This document discusses the anatomy, assessment, and management of tricuspid valve disease. It covers tricuspid stenosis and tricuspid regurgitation. For tricuspid stenosis, the most common causes are rheumatic fever and infective endocarditis. Symptoms include fatigue and swelling. Transthoracic echocardiogram is used to assess the mean gradient and valve morphology. For tricuspid regurgitation, the most common primary causes are rheumatic fever and carcinoid heart disease. Secondary causes are related to right ventricular dilation. Symptoms are similar to stenosis. Echocardiogram can assess the severity of regurgitation and pulmonary pressures. Management involves medical therapy depending on severity of disease.

1. By
Waseem Omar
A. Lecturer of cardiology

2. Agenda:
 Anatomy.
 How to assess???
 Tricuspid stenosis.
 Tricuspid regurgitation.
 Recommendation for management.

3. Anatomy

6. The tricuspid valve has been
described as having as few as
2 and as many as 6 leaflets

7. How to assess??
Transthoracic echo is the
modality of choice for
assessment of tricuspid
valve.

12. Tricuspid stenosis
 Almost rheumatic in origin and is generally accompanied
by mitral and aortic valve involvement.
 Most stenotic tricuspid valves are associated with clinical
evidence of regurgitation.
 Isolated TS less than 1% of general population.

13. causes
 Rheumatic : diffuse thickening of the leaflets with or
without fusion of the commissures. The chordae tendineae
may be thickened and shortened, left sided valves almost
affected.
 Congenital.
 Infective endocarditis: Large infected vegetations
obstructing the orifice of the tricuspid valve may produce
stenosis, in IV drug abuser.

14.  Carcinoid heart disease: in patients with GIT carcinoid
tumor secret vasoactive substance, manifest as fibrous
white plaques located on the valvular and mural
endocardium. The valve leaflets are thickened, rigid, and
reduced in area, affect right sided valves and spared left
sided valves.

15. symptoms
 Fatigue.
 Fluttering discomfort in neck.
 Right upper quadrant pain.
 Abdominal enlargement.
 Lower limb swelling.

16. signs
 Increases the jugular venous pulse and prominent A wave.
 Peripheral edema and ascites.
 The first heart sound may be split widely. The second
heart sound may be single.
 Diastolic rumbling murmur along the left sternal border
increases with inspiration.

17. ECG: P pulmpnale

18. Transthoracic echo
 Confirm diagnosis: mean gradient > 5 mmHg using
continous Doppler.
 Define leaflets morphology.
 Define coexisting valvular disease.

23. Tricuspid regurgitation
 Tricuspid regurgitation may result from structural
alterations of any or all of the components of the tricuspid
valve apparatus.
 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 right ventricular (RV)
dilatation.

24. Primary TR:
 Rhumatic: most common cause.
 Carcinoid heart.
 Endocarditis.
 Tricuspid valve prolapse (floppy tricuspid valve) varies
from 0.3-3.2%. The lesion appears to be associated with
prolapse of the mitral valve.

26.  Congenital: AV canal defect, TV cleft, VSD,
 And Ebstein anomaly: 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

28.  Papillary muscle dysfunction.
 Trauma to the RV.
 Connective-tissue diseases: dysfunction of other heart
valves is typically present.
 Medications that act via serotoninergic pathways may
cause valvular lesions, as medications used to treat
migraine, Parkinson disease, and obesity (eg,
fenfluramine)

29. Clinical Presentation
 In the absence of pulmonary hypertension, TR generally is
well tolerated.
 However, when pulmonary hypertension and TR coexist,
cardiac output declines and the manifestations of right-
sided heart failure become intensified.

30. Symptoms
 Fatigue.
 Throbbing pulsation in neck.
 Right upper quadrant pain.
 Abdominal enlargement.
 Lower limb swelling.

31. signs
 Evidence of weight loss, cachexia, cyanosis, and jaundice
often are present on inspection in patients with severe TR.
 AF is common.
 Jugular venous distention: absent x descents , prominent
systolic c-v wave , deep y descent.
 Pulsating enlarged tender liver.
 Ascites, periphral edema are frequent.

32. Auscultation:
 Systolic murmur over lower left sternal border increased
with inspiration.
 murmur usually is high-pitched, pansystolic, and loudest
with PHT, and usually of low intensity and limited to the
first half of systole in primary TR.
 S3.
 Accentuated P2.

33. Echocardiography in TR
 Detect TR.
 Estimate its severity.
 Assess pulmonary arterial pressure.
 Assess RV size and function.
 Assess associated left side heart disease.

34. Assessment of severity
1.jet area

35. 2.Vena contracta

36. 3.Hepatic vein Doppler

37. PA systolic pressure

38. RA pressure

39. RA pressure

40. RV size

41. RV function

47. Management

48. Medical management

50. Thanks