Tricuspid insufficiency I07.1

Tricuspid valve insufficiency (TI) is the inability to close the tricuspid valve located between the right atrium and right ventricle. The incompletely closing valve leads to a systolic reflux from the ventricle into the atrium (Bob 2001). The regurgitation volume flowing from the right ventricle into the right atrium due to the inability to close the tricuspid valve depends on the right ventricular systolic pressure and the size of the valve leak. The severity and symptomatology of TI is dependent:

• - systolic pulmonary pressure (provided there is no stenosis of the right ventricular outflow tract)
• of the diameter of the tricuspid valve annulus
• from the respiration-dependent changes in the right ventricular preload
• from the compliance of the right atrium

Inspiratorily, the filling of the right ventricle increases, while the effective cardiac output is reduced and does not increase under stress (Kasper 2015).

As long as pulmonary hypertension is not present, even severe TI is well tolerated over a long period of time. With the onset of pulmonary hypertension, however, there is a massive deterioration in hemodynamics. Thus, significant changes in the preload or afterload can lead to a severe TI if the TI is mild until then and vice versa (Pinger 2019).

In tricuspid insufficiency, a distinction is made between:

• primary TI (also known as valvular TI)
  • this can be congenital
  • or be acquired
  • In the primary form there are intrinsic changes of the valve itself (in the area of the sails, chordae tendineae and papillary muscle)
• secondary TI (also known as functional or relative TI)
• This form of TI is caused by a "remodeling", usually a consecutive alteration of the annulus and the valve retaining apparatus develops - caused by a dilatation of the right ventricle (Pinger 2019).

TI is often found in combination with mitral valve stenosis. However, it is not as common in Western Europe as mitral valve stenosis.

Women are more frequently affected than men (Kasper 2015).

Primary TI (also called valvular TI): It occurs rarely and when it does, it is usually a combined vitium [Krakow 2005]). Isolated hemodynamically effective tricuspid valve defects account for only about 4 % - 5 % of acquired heart valve defects and are therefore extremely rare (Erdmann 2006).

The secondary (functional or relative): This TI is much more common. Exact figures cannot be obtained (Bob 2001).

The primary or also called valvular TI) can be caused by:

• rheumatic fever (most common cause)
• bacterial endocarditis in e.g. drug addicts, after infection of a pacemaker cable, after application of indwelling catheters etc. (in 2006 Erdmann describes bacterial endocarditis as the most frequent cause in Western Europe) (Kasper 2015)
• congenital (e.g. with Ebstein disease, AV channel defect)
• Rupture of the Chordae tendineae
• iatrogenic (e.g. after radiotherapy, through multiple biopsies of the right ventricle, etc.)
• medically indicated by taking appetite suppressants (Pinger 2019)
• myxomatous
• Carcinoid heart syndrome (Kasper 2015)

Secondary TI (also known as functional or relative TI) can occur:

• as a consequence of right heart failure of various genesis (Bob 2001)
• in mitral valve cases by dilatation of the right ventricle and/or dilatation of the annulus
• after myocardial infarction in the area of the right ventricle
• Left heart diseases such as dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM) (Pinger 2019)
• chronic pacing in the area of the tip of the right ventricle (Kasper 2015)

A light to moderate TI is usually well tolerated. In most cases of TI, however, left-sided valve defects are also present, so that the symptoms of left ventricular dysfunction and/or pulmonary hypertension dominate.

First signs as an expression of a forward failure are:

• rapid physical exhaustion
• Dyspnea, initially especially under stress

As the disease progresses, patients report of:

• cervical pulsations
• reduced appetite with simultaneous weight gain
• painful oedema of the lower extremities
• abdominal fullness
• Muscular atrophy (Kasper 2015)

ECG: The ECG often provides clues to the possible cause of TI:

• z. e.g. Q- wave in the inferior leads as an indication of a posterior wall infarction).
• Sokolow- Lyon index ( RV1 +SV5/6 > 1.05 mV) (Bob 2001)
• high, slender R in V1, right deviation of the cardiac axis
• pre-excitations (can be found in patients with Ebstein anomaly)
• if sinus rhythm is present, evidence of enlarged right atrium may be found (e.g., P- dextroatrial, P in II and III is peak positive with > 0.2 mV and in V1 , V2 the positive portion of the P- spike is peak positive and higher than 0.15 mV)
• Atrial fibrillation (Kasper 2015)
• (in)complete right bundle branch block (Pinger 2019).

Echocardiography: Echocardiography is usually diagnostic.

A systolic pressure in the right ventricle:

• < 40 mmHg indicates primary TI in valve deformity.
• > 55 mmHg indicates secondary TI (Pinger 2019).

Otherwise, echocardiographic imaging can be performed:

On one- and two-dimensional echo:

• Dilatation of the right ventricle

• Dilatation of the right atrium

• the superior and inferior vena cava are dilated (>1 cm/m 2)

• during inspiration the systolic collapse of the inferior vena cava is abolished (Gerok 2007)

In CW- Doppler, systolic PAP can be estimated (Kasper 2015).

In contrast echo:

• when the tricuspid valve is plumbed, a return flow of contrast medium from the right ventricle into the right atrium is detectable

• when injected into the cubital vein, systolic reflux into the inferior vena cava and hepatic veins is found (Gerok 2007)

In Doppler echocardiography:

• Here, diastolic reflux signals can be visualized in the right atrium; the extent depends on the severity of TI (Gerok 2007).

In color Doppler echocardiography:

• there is systolic reflux into the hepatic veins

• as well as reflux into the right atrium (Gerok 2007).

The regurgitation volume detected by color Doppler is often increased in routine examinations. Evidence of mild TI is found in approximately 70% of normal subjects (Pinger 2019). (Kasper 2015). Color Doppler can also be used to determine the severity of TI (Kasper 2015).

Quantification of TI according to EAE 2010 / 2013:

• I. mild TI:
  • Morphology of the valve normal or abnormal.
  • V. contracta (mm) not defined
  • PISA radius (mm)x1 ≤ 5
  • EROA (mm 2) not defined
  • R vol (ml) not defined
  • PW- signal of inflow normal
  • CW- signal of TI weak/ parabolic
  • Hepatic venous flow systolic dominated
• II. moderate TI
  • Valve morphology normal or abnormal
  • V. contracta (mm) < 7
  • PISA radius (mm)x1 6 - 9
  • EROA (mm 2) not defined
  • R Vol (ml) not defined
  • PW- Signal of inflow normal
  • CW- signal of TI dense/ parabolic
  • Hepatic venous flow systolic attenuated
• III. severe TI
  • Morphology of the valve abnormal
  • V. contracta (mm) > 7
  • PISA radius (mm)x1 > 9
  • EROA (mm 2) ≥ 40
  • R vol (ml) ≥ 45
  • PW- signal of inflow E- waves dominated > 1 m/s.
  • CW- signal of TI dense, triangular with early peak (peak < 2m/s possible).
  • Hepatic venous flow systolic flow reversal (Pinger 2019).

A V. contracta > 6.5 mm indicates severe TI with a specificity of 93% (Pinger 2019).

The use of jet area-as described in sometimes in the literature-is not recommended for quantification according to EAE (Pinger 2019).

Another classification is the classification according to Carpentier and Brizard (2006), which is based AN the mobility and morphology of the valve leaflets.

• Type I: There is annulus dilatation or valve perforation with normal leaflet mobility.
• Type II: Excessive mobility of the leaflets due to prolapse.
• Type III: In type III, there is restrictive leaflet mobility resulting from valvulopathy or functional TI (Pinger 2019)

X-ray thorax: The x-ray shows the enlarged right ventricle and the also enlarged right atrium. The posterior-anterior ray path shows a triangular configuration of the heart with protrusion of the enhanced right border of the heart. In the lateral pathway, the outflow tract of the right ventricle bulges into the retrosternal space.

In primary TI, there is also:

• a relative insufficiency of blood flow to the lungs.

In secondary TI, there may be:

• signs of pulmonary hyperemia
• signs of hypertension

The mediastinum is usually widened (by the superior vena cava and the azygos vein). There may be a cranial displacement of the diaphragm (caused by ascites) (Erdmann 2006).

Cardiac MRI: In echocardiography sometimes cannot be accurately determined:

• severity of TI
• pulmoarterial pressure
• size and systolic function of the right ventricle.

If there are problems with this and a 3-D echocardiogram is not available, it is recommended that a cardiac MRI be performed (Kasper 2015).

Right heart catheterization: The following changes may occur with right heart catheterization:

• the mean pressure in the right atrium is elevated (RAP)
• there is an accentuation of the v- wave.

During inspiration these hemodynamic changes are intensified (so-called positive Kußmaul sign [Erdmann 2006])

• the Y-valley is intensified
• in severe TI, the contour of the right atrial pressure curve is very similar to the right ventricular pressure curve, but shows a lower amplitude (so-called ventriculized RA curve)
• Right ventricular end-diastolic pressure (RVEDP) is elevated (Pinger 2019).

Dextrocardiography: Angiographic quantification of a TI using dextrocardiography:

With dextrocardiography, it is possible to angiographically visualize TI as systolic contrast reflux into the right atrium. However, because regurgitation can also be induced by catheter position or by triggering extrasystoles during contrast administration, the diagnostic value of dextrocardiography is often doubted for this reason. Ideally, the shaft of the angiographic catheter should lie exactly in the middle of the ostium of the tricuspid valve, as this can prevent the valve from being artificially held open (Lapp 2014).

According to ACC / AHA 2014, there is a IIa- indication for catheter-based evaluation if only an inadequate assessment was possible by noninvasive diagnostics (Pinger 2019).

Angiographic quantification:

• Grade I: Only minimal regurgitation of the contrast medium into the right atrium is detectable
• Grade II: Only partial contrast of the right atrium is found; however, this remains during diastole
• Grade III: Complete and dense contrast of the entire right atrium.
• Grade IV: At this stage, there is contrast reflux in the hepatic veins and complete and immediate contrast of the right atrium, which additionally increases with each cardiac beat (Pinger 2019)

Inspection and Palpation:

• Pulsations at the left sternal border (due to pulsations of the right ventricle)
• Neck vein pulsations (typical sign in TI; allows conclusions to be drawn about the severity of the stenosis). (Bob 2001)
• Congested jugular veins (are a typical sign of PI)
• Hepatomegaly
• pleural effusions
• positive hepato- jugular reflux (Kasper 2015).

Auscultation. The following murmur phenomena may be present in TI:

• blowing holosystolic m urmur at the left distal edge of the sternum, which intensifies during inspiration and attenuates during expiration or Valsalva attempt: so-called Carvallo sign [Pinger 2019])
• paradoxical splitting of the 2nd heart sound (occurs due to the abnormally shortened expulsion time of the right ventricle; however, it is heard only occasionally)
• a right ventricular 3rd heart sound may be present
• if there is a concomitant relative tricuspid stenosis, a soft mesodiastolic low-frequency murmur can be heard (Bob 2001)
• the pulmonary valve closure sound may be accentuated (Pinger 2019)

Note: The sound of a TI can easily be confused with the auscultation sound of mitral regurgitation. The respiratory changes that are unique to TI may be of assistance in this regard (Kasper 2015).

ECG: The ECG often provides clues to the possible cause of TI:

• z. E.g. Q- jag in the inferior leads as an indication of posterior wall infarction).
• Sokolow- Lyon index ( RV1 +SV5/6 > 1.05 mV) (Bob 2001)
• high, slender R in V1, right deviation of the cardiac axis
• pre-excitations (can be found in patients with Ebstein anomaly)
• if sinus rhythm is present, evidence of enlarged right atrium may be found (e.g., P- dextroatrial, P in II and III is peak positive with > 0.2 mV and in V1 , V2 the positive portion of the P- spike is peak positive and higher than 0.15 mV)
• Atrial fibrillation (Kasper 2015)
• (in)complete right bundle branch block (Pinger 2019)

• Mitral valve regurgitation
• Ventricular septal defect

In both conditions, systolic volume does not increase on inspiration; in addition, the punctum maximum is different (Bob 2001).

• pericarditis constrictiva
• right ventricular dysplasia
• right ventricular infarction
• restrictive cardiomyopathy (Gerok 2007)

Secondary hyperaldosteronism: this occurs frequently; the cause is the pronounced hepatic congestion (Kasper 2015)

Basically, a distinction is made between conservative and surgical treatment:

conservative therapy:

• Diuretics (for signs of right heart failure)
  • Aldosterone antagonists (in secondary hyperaldosteronism; this is caused by the pronounced hepatic congestion
• for secondary TI therapy of the underlying disease

In principle, a valve reconstruction is preferable to implantation of a prosthesis. An annuloplasty with implantation of a ring is the method of choice. Unfortunately, there is uncertainty about the optimal time for the operation.

The indication for tricuspid annuloplasty should be generously set in case of an already planned operation of the mitral valve. It has been shown that the re-operation to correct a severe TI with a previously performed left-sided valve surgery has a significantly higher mortality (approx. 10 % to 25 %) (Pingler 2019).

The indication for surgical tricuspid valve surgery according to ACC / AHA 2014 exists:

• Class I: Patients with severe TI and planned left-sided valve surgery
• Class IIa:
  • Valve repair in patients with mild or moderate TI and planned left valve surgery with dilatation of the tricuspid valve annulus or in patients with right heart failure
  • Valve surgery for primary, severe, symptomatic TI and lack of response to medication
  • Valve repair in patients with moderate functional TI and planned left-sided valve surgery
• Class IIb:
  • Valve surgery for existing pulmonary hypertension
  • Valve surgery for asymptomatic patients or minimally symptomatic patients
  • with existing severe TI and increasing dilatation of the right ventricle and/or dysfunction of the right ventricle
  • Re-surgery for isolated tricuspid valve repair or tricuspid valve replacement in patients with severe functional TI and already performed left-sided valve surgery and postoperative persistent symptoms without concomitant severe pulmonary hypertension or dysfunction of the right ventricle (Pinger 2019)

Relative contraindications for surgical therapy include severe pulmonary hypertension or dysfunction of the right ventricle (Pinger 2019).

Basically, it can be said that in valve insufficiency, the resulting volume load, which leads to eccentric hypertrophy, has a more favourable prognosis compared to a pressure load with concentric hypertrophy (Herold 2018). In the case of a TI, however, the prognosis is unfavourable in the severe form of insufficiency.

The 1-year survival rate is

• in case of a mild TI 90 %.
• for a medium TI 79 %
• for heavy TI 64 % (Pinger 2019)

Isolated insufficiencies of the tricuspid valve are rarely found. The prognosis is usually good. Mostly, however, TI is combined with other Vitien, which rather has a negative influence on the prediction (Bob 2001).

The worst prognosis is found when liver congestion with consecutive loss of function, portal hypertension and ascites occurs (Erdmann 2006). In the majority of cases, however, TI is the secondary form. The course of the disease is largely determined by the disease underlying the insufficiency (Erdmann 2006).

The TI is probably the most frequently underestimated vitium. The prognosis of patients with severe TI is serious. About 35% of them die within the next 12 months. The operative risk for patients with severe TI is also high, it is about 20 % (Kasper 2015).

After survival of the perioperative phase the 1-year survival rate is 93 % (Pinger 2019).

The 10 year survival rate is about 37 % - with no difference between biological and mechanical valve replacement (Günther 2008) -, the 15 year survival rate is about 30 % (Zafer 2007). A functional improvement was shown postoperatively in 61 % of patients. However, this demonstrable improvement did not result in an improved survival prognosis (Pinger 2019).

The need for re-operation is minimal. It has been shown that there is no significant difference between valve reconstruction and implantation of a prosthetic valve (Günther 2008).

Patients with valve reconstruction or prosthetic heart valve have a significantly increased risk of endocarditis. The post-procedural bacteremia frequency after tooth extractions in gingivitis is up to 90%. For this reason, postoperative endocarditis prophylaxis is necessary for certain procedures. The standard therapy is administered as a single dose approx. 30-60 minutes before the procedure, e.g. amoxicillin or ampicillin 2 g orally or i.v., or in the case of penicillin allergy clindamycin 600 mg also orally or i.v. (Pinger 2019). For further details see Endocarditis prophylaxis

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