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1 Diagnosis of valvular heart disease Without echocardiography is like traveling on a horseback or at best on a steam train 1

2 Echocardiography 2D 2

3 Diagnosis of valvular heart desease Aortic valve disease Aortic stenosis congenital (bicuspid) (50% <70years) rheumatic (commissural fusion) degenerative (calcification) (50% >70 years) creates resistance to ejection the normal orifice=2-3 cm 2, reduction leads to systolic pressure drop "gradient" between the LV and aorta:lv pressure load concentric hypertrophy, compliance 3

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5 Clinical symptoms (AS) Fenyvesi 1.Chest pain,angina pectoris 2.Effort syncope:"graying out" or loss of consciousness. At times a few minutes after the patient stops the exercise. 3.heart failure, eventual depression of contractility,dilatation of LV 4.Sudden death (SCD), arrhythmia 5

6 Physical examination(as) Auscultation diamond shaped ejection murmur ending before S2,P.max in the aortic area transmitted to the carotid, thrill may be palpable may be musical at the apex differenciate from pansystolic:shape and S2 Ejection click : "blah","butter" after the onset of S1 0,03-0,06 s, valvular upward tensing of a mobile cusp, rare after the third decade of life 6

7 S2 soft the "absent A2" is only an illusion,caused by the very loud murmur prolonged LV systole may cause paradox splitting of S2 S4 very common caused by LV hypertrophy S3 only in heart failure Pulse parvus et tardus, a concomitant AR can "normalize" it Blood pressure: narrowed pulse pressure 7

8 Apex impulse :presystolic apical simultaneously with S4 not dysplaced, not hyperkinetic, a prolonged outward thrust in 2/3 of systole Physical signs of AS not reliable for severity-even with chest Rtg and ECG Echocardiography :LV thickness valve area Doppler gradient Catheterization,difficulties,peak-to-peak versus maximal gradient! 8

9 Calculating pressure gradients across stenotic valves 9

10 AS natural course Ross, Braunwald Circ

11 AS Aortic valve area< 1cm 2 11

12 Aortic regurgitation Valve incompetence: diastolic flow of blood from the aorta into the left ventricle Major causes: in the past:rheumatic fever, syphilis (!) recently :connective tissue diseases ankylosing spondylitis rheumatoid arthritis the Marfan-syndrome acute form:bacterial endocarditis Pathology :disease of the aorta or of the valve 12

13 Pathopysiology: volume load, LV dilatation if not accompanied by increase in wall thickness it leads to increased wall stress extreme increase in stoke volume Clinical symptoms: asymptomatic for many years symptoms of LV failure: fatigue, dyspnea,oedema more specific: palpitation, pulsation in the neck, dizziness 13

14 Physical signs in AR i The peripheral circulation Pulse :celer et altus (Corrigan's pulse) Duroziez' murmur :a biphasic bruit over any larger artery Traube sign : booming syst and diast sound capillary pulsation(quincke) uvula pulsation (Müller's sign) Musset's sign :bobbing of the head with each pulsation Hill's sign:an exaggerated difference between popliteal and brachial blood pressure > 60 mmhg 14

15 Blood pressure Extreme widening of the pulse pressure diastolic approaching zero Apex impulse displaced down and to the left, hyperdynamic,a prolonged diastolic filling wave 15

16 Auscultation of AR Murmurs : protodiastolic,high pitched,p.max left sternal border,"safety belt radiation",the patient must stop breathing-sitting leaning foreward systolic ejection murmur --increased stroke volume diastolic rumble :the Austin Flint murmur S1 normal, possible systolic click S3 is a rule in A.R. 16

17 protodiast Compare With AS 17

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21 severe AI 21

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23 Chest X-ray dilatation of the LV, elongation of the apex inferiorly and posteriorly dilatation of the ascending aorta Echocardiography anatomical information on the valve LV chamber dimensions flow-regurgitation Doppler measurement non-invasive haemodynamics Cardiac catheterization invasive haemodynamics coronary arteries 23

24 Calculating pressure gradients across stenotic valves 24

25 Mitral stenosis Resistance to flow through the mitral apparatus during diastolic filling of the left ventricle Major causes : recurrent rheumatic endocarditis congenital calcification(valvular or annulus) thrombus myxoma 25

26 Mitral stenosis Pathology: commissural adhesions and fusion chordal scarring and contraction resulting in a funnel shaped structure the orifice area is reduced from the normal 4-6 cm2 to < 1,5 26

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28 Pathophysiology A pressure gradient is created between the left atrium and LV LA pressure pulmonary veins capillaries PA right heart (disproportionate pulmonary hypertension) RV hypertrophy 28

29 Clinical symptoms: dyspnoe(paroxysmal), fatigue,palpitation(due to atrial fibrillation) systemic or cerebral embolism chronic RV failure, haemoptoe chest pain 29

30 Physical examination(ms) No specific general signs "mitral facies Inspection of the face: For by his face straight shall you know his heart Shakespeare, King Richard III Act III, scene IV-53 Palpation Apex impulse:usually normal,rv hypertrophy may cause sustained parasternal lift in systole 30

31 Physical examination(ms) Auscultation: one of the most fascinating sound-murmur combinations 1.Accentuation of S1: the M1 is late (Q-S1) because of increased LA pressure The sudden halting of the valve at its upward motion happens at a higher rate of LV pressure rise 31

32 2.Opening snap (OS) at the maximal excursion of the anterior mitral leaflet.the higher the atrial pressure the shorter the A2-OS P.max; lower sternal area glossary of time intervals: "blah" 0.03 s "butter" 0.06 "d-t" 0.08 "pa-pa" Diastolic rumble p.max apex, lying on the left side or just turning low pitched 32

33 Mitral stenosis auscult opening snap 33

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35 54 4.Presystolic accentuation of the diastolic murmur. Atrial systole is the most accepted explanation: no if AF?! or a high velocity antegrade flow thru a progressively narrowing mitral orifice during early ventricular systole 5.in some cases pulmonary regurgitant murmur caused by the pulmonary hypertension: Graham Steell murmur 35

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37 ECG dr.fenyvesi "mitral " P wave, notched P in II and a negative deflection in V1 AF is common Chest Roentgenogram left atrial enlargement with LA appendage straightening of the left cardiac border on the p-a chest film pulmonary venous alterations prominent pulm artery right ventricular enlargement 37

38 a convex left atrial border LA appendage Chr interstit pulm edema LA bulging into the esophagus 38

39 Echocardiography The most reliable diagnostic technique anatomical diagnosis: leaflet movement orifice size and area noninvasive haemodynamics: Doppler estimate of diastolic gradient LV function Catheterization "standard" technique, now not necessary, except over age of 4o-45? to exclude coronary artery disease before surgery 39

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44 Mitral regurgitation occurs when contraction of the left ventricle ejects blood into the left atrium as a result of abnormalities of the mitral apparatus 44

45 Mitral regurgitation Major causes: rheumatic fever coronary heart disease: myocardial infarction LV dilatation, papillary muscle dysfunction mitral valve prolapse : the most common cause bacterial endocarditis : rupture,penetration 45

46 Pathopysiology Volume overload on the LV and LA systolic elevation of LA, PV and P capillary pressure dilatation of LV to accomodate stroke volume ( the diastolic filling volume of LV: 1.syst output of RV + 2.amount of previous regurgitant volume) 46

47 In early rapid filling S3! "diastolic gallop" LV wall thickening In coronary heart disease impaired muscle function and LV shape m.r. 47

48 Fenyvesi Physical examination LV impulse is displaced downward and to the left,hyperdynamic Parasternal impulse is caused by the filling of a large left atrium Diastolic impulse is felt at the apex simultaneously with the S3 48

49 Auscultation in MI Holosystolic murmur: high pitched,radiates to the left axilla S1 is usually diminished,the systole is short early A2 splitting of S2 S3 a "protodiastolic gallop" high velocity rapid filling of LV In mitral prolapse a midsystolic click late systolic murmur is characteristic 49

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52 ECG signs of LA and LV enlargement in CHD signs in prolapse :ST-T changes,qt prolongation,t negativity in inferior leads Chest Roentgenogram in chronic MR LV and extreme LA enlargement double contour along the right border in prolapse normal 52

53 RA LA Straightening of the left heart border 53

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56 Echocardiography Fenyvesi Mitral regurgitation Valve anatomy:thickness,calcification of the mitral apparatus, valve area Valve motion Noninvasive haemodynamics:assessment of regurgitant volume Doppler technique LV function Prolapse direct evidence:billowing leaflets, myxomatous degeneration 56

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61 Mitral stenosis and regurgitation 61

62 Cardiac catheterization decreasing significance with new echo techniques quantitation of mitral regurgitation, left atrial size LV function large V wave on "wedged pressure" curve Coronary anatomy 62

63 Mitral prolapse syndrome idiopatic(?) or familial autosomal, dominant The systolic click-murmur noticed long ago, but considered of extracardiac origin P.D. White st description Barlow J.B detailed analysis of pathophysiology Barlow syndrome Extrasystolia, syncope 63

64 Clinical symptoms of MR are present Well tolerated for many years fatigue, dyspnea, palpitations, chest discomfort, anxiety, "panic syndrome"(?) 64

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66 Dynamic: auscultation Decrease of LV volume moves prolapse earlier in systole Increase of LV volume moves prolapse and click-murmur later 66

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68 Venous return decreases, hence LV volume also 68

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70 TEE echo posterior mitral leaflet prolapse 70

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74 Posteriorly oriented MI jet restricted posterior leaflet 74

75 Mitral valve prolapse 75

76 Mitral prolapse, high grade mitral regurg 76

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78 Tricuspid valve disease Tricuspid stenosis Rheumatic etiology, never isolated -in 14% of all rheumatic autopsies,high prevalence in India usually associated with MS,female! Pathophysiology:right atrial-right ventricular pressure gradient on inspiration in sinus rhythm giant atrial "a" wave, decreased cardiac output Clinical symptoms:fatigue,hepatomegaly,ascites, edema(and patient conspicuously lying flat), pulsation in the neck(venous) suspicion of MS, but no pulmonary congestion 78

79 Physical signs:increased venous pulsation in the neck OS after a mitral OS, p.max left parasternal harsh presystolic murmur diastolic murmur and OS inspiration ECG :right atrial hypertrophy P II and V1 greater than 0,25mV often combined MS wide P II,III, avf and +- V1 Chest X-ray:enlarged right atrium,wide superior vena cava, no pulm.engorgement Echocardiography: direct evidence 79

80 Fenyvesi Tricuspid regurgitation Usually not a primary valvular disease: right ventricular dilatation pulmonary hypertension "functional" mitral stenosis TI cor pulmonale or valvular pathology: Ebstein's anomaly rheumatic myxomatous degeneration endocarditis carcinoid syndrome 80

81 Clinical symptoms of TR Decreased cardiac output "right sided heart failure", usually accompanies mitral disease, thus may alleviate symptoms of left-sided heart failure (as pulmonary congestion,dyspnoe..) 81

82 Physical signs Jugular veins dilated, no x descent, + r v and y see figure!! right ventricular impulse Liver enlarged, pulsating S3 on inspiration, P2! Pansystolic murmur,p.max 4th interspace on inspiration :Carvallo sign 82

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86 Prosthetic cardiac valves 86

87 Starr-Edwards 1960!! Omniscience Medtronic-Hall St.Jude Carbomedics 87

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90 Hancock porcine Carpentier-Edw pericardial cryopreserved homograft 90

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104 A University should be a place of light of liberty, and of learning. Benjamin DISRAELI,

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