Valvular Heart Disease

Transcription

1 GP Update Refresher 18 th January 2018 Valvular Heart Disease Dr. Alexander Lyon Senior Lecturer and Consultant Cardiologist Clinical Lead in Cardio-Oncology Royal Brompton Hospital, London UK President of British Cardio-Oncology Society Heart Failure Association of the ESC Board Member Chair of HFA Cardio-Oncology Study Group of ESC Cardiology advisor to Macmillan Cancer

2 Overview General Principles Aortic Stenosis Mitral Stenosis Mitral Regurgitation New Advances

3 Valvular Function Stenosis or Regurgitation Aortic, Mitral, Pulmonary and Tricuspid valves Mild, Moderate, Severe Moderate or Severe Probably relevant to clinical symptoms Consider formal Cardiology opinion Trivial and Mild very common

4

5 General Principles

6 General Principles Regurgitant valves Aortic regurgitation (AR) and Mitral regurgitation (MR) Volume load on left ventricular LV dilatation Supranormal LVEF Vasodilators e.g. ACE inhibitors may be helpful Symptoms not reliable guide If LVESD starts enlarging LV failure?valve leaflet vs annular cause

7 General Principles Stenotic valves Aortic stenosis and Mitral stenosis (AS and MS) Fixed limitation of flow Pressure load Left ventricle (AS) Left atrium and pulmonary circulation (MS) Limit cardiac output Avoid vasodilators Need replacement if symptomatic If LV impairment AS gradient underestimated

8 Endocarditis Prophylaxis High risk cases merit antibiotics Prosthetic heart valves Previous endocarditis Cyanotic congenital heart disease Congenital heart disease repaired with prosthetic material Amoxycillin 2g or Clindamycin 600mg po minutes before dental procedure

9 Choice of prosthetic valves Mechanical vs Biological

10 Target INR for mechanical valves Risk factors: Mitral or tricuspid position Previous PE or DVT Previous valve-related thrombosis Atrial Fibrillation LVEF <35%

11 Aortic Stenosis Aetiology CONGENITAL Bicuspid Aortic Valve Presents with symptoms at a spectrum of ages Depending upon severity Peak is in the 4 th decade Male : female ratio 3:1 Coarctation in 6% cases ACQUIRED Rheumatic heart disease Valves can be both stenotic and regurgitant NB Mitral Valve is always also involved Senile degenerative calcification Most common cause in age group more than 65 Increasing prevalance

12 Aortic Stenosis Pathophysiology Increased afterload due to left ventricular outflow tract obstruction Progressive left ventricular hypertrophy to maintain the LV output Establishment of a large pressure gradient between the LV and the Aorta This can be present for many years without a reduction in cardiac output or the onset of symptoms Reduction in systemic and coronary blood flow

13 Aortic Stenosis (AS) Calcified leaflets, tricuspid or bicuspid Peak gradient severe >64mmHg Mean gradient severe >40mmHg Causes severe LV hypertrophy with EF>50% If low LVEF then caution needs specialist review

14 Aortic Stenosis Natural History Truly asymptomatic patients have an excellent prognosis regarding survival with an expected death rate of less than 1% per year Symptomatic patients with severe AS treated medically, the mortality rate from symptom onset is high: 25% in 1 year 50% in 2 years Valve area may decline by cm 2 / year Pressure gradient may rise by 10 15mmHg/year AS progresses more rapidly in patients with Degenerative calcification than in those with Congenital or Rheumatic heart disease.

15 Aortic Stenosis Time interval from onset of symptoms to death

16 Aortic Stenosis AUSCULTATORY FINDINGS Classical diamond shaped crescendo decrescendo murmur best heard in the lower left or upper right parasternal border Harsh and rasping in quality Radiates to the carotids Sometimes it may be heard loudest at the apex, especially in the elderly with calcific AS leading to misinterpretation as MR murmur It is not the intensity of the murmur that corresponds to the severity of AS but the timing of the peak and duration of the murmur.

17 Aortic Valve Replacement Aortic Valve Replacement Transcatheter Aortic Valve Implantation (TAVI) Biological Mechanical Stented Sutureless Conventional Stentless Allograft (Ross) Xenograft

18 TAVI growing as suitable choice for High risk patients with severe AS Mr. Ulrich Rosendahl M.D. F.E.T.C.S Consultant Cardiac Surgeon Royal Brompton Hospital

19 Mechanical vs Biological valves Mechanical Valve Replacement Bioprosthetic Valve Replacement Operative mortality 1.5% 1.5% Death at re-operation (Risk of re-operation x risk of death at re-operation) Valve-related mortality (cumulative for 30 years) Valve-related morbidity (cumulative for 30 years) Total risk of morbidity and mortality over 30 years 2.1% 5.8% (+ 10.8% for second re-operation) 27% 29% 78% 12% 108.6% 48.3% (59.1% if two reoperations)

20 Mitral Valve Structure 3 parts of the Mitral Valve 1. MV Annulus 2. MV Leaflets 3. Subvalvular Apparatus (Chordae and Papillary Muscles)

21 Mitral Stenosis

22 Mitral Stenosis Aetiology Primarily a result of rheumatic fever (~ 99% of surgery show rheumatic damage) Scarring & fusion of valve apparatus Pure or predominant MS occurs in approximately 40% of all patients with rheumatic heart disease Two-thirds of all patients with MS are female Rarer non-rheumatic calcified MS Annular calcification Elderly, renal failure

23 Anatomy in Mitral Stenosis

24 Mitral Stenosis Pathophysiology Right Heart Failure: Hepatic Congestion JVP Tricuspid Regurgitation RA Enlargement Pulmonary HTN Pulmonary Congestion LA Enlargement Atrial Fibrillation LA Thrombi LA Pressure RV Pressure Overload RVH RV Failure LV Filling

25 Fatigue Palpitations Cough SOB Left sided failure Orthopnoea PND Palpitation Right sided failure Hepatic Congestion Oedema Mitral Stenosis Symptoms Atrial fibrillation Systemic embolism Pulmonary infection Haemoptysis Worsened by conditions that require cardiac output. Exertion,fever, anaemia, tachycardia, intercourse, pregnancy, thyrotoxicosis

26 Mitral Stenosis Examination Clinical signs: Mitral facies Elevated JVP In SR- prominent a wave In AF- x descent disappears, and prominent v or c-v wave

27 Mitral Stenosis Examination S1 S2 OS S1 First heart sound (S1) is accentuated and snapping Opening snap (OS) after aortic valve closure Low pitch diastolic rumble at the apex Pre-systolic accentuation (if in sinus rhythm) RV heave and loud P2

28 Mitral Stenosis Natural History Progressive, lifelong disease Usually slow & stable in the early years Progressive acceleration in the later years year latency from rheumatic fever to the onset of symptoms. Additional 10 years before disabling symptoms

29 Mitral Stenosis Prognosis If untreated: 10-year survival is 50-60% Asymptomatic patient: >80% 10-year survival, with 60% of patients have no progression of symptoms. BUT once symptomatic: 0-15% 10-year survival Severe pulmonary hypertension - mean survival <3 years

30 Mitral Stenosis Complications Atrial dysrrhythmias Systemic embolization (10-25%) Risk of embolization is related to, age, presence of atrial fibrillation, previous embolic events Congestive heart failure Pulmonary infarcts (result of severe CHF) Haemoptysis Massive: 2 0 to ruptured bronchial veins (pulm HTN) Streaking/pink froth: pulmonary oedema, or infection Endocarditis Pulmonary infections

31 Mitral Stenosis Treatments Percutaneous Mitral Balloon Valvuloplasty Selected cases only Minimally calcified valves No mitral regurgitation Surgical Mitral commissurotomy Mitral Valve Replacement Mechanical Bioprosthetic

32 Percutaneous Balloon Valvulotomy

33 Percutaneous Balloon Valvulotomy

34 Mitral Regurgitation

35 Mitral regurgitation (MR) Primary or Degenerative Problem originating from the mitral valve Mitral valve prolapse Degenerative Endocarditis Rheumatic Fever Treat the valve Secondary or Functional Problem secondary to ventricular dysfunction Treat the ventricle

36 Mitral Regurgitation Symptoms are NOT a reliable guide!

37 Survival in patients with mitral valve prolapse according to categories of baseline risk factors (RFs). Primary RFs were moderate-to-severe mitral regurgitation (MR) and ejection fraction less than Secondary RFs were mild MR, left atrium larger than 40 mm, flail leaflet, atrial fibrillation, and age older than 50 years.

38 Surgery for Primary Mitral Regurgitation

39 MR secondary to LV Dysfunction Due to annular dilatation and lateral papillary muscle displacement Coaptation point is displaced in the apical direction MR does not deteriorate with Dobutamine stress (unlike valvular MR) Treat ischaemia if present Treat LV dysfunction with appropriate medical therapy and CRT if indicated CRT treats presystolic MR and with reverse remodelling MR may resolve

40 New Advances

41 New percutaneous treatments for Mitral regurgitation Royal Brompton Hospital Transcatheter Mitral programme Sapien III Direct Flow Tendyne Harpoon NeoChord

42 The Tendyne TMVR System Tri-leaflet porcine pericardial valve in an apically tethered, self-expanding nitinol frame D-Shaped Self-Expanding Nitinol Outer Frame Circular Self-Expanding Nitinol Inner Frame Fully retrievable and repositionable Large Valve Size Matrix to Treat Varying Anatomies Valve Tether to Apex Provides Valve Stability - Designed to Reduce PVL Apical Pad Assists in Access Closure

43 Type of Bicuspid Aortic Valve Royal Brompton and Harefield National Foundation Trust

44 Biology of Bicuspid Aortic Valve and Aortopathy Tadros T M et al. Circulation 2009;119:

45 Modern 3D Cardiac Imaging CT and CMR

46 Patterns of aortopathy Normal Marfan Whole Ao. Asc.Ao.An. Ao root + Asc.Ao. Late after TOF repair

47 Hybrid Theatre at Royal Brompton Hospital The hybrid aortic arch repair, with debranching and reimplantation, or bypass of aortic arch vessels and TEVAR with endografting of the aortic arch

48 Personalised aortic root support 3D Designer grafts Personalised External Aortic Root Support PEARS

49 Exostent for selected cases of BAV Age 19 Progressive dilatation of aortic root (47mm) Normally functioning BAV Off-pump procedure

50 Dr. Alexander Lyon Senior Lecturer and Consultant Cardiologist Royal Brompton Hospital, London Tel: Mobile: Fax: Thanks to Mr Ulrich Rosendahl, Prof John Pepper, Mr Neil Moat, Mr Cesare Quarto and Miss Rashmi Yadhav Valve surgeons, Royal Brompton Hospital