TRICUSPID VALVE DISEASE (TVD) o Dyspnea

o hepatomegaly, ascites, and edema

- Advanced TS and/or TR = fatigue secondary to a low CO and
Tricuspid Stenosis
discomfort due to refractory edema, ascites, and marked
Etiology hepatomegaly.
- Much less prevalent than MS in North America and Western - Uncomfortable fluttering in the neck has been reported in
Europe patients with TV disease
- Generally rheumatic in origin
- More common in women than men Physical Findings:
- Does not occur as isolated lesion; assoc. with MS - Severe TS is assoc. w/ marked hepatic congestion, often
- Rheumatic TS commonly assoc. with tricuspid regurgitation resulting in cirrhosis, jaundice, serious malnutrition,
(TR) anasarca, and ascites
- The jugular veins are distended
- In patients with sinus rhythm
o giant a waves
o v waves are less conspicuous
o tricuspid obstruction impedes RA emptying during
diastole = slow y descent
o prominent presystolic pulsations of the enlarged liver
- Auscultation:
o OS of the tricuspid valve rarely heard ~0.06 s after
pulmonic valve closure.
o The diastolic murmur of TS
 Heard best along the L lower sternal border and over
the xiphoid process
 Most prominent during presystole in patients with
sinus rhythm
 Augmented during inspiration; reduced during
expiration
 particularly reduced during the strain phase of the
Valsalva maneuver, when tricuspid transvalvular
Pathology flow is reduced
- Commissure fusion
- In the case of rheumatic disease, mixed TS and TR may result Laboratory Examination
from fusion and shortening of the chordae tendineae + ECG:
commissure fusion = retraction of the valve leaflets. - RA enlargement
- Dilated RA and thickened in chronic TS - Tall, peaked P waves in lead II
- Chronic obstruction to RV filling often produces signs of - Prominent, upright P waves in lead V1
systemic venous congestion (ie. hepatomegaly and - Absence of RVH if pt has right-sided heart failure suspected
splenomegaly) to have MS should suggest assoc. TVD

Pathophysiology
- A diastolic pressure gradient between the RA AND RV
defines TS.
o Augmented when the transvalvular blood flow inc
during inspiration & declines on expiration
o Mean diastolic pressure gradient of 4 mmHg can elevate
the mean RA pressure = systemic venous congestion;
can cause…
 Hepatomegaly
 Ascites
 Edema
- In patients with sinus rhythm:
o Tall RA a wave
o Prolonged y descent
- CO at rest is usually depressed; fails to rise during exercise
- The low CO is responsible for the normal or slightly elevated
LA, PA & RV systolic pressures despite MS
- Presence of TS can mask the hemodynamic and clinical
features of any associated MS
- Severe TS = valve area <1.0 cm2
CXR:
- Combined TS and MS:
o prominence of the RA and SVC w/o much PA
enlargement
o less evidence of pulmonary vascular congestion than
occurs in patients with isolated MS
o engorgement of the azygos vein
Transthoracic echocardiographic (TTE) examination:
- Tricuspid valve is usually thickened and domes in diastole
- the transvalvular gradient can be estimated by continuous
wave Doppler echocardiography.
o Severe TS = valve area ≤1 cm2 or pressure half-time of
≥190 ms.
- The RA and IVC are enlarged
- Provides additional information regarding the severity of any
associated TR, mitral valve structure and function, LV and
RV size and function, and PA pressure.
Cardiac catheterization is not routinely necessary for assessment
of TS.

Clinical manifestations Treatment

Symptoms: - If w/ systemic venous congestion: salt restriction, bed rest,
- Development of MS generally precedes that of TS; initial sx and diuretic therapy
of pulmonary congestion and fatigue
- Severe TS: Surgical treatment:
- Preferably at the time of surgical mitral valvotomy or MVR
for mitral valve disease
- In patients with moderate or severe TS who have mean
diastolic pressure gradients > ~4 mmHg and tricuspid orifice
areas <1.5–2 cm2.
- May permit substantial improvement of tricuspid valve
function.
- If repair cannot be accomplished= tricuspid valve
replacement
- Mechanical valves in the tricuspid position are more prone to
thromboembolic complications
- PTBV for isolated severe TS without significant TR is very
rarely performed.
Tricuspid Regurgitation
Etiology
- > 80% of TR cases are 2ry (functional) in nature
- R/t tricuspid annular dilatation and leaflet tethering in the
setting of RV remodeling caused by pressure
and/or volume overload, myocardial infarction (MI) or
trauma
- Secondary TR:
o seen in the late stages of heart failure
o due to rheumatic or congenital heart disease with severe
PA HTN (PA systolic pressure >55 mmHg)
o can be caused by other types of left-sided valvular (e.g.,
mitral regurgitation) or myocardial diseases (e.g.,
cardiomyopathies).
o It is reversible in part if PA HTN can be relieved.
o Can also develop from chronic RV apical pacing and
dyssynchronous contraction; in some patients, the RV
leads may also perforate or entrap the TV leaflets.
- TR can often emerge in the setting of new onset
a-fib (AF) esp in elderly patients.
- Rheumatic fever may produce primary TR, often associated
with TS.
- Less commonly, primary TR results from congenitally
deformed tricuspid valves, and can occur with defects of the
AV canal, as well as with Ebstein’s malformation of the
tricuspid valve
Pathology
- Dilation and deformation of the tricuspid annulus
- Valve leaflets appear stretched but pliable and normal in
appearance.
- If TR is caused by carcinoid syndrome: white fibrous
carcinoid plaques are found on the ventricular surfaces of the
TV >> cusps to adhere to the underlying RV wall >> stents
the valve open
Pathophysiology
- Incompetent tricuspid valve allows blood to flow backward
from the RV into the RA
- The volume of back flow is dependent on the:
o driving pressure (i.e., RV systolic pressure)
o size of the regurgitant orifice
- RV filling is increased during inspiration.
- Forward CO is reduced and does not augment with exercise.
- RA enlargement and elevation of the RA and JVP with
prominent c-v waves in the pulse tracings.
- Progressively severe TR can lead to “ventricularization” of
the RA wave form
- Severe TR:
o RV dilation (RV volume overload)
o Eventual systolic dysfunction; progression can be
accelerated by:
 concomitant pressure load from PA HTN
 myocardial fibrosis from previous injury
Clinical manifestation
Symptoms:
- Mild or moderate degrees of TR are usually well tolerated in
the absence of other hemodynamic disturbances.
- LV dysfunction (TR coexist w/ left-sided valve lesions)
and/or PA HTN sx
- Fatigue and exertional dyspnea due to reduced forward CO
are early sx of isolated, severe TR.
- As the disease progresses:
o RV function declines
o cervical pulsations
o abdominal fullness/bloating
o diminished appetite
o muscle wasting, although with progressive weight gain
o painful swelling of the lower extremities
Physical findings
- Severe TR:
o Distended neck veins
o Prominent c-v waves and rapid y descents (in the absence
of TS).
- May include marked hepatomegaly with systolic pulsations,
ascites, pleural effusions, edema, and a positive hepatojugular
reflux sign.
- Characteristic findings:
o Prominent RV pulsation along the left parasternal region
o blowing holosystolic murmur along the lower L sternal
margin, w/c may be intensified during inspiration
(Carvallo’s sign); reduced during expiration/strain phase
of Valsalva maneuver
- Murmur of TR may sometimes be confused with that of MR
unless attention is paid to its variation during the respiratory
cycle and extent of RV enlargement
- AF is usually present in the chronic phase
Laboratory examination
ECG:
- Inferior Q-wave MI suggestive of a prior RV MI, RVH, or a
bizarre right BBB-type pattern with preexcitation in patients
with Ebstein’s anomaly.
- Enlargement may be present in patients with sinus rhythm;
AF is frequently noted.
CXR:
- RA and RV enlargement, depending on the chronicity and
severity of TR
TTE:
- definitive with demonstration of RA dilation and RV volume
overload
- shows prolapsing, flail, scarred or displaced/tethered
tricuspid leaflets with annular dilatation
- Dx & assessment of TR = color flow Doppler imaging
- Severe TR is accompanied by hepatic vein systolic flow
reversal.
- Continuous wave Doppler of the TR velocity profile is useful
in estimating PA systolic pressure, except when the TR is
very severe and the jet velocity is blunted by rapidly
increasing RA pressure.
- In patients with severe TR:
o CO is usually markedly reduced
 o RA pressure pulse may not exhibit an x descent during
early systole
o RA pressre pulse may show a prominent c-v wave with a
rapid y descent.
- Elevated mean RA and RV end-diastolic pressures

Exercise testing can be used to assess functional capacity in

patients with asymptomatic severe TR.
Resources:
Harrisons
Schwartz