Tricuspid regurgitation
- Signs
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- Raised JVP
- Pansystolic murmur over left sternal edge and loudest in inspiration
- Pulsatile hepatomegaly
- Peripheral oedema
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- If mild or moderate, usually no haemodynamic consequences
- Severe TR can cause right sided heart failure, and is often associated with functional MR
- Causes
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- Usually functional ie secondary to dilated RV and/or RA, which itself can be caused by pulmonary hypertension / respiratory disease, dilated cardiomyopathy, RV MI, mitral valve disease.
- Primary TR (9%) – anatomical abnormality of the valve, can be due to IE (in IVDUs), carcinoid, rheumatic heart disease, Ebstein’s anomaly, previous radiotherapy, myxomatous disease, trauma/iatrogenic
- Can be related to implantable devices (lead-induced). Managed differently
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- Investigations
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- ECG may suggest RVH
- Echo – can suggest a cause, impact of the TR, and severity (assess when euvolaemic)
- Severe TR is suggested by effective regurgitant orifice area >40mm², RVol >45mL/beat, RF >50%
- In the setting of severe TR, RV function is often overestimated, and pulmonary pressures and often underestimated
- CMR better at assessing RV size and function (if this is key to decision making)
- Right heart catheter and gated CTCA often done prior to valve interventions
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- Severe TR has a poor prognosis / debilitating symptoms
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- Patients are often on massive doses of diuretics (or have recurrent admissions for offloading) and lots of oedema
- AF, SOB and fatigue are very common
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- Management
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- Depends a bit on aetiology, but diuretics and ACE-I commonly used
- HF and AF treated in usual way
- Medical treatment has little impact on evolution/severity of TR
- If device-related – may need lead extraction
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- Surgery
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- Patients often referred late (hence why TV surgery is often high risk)
- Generally considered if:
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- Primary severe TR with symptoms
- Symptomatic severe secondary TR
- Asymptomatic severe TR with RV dilatation or deterioration
- Moderate or severe TR and the patient also requires left sided valve surgery
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- No role for surgery if severe LV or RV dysfunction or pulmonary hypertension (risks too high)
- Transcatheter repair for TR (Tricuspid TEER)
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- Can repair the tricuspid valve if TR moderate/severe and patient is having MV or AV surgery
- Only done in a few centres
- Improves quality of life, unclear about effect on mortality (none noted yet)
- Not recommended if life expectancy is very limited – can use a scoring system
- Refer if severe TR with lots of symptoms on maximal medical therapy (though not he capacity currently to help everyone)
- Lots of diuresis before the procedure is important
- TOE for planning
- Single anti-platelet afterwards if not anticoagulated
- 2% risk of single leaflet detachment – sudden worsening of TR down the line. May need another corrective procedure
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- Valve replacement is usually reserved for advanced disease with annular dilation and leaflet tethering, or if repair fails
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- Follow up
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- If TR severe or moderate – echo and clinical review every 6 months
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Tricuspid Stenosis
- Rare
- Causes
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- Rheumatic heart disease (often with combined TR)
- Whipple’s disease
- Fabry’s disease
- Carcinoid
- Mediations (fenfluramine or methysergide)
- IE
- Device-associated thrombus
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- Clinical features – presystolic murmur and mid diastolic murmur
- Echo – A mean diastolic transvalvular gradient of >5 mmHg at a normal heart rate indicates severe TS
- Management
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- Medical therapy as bridge to surgery, often with diuretics
- Surgery is advised in severe TS
- Consider repair if young, but valve replacement is often done
- Tissue valves best (metal valves have a high risk of clotting off in the low-pressure system)
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Pulmonary valve lesions
- Both PS and PR can have an ejection systolic murmur
- Pulmonary stenosis
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- Usually congenital, can be part of Fallots
- Occasionally due to rheumatic fever or carcinoid
- Associated with Noonan’s syndrome
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- Pulmonary regurgitation
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- Usually due to pulmonary hypertension
- Can also have Graham Steel murmur (decrescendo early diastolic)
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