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Management of Pulmonary Regurgitation Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery.

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Presentation on theme: "Management of Pulmonary Regurgitation Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery."— Presentation transcript:

1 Management of Pulmonary Regurgitation Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery

2 Pulmonary Infundibulum  Roles of interrelation The pulmonary infundibulum might not be limited to its systolic function. The fact that it remains contracted until late in diastole is probably essential to pulmonary valve competence Pulmonary valve has the peculiarity of being inserted inside the inner shell of an exclusively muscular cylinder. Contraction of this cylinder inevitably approximates the pulmonary cusps to each other and increases their coaptation length The pulmonary pressure that the pulmonary valve could withstand without leaking was greater when the pulmonary infundibulum was stimulated by adrenergic stimulation.

3 Pulmonary Infundibulum  Functional roles The outlet portion of the right ventricle had not only a passive role in right ventricular contraction, and the peristaltic mode may be crucial to achieving a complete emptying of the right ventricular cavity. The delayed opening of the pulmonary valve might be more suitably explained by the peristaltic mode of function of the right ventricle than by its intrinsic power The pulmonary infundibulum ejecting the blood that it had accumulated at a time when the rest of the right ventricle was already relaxing.

4 Interaction of Ventricles  RV-LV-cross talk- While the deeper layer of myocardial fibers are separated, there are shared superficial fibers that encircle the normal LV and RV. Furthermore, in some forms of CHD, such as TOF, the deeper layers of RV and LV may be contiguous within the interventricular septum. The function of the two ventricles is therefore linked, in both the structurally normal and abnormal heart.

5 Risk Factors for Late Death  Causes after TOF repair Residual VSD Residual RV outflow stenosis Severe PR Severe TR Older age at repair Previous Potts, or Waterston shunt

6 Causes of Sudden Death  Approaches after TOF repair Bradyarrhythmias such as complete AV block, bifascicular block, SSS VT and residual RVOTO and RV dysfunction Complex ventricular arrhythmias by Holter monitoring Monomorphic VT and severe PR, peripheral PS, RV dilation, QRS duration more than 180ms

7 Arrhythmia & Sudden Death  Approaches after TOF repair QRS Easy to measure Reflects RV size Dynamic nature, QRS change important New QRS cutoff values for contemporary cohorts QT dispersion Refines risk stratification Less dynamic May reflect initial ventriculotomy scar/ VSD closure

8 Right Ventricular Dilatation  Predictive factors Degree of pulmonary insufficiency Duration of pulmonary insufficiency Identification of akinetic or dyskinetic area in right ventricular outflow tract Right ventricular outflow tract damage

9  Indications of PVR 1. Free pulmonary regurgitation with progressive or moderate right ventricular dilation 2. Sustained arrhythmias & or symptoms 3. Important tricuspid regurgitation 4. Symptoms of deteriorating exercise performance Pulmonary Regurgitation

10 Pulmonary Valve Replacement  Indications 1. Impaired pulmonary artery runoff (Mayo) 1) Peripheral stenosis 2) Vascular obstructive diseases 3) Single pulmonary artery 4) Absent valve with aneurysm of central PA 2. Functional impairment (Ilbawi) 1) Progressive cardiomegaly & TR 2) Evidence of RV dilation or dysfunction

11 Pulmonary Valve Replacement  Indication after TOF repair History of VT( especially sustained), syncope RV hypertension(>60mmHg) Longer QRS(>180ms) or increased QRS Increased CTR Increased RV volume, low RVEF (RV dysfunction) Free PR with or without peripheral PS, More than moderate TR Decreased exercise tolerance EPS inducible sustained VT New onset atrial fibrillation or flutter

12 Subannular PVR  After TOF Repair A; mattress suture securing the anterior SPV commissural posts to RVOT B; sutures spacing posterior posts at 120 distance C; continuous proximal suture with anterior patch

13 RVOT Reconstruction Medtronic freestyle valve before and after excising the coronary remnants Generous excision of graft surrounding coronary to be oriented anteriorly. Note that both the RVOT and neopulmonary artery have been enlarged with a PTFE patch.

14 PVR (CE Perimount Valve) (F/19y, PR, s/p TOF total correction)

15 Pulmonary Valved Conduit Shelhigh Valved Conduit

16 Pulmonary Valve Replacement  Percutaneous replacement Surgical pulmonary valve replacement is associated with low morbitity and mortality; however, reoperations during mid- and long-term follow-up are very common. The risk of extracorporeal circulation, infection, and also special reoperation risks remain Percutaneous pulmonary valve implantation is emerging as an alternative or additional option for a successful surgical scheme, recently even being introduced into clinical practice.

17 Monocuspid Valve Insertion  Residual or recurrent PR 1. Long distance to be covered during rapid closure, or irregular movement 2. Being tailored too wide 3. Loss of movement due to degeneration or calcification

18 Pulmonary Monocuspid Valve 1. Materials 1) Autogenic tissue 2) Autologous pericardium 3) Xenograft 4) Prosthetic membrane (Gore-Tex membrane) 2. Indications 1) Elevated PAP 2) Presence of multiple pulmonary stenosis 3. Technique 1) 30% longer than the width of the outflow tract patch 2) Cover the upper round margin of the RVOT sufficiently 4. Expectation 1) Prevent PR especially immediate postoperatively 2) Potentially improve hemodynamic function

19 Preparation of Valved Stents Self-expanding stents are assumed to improve preservation of the valve in its folded condition in the application device and the valve’s long-term functioning

20 Glutaraldehyde Stabilization 1. Benefits 1) Satisfactory hemodynamics 2) Low thrombogenecity 3) Reduced antigenecity 2. Disadvantages 1) Leaflet calcifications 2) Cytotoxicity caused by unreacted glutaraldehyde reagent 3) Alteration of the natural biochemical properties of the valve


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