Patterns, pearls and practical medicine

Right sided valve disease

Tricuspid regurgitation

  • Signs
      • Raised JVP
      • Pansystolic murmur over left sternal edge and loudest in inspiration
      • Pulsatile hepatomegaly
      • Peripheral oedema
  • If mild or moderate, usually no haemodynamic consequences
  • Severe TR can cause right sided heart failure, and is often associated with functional MR
  • Causes
      • 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
  • Investigations
      • 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
  • Severe TR has a poor prognosis / debilitating symptoms
      • 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
  • Management
      • 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
  • Surgery
      • Patients often referred late (hence why TV surgery is often high risk)
      • Generally considered if:
          • 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
      • No role for surgery if severe LV or RV dysfunction or pulmonary hypertension (risks too high)
      • Transcatheter repair for TR (Tricuspid TEER)
          • 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
      • Valve replacement is usually reserved for advanced disease with annular dilation and leaflet tethering, or if repair fails
  • Follow up
      • If TR severe or moderate – echo and clinical review every 6 months

Tricuspid Stenosis

  • Rare
  • Causes
      • Rheumatic heart disease (often with combined TR)
      • Whipple’s disease
      • Fabry’s disease
      • Carcinoid
      • Mediations (fenfluramine or methysergide)
      • IE
      • Device-associated thrombus
  • 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
      • 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)

Pulmonary valve lesions

  • Both PS and PR can have an ejection systolic murmur
  • Pulmonary stenosis
      • Usually congenital, can be part of Fallots
      • Occasionally due to rheumatic fever or carcinoid
      • Associated with Noonan’s syndrome
  • Pulmonary regurgitation
      • Usually due to pulmonary hypertension
      • Can also have Graham Steel murmur (decrescendo early diastolic)

 

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