valvular heart diseases

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VALVULAR HEART DISEASEs SREELAKSHMI P

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CONTENTS MITRAL STENOSIS MITRAL REGURGITATION AORTIC STENOSIS AORTIC REGURGITATION

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Normal mitral valve ANATOMY -FUNNEL SHAPED MITRAL APPARATUS: ANNULUS LEAFLETS TENDINOUS CORDS PAPILLARY MUSCLES ATRIAL AND VENTRICULAR MYOCARDIUM OBLIQUE LOCATION

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2 leaflets of MV - unequal size, but of identical surface area PML - attached and is part of mural endocardium of LA AML – no true annulus, continuous with the wall of ascending aorta

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2 MV leaflets attached by 120 chordae to the two papillary muscles Each leaflet by means of chordae to both PM

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MITRAL STENOSIS

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AETIOLOGY Rheumatic – most common Heavy calcification – elderly Congenital SLE, Rheumatoid arthritis Drugs - methysergide

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Pathology Pathologic features: Initial attack of RF with carditis – tiny transluscent nodules along the line of closure – Carey Coomb’s murmur. No significant obstruction Decades from the onset of rh. Carditis – significant symptomatic obstruction of MV. Initial valvulitis – abnormal flow pattern across valve leaflets – thickening, fibrosis and calcification of leaflets Selzer and Cohn’s hypothesis Latent period - West : 5-10 yrs, India : 2-3 yrs

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PATHOPHYSIOLOGY

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MV area : 4 - 6 cm2 (4cm2/sq.m.bodysurface area) No pressure gradient even with exercise normally. MS – MVA < 2.5 cm2 HEMODYNAMIC HALLMARK: LEFT ATRIOVENTRICULAR PRESSURE GRADIENT

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Mitral stenosis Pathophysiology Impaired blood flow through mitral valve Increase in LA pressure Passively elevated pulmonary venous Pressure

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Reactive pulmonary HTN (protection from lung congestion) Fixed pulmonary HTN (organic intimal & medial changes) RV pressure overload,RVH,RV failure TR.,RA enlargment

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Mitral Stenosis

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Clinical features Low CO-fatigue,syncope Dyspnoea, orthopnoea, PND – Lt. Heart failure Palpitation – AF Haemoptysis Cough – Pulmonary congestion Chest pain – Pulmonary HTN Thromboembolic complications Oedema, Ascites – Rt. Heart failure HOV

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Mitral stenosis Symptoms Dyspnoea , orthopnoea , PND Stenosis ? obstruction to LV inflow ? LA pressure ? ? pul.venous hypertension ? ? pul. Cap.pressure ? fluid is driven out of the pul.capillaries ? this transudate ?ses the compliance of lungs

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HEMOPTYSIS 1.Pul. apoplexy with rupture of pulmonary bronchial venous connections 2.PND- blood stained sputum 3. Pul. oedema with rupture of alveolar capillaries 4. Winter bronchitis 5. Pul embolism inducing pul.infarction 6.Anticoagulation

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Fever due to Infective endocarditis : relatively uncommon in isolated MS.More frequent if complicated by AR or MR. Syncope: Arrythmia, PAH, Ball valve thrombus Chest pain: PAH, RV infarction,RV ischeamia,Coronary microemolism

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PHYSICAL EXAMINATION FINDINGS General appearance Most patient: No distinguishing feature Mitral facies: Patchy,pinkish,purple appearance of cheek resulting from Dilated vien; seen in severe MS with PHT Advanced MV disease : typically thin,often have acrocyanosis and peripheral edema

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VITALS Pulse : Normal or low volume Irregular if AF Absent in embolism BP : usually normal, low pulse pressure in severeMS JVP : ? with RV failure absent a wave if AF Prominent a wave with PAH, v wave with asso.TR

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Palpation: Tapping apex beat due to tap of S1 Diastolic thrill at apex Left parasternal heave due to RVH Palpable P2 if PAH pulsations of PA in pul. area if PA is dilated

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Mitral Stenosis AUSCULTATION Loud S1 Opening Snap RVS4 in case of pul HTN Diastolic Apical Rumble (murmur) May be associated with: Right Sided Murmurs PR – Graham Steel Murmur TR MR or AS

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Mitral Stenosis: Physical Exam ‘’Low pitch rough rumbling mid diastolic murmur at the apex with presystolic accentuation with bell of steth and the patient in left lateral position with breath holding in expiration’’ S1 S2 OS S1

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A2-P2 A2-OS Widen on inspiration Narrows Narrow on standing Widens site

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A2-S3 A2-OS Low pitched high pitched Only at apex radiate widely Soften on standing Widens No change on inspiration Narrows

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DD of MDM LEFT SIDED RIGHT SIDED SEVERE MR SEVERE TR SEVERE AR SEVERE PR ATRIAL MYXOMA CAREY-COOMB’S MURMUR RYTANDS MURMUR FLOW- MDM : VSD,PDA ASD

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Clinical feature identifying the severity Histoty ---symptomatic patient Examination –Short A2-OS intrvel --Long duration of MDM Feature of PHT,CCF

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CXR - LA ENLARGEMENT PA view LEFT ATRIAL ENLARGEMENT Enlargement of LA appendage (Straightening of left heart border) LA bulges to the right (Double shadow seen through the right side of heart) Elevation of left main bronchus with widening of carinal angle Displace descending thoracic aorta to the left Displace oesophagus to the right Atelectasis of Left lower lobe.

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Lateral View Displaces Left main bronchus posteriorly Localised posterior displacement of barium filled oesophagus at the level of upper posterior heart border.

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Lateral view

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PULMONARY FIELD CHANGES INVERTED MOUSTACHE APPEARANCE OF PROMINENT UPPERLOBE VEINS KERLEY B LINES BATSWING APPEARANCE OF PUL EDEMA PERIPHERAL HYPERTRANSULENCY MILIARY MOTTLING OF BASAL CALCIFICATION IN HEMOSIDEROSIS

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CALCIFICATION OF MITRAL VALVE

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The ECG in mitral stenosis Mild MS –Insensitive AF - common. In sinus rhythm, p mitrale is present: Prolonged m-shaped p wave (duration >0.12 sec in lead II) Marked terminal negative component to the p wave in lead V1 RVH ( Severe MS): Right axis deviation R wave > S wave in lead V1

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Management Medical CMV, BMV Surgical OMV MVR

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Mitral stenosis Medical therapy Avoid occupation requiring sternuous exertion in moderate MS SBE prophylaxis and Pencillin prophylaxis for RHD Salt restriction Diuretics ? blockers Digitalis (in AF) Anticoagulants

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Mitral stenosis Options for mechanical relief Closed mitral commisurotomy Open mitral commisurotomy Mitral valve replacement Mechanical Biological Percutaneous balloon mitral valvuloplasty (PBMV)

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PERCUTANEOUS MITRAL BALOON VALVULOPLASTY CRITERIA: Significant symptoms Isolated MS No subvalvular pathology Mobile non-calcified valve Left atrium free of thrombus

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Catheter is inserted into a vein in leg & up into the heart A baloon in the tip of catheter is inflated – widening of MV

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Closed or open mitral valvotomy if facilities of PMBV are unavailable Antibiotic prophylaxis against IE after PMBV or mitral valvotomy Follow up at 1-2 yr intervals as re-stenosis can occur If vales are not suitable for repair – MV replacement

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MITRAL REGURGITATION

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AETIOLOGY ACUTE Endocarditis Papillary muscle rupture(post MI) Trauma Chordal rupture/leaflet flail(MVP,IE) CHRONIC Myxomatous(MVP) Rheumatic fever Endocarditis (healed) Mitral annular calcification Congenital(cleft AV canal) HOCM with SAM Ischemic (LV remodeling) Dilated cardiomyopathy

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Mitral Regurg – pathophysiology

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Pathophysiology A form of volume overload that affects the left ventricle and the left atrium. A portion of each systolic stroke volume is ejected retrograde into the left atrium. This results in abnormal left atrial expansion with resulting left atrial dilation Left ventricular eccentric hypertrophy develops as new myocardial sarcomeres are added end to end (i.e., in series).

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Total left ventricular volume increases progressively LV dilatation changes the spatial relationship between the papillary muscles and the mitral valve annulus These spatial changes lead to increases in the volume of mitral regurgitant flow. Thus, mitral regurgitation worsens over time as a result of left ventricular remodeling.

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PATHOPHYSIOLOGY CHRONIC MR Less symptoms Compensatory dilatation of left atrium without increase in pressure. Gradually progress to pulmonary congestion.

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ACUTE MR Sudden increase in left atrial pressure, because the left atrium is not dilated to occupy the increased blood volume So very symptomatic

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SYMPTOMS Breathlessness – pulm congestion Fatigue – low cardiac output Palpitation – AF Pedal oedema – right heart failure Chest pain, cough, haemoptysis – pulmonary hypertension

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Physical Examination Pulse Normal in mild MR Hyperkinetic in moderate to severe Small water-hammer [quick raising poorly sustained low amplitude] in severe MR irregularly irregular in AF May absent in embolism

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JVP Usually normal Prominent a wave in PAH Prominent v wave in TR Absent a wave in AF

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Palpation Apex beat:forceful displaced to the left and down Systolic expansion of the enlarged left atrium may result in a late systolic thrust in the parasternal region/ due to PAH Thrill at apex

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AUSCULTATION S1 soft --defective apposition valve cusps Wide splitting of S2 is common--- results from the shortening of left ventricular ejection

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S3 is common LV S4 –Never a feature of rhumatic MR Seen IN acute MR RVS4 --Severe PHT

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The systolic murmur The holosystolic murmur of chronic MR is usually constant in intensity,soft blowing, high-pitched, and loudest at the apex with radiation to the left axilla and left infrascapular area.

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Type of systolic murmur in MR Holosystolic with plateau configuration eg Rhumatic MR S1 S2

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COMPLICATIONS CARDIAC FAILURE INFECTIVE ENDOCARDITIS AF PAH EMBOLISM RECURRENT INFECTIONS

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INVESTIGATIONS X-RAY Enlarged left atrium Enlarged left ventricle Venous congestion Pulmonary oedema ECG left atrial hypertrophy left ventricular hypertrophy

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Echocardiography Dilated LA,LV Structural mitral valve abnormalities Doppler regurgitation Cardiac catheterisation Dilated LA & LV, MR Pulmonary hypertension

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MANAGEMENT MEDICAL Ischemic /nonischemicDCM Diuretics Vasodilators, e.g. ACE inhibitors,Beta blockers Digoxin Anticoagulants if atrial fibrillation is present Antibiotic prophylaxis against infective endocarditis

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ACUTE SEVERE MR Urgent stabilisation and preparation for surgery Diuretics IV vasodilators

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SURGICAL Mitral valve replacement or repair Inserting an annuloplasty ring to overcome annular dilatation

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MITRAL VALVE PROLAPSE

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systolic click-murmur syndrome Barlow's syndrome floppy-valve syndrome billowing mitral leaflet syndrome

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AETIOLOGY MOSTLY NOT KNOWN DEFECTIVE SYNTHESIS OF TYPE 3 COLLAGEN MARFANS,EDS,OSTEOGENESIS IMPERFECTA STRAIGHT BACK SYNDROME

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PATHOLOGY MYXOMATOUS DEGENERATION OF EXCESSIVE MITRAL LEAFLET TISSUE INCREASED CONC. OF GAG

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CLINICAL FEATURES Asymtomatic Palpitation Syncope Chest pain Breathlessness

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AUSCULTATION Mid/late systolic click high-pitched, late systolic crescendo- decrescendo murmur ("whooping" or "honking" ) and is heard best at the apex.

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COMPLICATIONS Mitral regurgitation Sudden death – arrhythmias, AF CCF - MR

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INVESTIGATIONS ECG Normal May show biphasic or inverted T waves in leads II, III, and aVF occasionally supraventricular or ventricular premature beats Echocardiography Catheterisation

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MANAGEMENT IE prophylaxis – if previous IE ß-blockers – for chest pain, palpitation Antiplatelet agents (eg.aspirin) or anticoagulants – for TIA Treat MR if present

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THANK YOU…

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