.05-0.34 mg/kg/d PO; 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, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects include oral 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

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

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

More on Tricuspid Stenosis

Overview: Tricuspid Stenosis
Differential Diagnoses & Workup: Tricuspid Stenosis
Treatment & Medication: Tricuspid Stenosis
Follow-up: Tricuspid Stenosis
Multimedia: Tricuspid Stenosis
References

References

  1. Lev M, Liberthson RR, Joseph RH, Seten CE, Eckner FA, Kunske RD, et al. The pathologic anatomy of Ebstein's disease. Arch Pathol. Oct 1970;90(4):334-43. [Medline].

  2. Waller BF. Morphological aspects of valvular heart disease: Part I. Curr Probl Cardiol. Oct 1984;9(7):1-66. [Medline].

  3. Waller BF. Morphological aspects of valvular heart disease: Part II. Curr Probl Cardiol. Nov 1984;9(8):1-74. [Medline].

  4. Acikel M, Erol MK, Yekeler I, Ozyazicioglu A. A case of free-floating ball thrombus in right atrium with tricuspid stenosis. Int J Cardiol. Apr 2004;94(2-3):329-30. [Medline].

  5. Faletra F, La Marchesina U, Bragato R, De Chiara F. Three dimensional transthoracic echocardiography images of tricuspid stenosis. Heart. Apr 2005;91(4):499. [Medline].

  6. Arnett EN, Roberts WC. Pathology of active infective endocarditis: a necropsy analysis of 192 patients. Thorac Cardiovasc Surg. Dec 1982;30(6):327-35. [Medline].

  7. Block PC, Bonhoeffer P. Percutaneous approaches to valvular heart disease. Curr Cardiol Rep. Mar 2005;7(2):108-13. [Medline].

  8. DiSesa VJ, Mills RM Jr, Collins JJ Jr. Surgical management of carcinoid heart disease. Chest. Nov 1985;88(5):789-91. [Medline].

  9. Kratz JM, Crawford FA Jr, Stroud MR, et al. Trends and results in tricuspid valve surgery. Chest. Dec 1985;88(6):837-40. [Medline].

  10. Miller BR, Vohr FH, Christian FV, Singh AK. Cardiac valvular replacement in carcinoid heart disease. Am J Med. Nov 1983;75(5):896-8. [Medline].

  11. Morgan JR, Forker AD, Coates JR, Myers WS. Isolated tricuspid stenosis. Circulation. Oct 1971;44(4):729-32. [Medline].

  12. Mukhopadhyay S, Suryavanshi S, Yusuf J, et al. Isolated thrombus producing tricuspid stenosis: an unusual presentation in primary antiphospholipid syndrome. Indian Heart J. Jan-Feb 2004;56(1):61-3. [Medline].

  13. Sakata Y, Koibuchi N, Xiang F, et al. The spectrum of cardiovascular anomalies in CHF1/Hey2 deficient mice reveals roles in endocardial cushion, myocardial and vascular maturation. J Mol Cell Cardiol. Oct 18 2005;[Medline].

  14. Sharieff S, Saghir T, Shah-e-Zaman K, et al. Concurrent percutaneous valvuloplasty of mitral and tricuspid valve stenoses. J Invasive Cardiol. Jun 2005;17(6):340-2. [Medline].

Further Reading

Keywords

tricuspid stenosis, tricuspid valve, rheumatic heart disease, mitral stenosis, carcinoid, Ebstein anomaly, tricuspid valve dysfunction, myocardium aberrations, stenotic tricuspid valves, rheumatic fever, carcinoid syndrome, endocarditis, endomyocardial fibrosis, lupus, congenital tricuspid atresia, rheumatic fever, congenital tricuspid stenosis, atrial fibrillation, peripheral edema, ascites, congenital abnormalities, metabolic abnormalities, enzymatic abnormalities, active infective endocarditis, rheumatic tricuspid stenosis, carcinoid heart disease, infective endocarditis, Fabry disease, giant blood cysts, supravalvular obstruction from congenital diaphragms, intracardiac tumor, extracardiac tumor, thrombosis, emboli, large endocarditis vegetations

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

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.

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.

 
 
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