Tricuspid valve disease Jeff Macemon MBChB PGDMSM RACS Cardiothoracic Trainee Waikato Cardiothoracic Unit

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Functional (Secondary) TR RV dysfunction and Dilatation (Usually as a consequence of Left sided disease in association with PHTN) Tricuspid annulus dilated and fails to shorten during systole (normally 15-20%) Annular Dilatation along Anterior and Posterior leaflets (Septal leaflet portion relatively fixed with the fibrous skeleton between left/right trigones) Diameter Threashold approx. 34mm  Failure of leaflet coaptation Source: Kirklin/Barratt-Boyes Cardiac Surgery (Kouchoukos)

Source: Kirklin/Barratt-Boyes Cardiac Surgery (Kouchoukos)

Primary causes of Tricuspid Disease Rheumatic Stenosis and Regurgitation Endocarditis Traumatic injury Carcinoid Disease

Rheumatic Tricuspid Disease In association with Mitral Rheumatic Disease +/- Aortic Rheumatic Disease Not seen as an isolated lesion Typically results in Regurgitant valve with varying stenosis Rarely pure stenosis In stenosis the annulus is typicaly larger than in Mitral stenosis, owing to the preload pressure difference between left and right sides Diastolic gradient of 4-5mmHg indicates important stenosis

Tricuspid Valve Endocarditis Associated with IVDU Pseudomonas ++ Staph aureus + Rarely Candida

Traumatic Injury of the Tricuspid Valve Blunt, non penetrating, rapid deceleration injuries In association with rupture of papillary muscles or chordae Ususlly Anterior leaflet flail Rarely due to traumatic VSD Perforation, laceration, scarring in relation to: PPM leads Cryo or RFA ablation procedures Repeated RV biopsy in transplant patients

Carcinoid Tricuspid Valve Disease Failure of serotonin inactivation in the liver, eg. From hepatic metastatic disease Carciniod Syndrome Bronchospasm, diarrhoea, nausea, malabsorption, flushing, telangiectasia Tricuspid, Pulmonary valve, and endocardial plaques Mixed TS/TR

Tricuspid Stenosis features Diastolic Gradient >4mmHg Mid-diastolic, often high-pitched murmur LLSE Maximal on inspiration Prominent P wave (ECG)) owing to atrial hypertrophy Elevated a wave of CVP trace Natural history is predominantly determined by Left sided disease

Tricuspid Regurgitation features JVP shows dominant and fused c and v waves Pansystolic, high pitched murmur LLSE, increases on inspiration Severe TR manifests by: Progressive fatigue/weakness, reduced CO Ascities, congestive hepatosplenomegaly Peripheral oedema Source:http://www.phaonlineuniv.org

Severe Tricuspid Regurgitation features Vena contracta often >0.7mm Dilation of IVC with flow reversal in hepatic veins Maximal annular circumference 14+/-0.7cm Cf normal 11.9+/-0.9cm Despite these, as RV function is dynamic, features of TR are best assessed in the OR under ideal haemodynamics

Tricuspid Regurgitation features Severe Functional TR is present in ~30% of patients with Mitral Regurgitation 2/3 of patients returning for Tricuspid surgery only had mild TR at the time of mitral valve surgery The tricuspid annulus does not remodel after left sided surgery Importance of recognising dilatation at initial surgery as this is a predictor of late TR

Important features of Tricuspid Surgery Anatomical considerations AV node Aortic annulus, non coronary cusp Coronary sinus Right Coronary artery Potential for PPM Repair vs replacement Choice of prosthetic device

Annuloplasty technique Plication of the anterior and posterior septal portions Reducing annular circumfrence Effectively “bicuspidising” the valve Band vs ring De Vega annuloplasty