The document discusses mitral stenosis and mitral regurgitation. For mitral stenosis, rheumatic heart disease is the leading cause and results in thickening and fusion of the mitral valve leaflets. This narrowing of the valve orifice leads to elevated left atrial pressures and pulmonary hypertension. Symptoms include dyspnea and palpitations. Mitral regurgitation can be acute or chronic, and has various etiologies such as rheumatic heart disease. Chronic mitral regurgitation results in left ventricular and left atrial enlargement, while acute mitral regurgitation can cause pulmonary edema due to a sudden rise in left atrial pressures. Echocardiography is important for evaluating

1. VALVULAR HEART DISEASE
BY: Dr.Kifle Alamirew(MD)
1

2. MITRAL STENOSIS
2

3. ETIOLOGY OF MS
 Rheumatic heart disease
 is the leading cause of mitral stenosis (MS) although only 50 to
70 percent of patients report a history of rheumatic fever
 In rheumatic MS, the valve leaflets are diffusely thickened by
fibrous tissue and/or calcific deposits. The mitral commissures
fuse, the chordae tendineae fuse and shorten, the valvular cusps
become rigid, and these changes, in turn, lead to narrowing at
the apex of the funnel-shaped ("fish-mouth") valve
 Calcification of the stenotic mitral valve immobilizes the leaflets
and narrows the orifice further
3

4. CONT’D……
 Other less common causes:
o Congenital mitral valve stenosis
o Cor triatriatum
o Mitral annular calcification with extension onto the leaflets
(degenerative)
o Left atrial myxoma
o Infective endocarditis with large vegetations
o Carcinoid heart disease
o Endomyocardial fibrosis
o Systemic lupus erythematosus
o Rheumatoid arthritis
4

5. PATHOPHYSIOLOGY OF MS
 When the orifice diameter < 2cm - blood can
flow from the LA to the left ventricle (LV) only if
propelled by an abnormally elevated left
atrioventricular pressure gradient during
diastole, the hemodynamic hallmark of MS
 The elevated left atrial pressure is reflected backward,
causing an increase in pulmonary venous, capillary, and
arterial pressures and resistance
5

6. CONT…
 With mild to moderate MS, symptomatic at exertion or at
increased HR.
 Occur at rest when it becomes severe MS
 The LV diastolic pressure and ejection fraction (EF) are
normal in isolated MS
6

7. CONT…
 Pulmonary hypertension results from:
 Passive backward transmission of the elevated LA pressure
 Pulmonary arteriolar constriction.
 Interstitial edema in the walls of the small pulmonary
vessels
 Organic obliterative changes in the pulmonary vascular
bed
7

8. SYMPTOMS OF MS
 The interval between the episode of rheumatic fever and the
clinical presentation of MS varies geographically
 Dyspnea, cough,orthopenia and PND
 Palpitation,
 Hemoptysis,
 Hoarsness-ortner syndrome
 Thromboembolism
 Chest pain
 Infective endocarditis
 Right sided HF
8

9. SIGNS OF MS
Physical Signs
 Inspection
 Mitral facies –pinkish purple patchs over
the cheek
 Palpation
 Decreased arterial pulse
 Prominent a wave (sinus rhythm)- increased
JVP
 Right ventricular heave
 Palpable P2
 Apical Diastolic thrill
9

10. CONT’D…..
 Auscultation
  S1 (the first heart sound (S1) is loud,
  P2
 Opening snap (OS)
 murmur of MS:
 is a low-pitched, diastolic, rumbling murmur
 is most prominent at the apex
 It is heard best in a quiet room with the patient lying on the left
side in held expiration and by using the bell of the stethoscope.
 Other murmurs: functional TR, Graham steel murmur of PR
especially if pulmonary hypertension present
 Sign of right ventricular heart failure 10

11. INVESTIGATIONS
ECG in MS
 M-mitrale: P wave that becomes broader (duration in lead II>0.12
sec), is of increased amplitude, and is notched
 P-pulmonale
 Right axis deviation and right ventricular hypertrophy: the frontal
axis shifts to the right (S>R in lead I and aVL) and a tall R wave
develops in V1 and V2 (R>S or R/S ratio >1)
11

12. CONT’D…..
CHEST X-RAY in MS
 Left atrial enlargement
o A "double density"
o The left heart border becomes straightened
o The left bronchus is elevated
o On the lateral projection, the left atrium is displaced posteriorly,
impinging on the esophagus
 Pulmonary vascular congestion
o Redistribution or "cephalization" of pulmonary blood flow to the upper
lobes
o Dilated pulmonary vessels,
o Kerley B lines at the bases, and interlobar effusions (Kerley C lines)
o In more severe cases, Kerley A lines (straight dense lines running toward
the hilum)
12

13. CONT’D……
 ECHOCARDIOGRAPHY IN MS
 The mitral leaflets are thickened, have reduced motion during
diastole, and show doming
 The mitral valve area can be accurately measured
 Estimates of leaflet motion, the degree of calcification and fibrosis
of the leaflets, and assessment of the subvalvular apparatus can help
establish the role for surgical or balloon valvotomy
 Left atrial size, and left and right ventricular size and systolic
function can be assessed
 Vegetations
 Left atrial thrombus
13

14. ECHOCARDIOGRAPHIC ASSESSEMENT OF
SEVERITY OF MS IN ADULTS
14

15. CONT’D…..
 OTHER INVESTIGATIONS IN MSS
 Stress ECHO
 Cardiac catheterization
 MRI
 Base line investigations (CBC, RFT, electrolytes)
 Coagulation profile
15

16. MANAGEMENT OF MS
 Avoid strenous exercise and physical activity
 Diuretcs with salt restriction
 Digoxin, B blockers: AF + HF
 Secondary prevention of rheumatic fever
 Prevention of endocarditis
 Prevention of thromboembolism
 Management of AF – warfarin
 surgery
16

17. MITRAL REGURGITATION
 Acute vs chronic
 Abnormality may be on
valve leaflets, valve
annulus, chorda
tendinae, papillary
muscle or others
17

18. ETIOLOGY OF MR
 Rheumatic heart disease is the cause of chronic
MR in only about one-third of cases and occurs
more frequently in males.
 The rheumatic process produces rigidity,
deformity, and retraction of the valve cusps and
commissural fusion, as well as shortening,
contraction, and fusion of the chorda tendinae
18

19. CONT’D….
19

20. PATHOPHYSIOLOGY OF MR
 Chronic mitral regurgitation is a state of volume overload leading
to the development of left ventricular hypertrophy.
 The left atrium also enlarges to accommodate the regurgitate
volume. This compensated phase of mitral regurgitation varies in
duration but may last many years
 The prolonged state of volume overload may eventually lead to
decompensate mitral regurgitation. This phase is characterized by
impaired left ventricular function, decreased ejection fraction and
pulmonary congestion
20

21. PATHOPHYSIOLOGY OF MR
 In acute severe MR, the regurgitant volume is delivered into a
normal-sized LA having normal or reduced compliance. As a result,
LA pressures rise markedly for any increase in LA volume. LA and
pulmonary venous pressures are markedly elevated, and pulmonary
edema is common
 Patients with chronic severe MR, on the other hand, develop marked
LA enlargement and increased LA compliance with little if any
increase in LA and pulmonary venous pressures for any increase in
LA volume. These patients usually complain of severe fatigue and
exhaustion secondary to a low CO, while symptoms resulting from
pulmonary congestion are less prominent initially
21

22. SYMPTOMS OF MR
 Patients with chronic mild-to-moderate isolated MR are
usually asymptomatic
 Fatigue, exertional dyspnea, and orthopnea are the most
prominent complaints in patients with chronic severe MR.
 Palpitations are common and may signify the onset of AF
 Right-sided heart failure, with painful hepatic congestion,
ankle edema, distended neck veins, ascites, and secondary TR,
occurs in patients with MR who have associated pulmonary
vascular disease and marked pulmonary hypertension,
pulmonary edema not common
22

23. SIGN OF ACUTE MR
 The patient with acute MR is often in pulmonary edema and there
is evidence of poor tissue perfusion with peripheral vasoconstriction,
pallor, and diaphoresis
 The arterial pulse is often rapid and of low amplitude or thready
due to the reduction in forward output.
 The cardiac impulse is hyperdynamic but is usually normal in
location because left ventricular size is normal.
 There is often a hyperdynamic precordium with a right ventricular
lift due to the acute increase in pressure within this chamber
 The murmur of acute mitral regurgitation may be early, midsystolic,
or holosystolic; often soft, low pitched and decrescendo, ending
before well before S2;often best heard along the left sternal border
and base of the heart, generally without a thrill, and may radiate to
the back
23

24. CONT’D……….
 S3 is commonly heard
 P2 is increased in intensity and the murmurs of pulmonary and
tricuspid regurgitation may be appreciated
 Approximately 50 percent of patients with moderate to severe MR
have no audible murmur, particularly those with acute ischemic MR
 The presumed mechanism of silent MR is a relatively low pressure
gradient in systole between the left ventricle and left atrium due to
the combination of a low systemic blood pressure and elevated left
atrial pressure. In addition, acoustic transmission of the murmur may
be obscured by obesity and respiratory distress. Thus, the absence of
a systolic murmur does not reliably exclude the diagnosis of acute
severe MR
24

25. SIGN OF CHRONIC MR
 The arterial pulse may be reduced in volume, but is usually brisk in upstroke,
reflecting the increased ejection rate and normal ejection fraction.
 Apical impulse is laterally displaced and it is usually brisk or hyperdynamic.
 Signs of right-sided congestive heart failure are typically absent unless there is
associated mitral stenosis or the MR is of long standing and is very severe
 S1 is diminished, reflecting failure of the mitral leaflets to close properly
 Wide splitting of S2 is not infrequent
 S3 gallop, which becomes particularly prominent if left ventricular failure occurs
(it is a sign of severe MR)
25

26. SIGN OF CHRONIC MR
 The murmur of chronic MR:
 is holosystolic, commencing immediately after S1 and continuing up
to and sometime beyond and obscuring A2, a result of the
persistent pressure gradient between the left ventricle and atrium
 is heard best over the apex,
 radiating to the axilla and when very loud may often radiate to the
back.
 It is most often blowing and high pitched in quality
26

27. INVESTIGATIONS
 ECG: LA enlaregement,LVH and if they develop pulmonary
hypertension LA enlargement and RVH can be seen
 CXR: the most common finding on the chest radiograph is
cardiomegaly, resulting from enlargement of the left ventricle and
left atrium
 ECHO: is essential for establishing the etiology and hemodynamic
consequences of mitral regurgitation .Other important features on
echocardiography are evaluation of the left atrium, left ventricle, and
pulmonary artery pressures
 Base line, coagulation profile,
 Cardiac catheterization and angiography
27

28. 28

29. MANAGEMENT OF MR
 Medical
 Surgery
29

30. AORTIC STENOSIS
30

31. ETIOLOGY OF AS
 Rheumatic heart disease
 Rheumatic AS is almost always associated with involvement of the mitral valve
and with AR
 Worldwide, rheumatic valve disease is the most common cause of AS
Congenital (bicuspid,unicaspid)
The congenitally affected valve may be stenotic at birth and may become
progressively more fibrotic, calcified, and stenotic or
 Bicuspid valve : abnormal architecture makes its leaflets susceptible to otherwise
ordinary hemodynamic stresses, which ultimately lead to valvular thickening,
calcification, increased rigidity, and narrowing of the aortic orifice
Age related degenerative calcific AS
31

32. PATHOPHYSIOLOGY
 When AS becomes hemodynamically significant, it
results in obstruction to left ventricular ejection
 adaptive changes in the left ventricle leads to
concentric hypertrophy
 AS is rarely of clinical importance until the valve
orifice become 1.0 cm2
 Remodeling continue
32

33. SYMPTOMS OF AS
 Dyspnea
 Diziness and Syncope
 Angina due to:
 Increased left ventricular oxygen demand as a result of
increased left ventricular
 Compression of intramyocardial coronary arteries from
prolonged contraction and impaired myocardial relaxation
 Reduced diastolic coronary perfusion time during tachycardia
 Accompaning coronary artery disease
 AF
 In severe case there will be manifestation of Decreased CO
and congestion
33

34. SIGNS OF AS Physical findings
 BP -  late and pulse pressure narrows
 Slow rising pulse
 Prominent a wave
 Carotid thrill
 Palpation
 Apical impulse is forceful, sustained and is
initialy normal in location but later displaced(Left
side HF)
 Palpable S4
 A systolic thrill may be felt at the base of the heart or at the
sternal notch, especially during full expiration with the patient
leaning forward 34

35. CONT’D…..
 Auscultation
 Soft S2,Paradoxical S2 split,Ejection click,
 Apical S4 gallop is common
 The murmur of AS:
 is an ejection (mid) systolic murmur that commences shortly after the S1,
increases in intensity to reach a peak toward the middle of ejection, and ends
just before aortic valve closure.
 is low-pitched, rough and rasping in character,
 Is loudest at the base of the heart, most commonly in the second right
intercostal space and
 is transmitted upward along the carotid arteries (the murmur is transmitted
well and equally to the carotid arteries).
35

36. CONT’D……..
 The murmur may also radiate to the apex of the heart where it
may have a different quality (musical due to high frequency
vibrations) and may be louder, suggesting that the patient also has
mitral regurgitation. This is known as the Gallavardin phenomenon.
 In almost all patients, AS is associated with a small degree of aortic
regurgitation since the stiff, calcified, and rigid aortic valve leaflets
may not coapt normally
 The duration and intensity of AS murmur has correlation with
severity of AS
36

37. INVESTIGATIONS
 ECG: LV hypertrophy and in advanced cases, ST-segment depression and T-wave
inversion (LV "strain")
 ECHO: LVH,nature of the valve,severity grading,LV function,etiology of the
AS,complications of AS,concomitant other valvular lesions
37

38. CONT’D…..
 CXR
 The chest x-ray may show no or little overall cardiac enlargement for many years
 Hypertrophy without dilatation may produce some rounding of the cardiac apex in the
frontal projection and slight backward displacement in the lateral view
 Aortic calcification is usually readily apparent on fluoroscopic examination or by
echocardiography; the absence of valvular calcification in an adult suggests that severe
valvular AS is not present
 In later stages of the disease, as the LV dilates there is increasing evidence of LV
enlargement, pulmonary congestion, and enlargement of the LA, PA, and right side of the
heart
 CT/MRI scan
 Cardiac catheterization
38

39. AORTIC REGURGITATION
 Acute vs chronic
 Aortic regurgitation (AR, also called aortic
insufficiency) is due to inadequate closure of the aortic
valve leaflets.
 It can be induced either by damage to and dysfunction
of the aortic valve leaflets or by distortion or dilatation
of the aortic root and ascending aorta.
39

40. ETIOLOGY OF AR
40

41. PATHOPHYSIOLOGY OF AR
 All forms of AR produce a similar hemodynamic abnormality
 The inability of the aortic valve leaflets to remain closed or coapted
during diastole results in a portion of the left ventricular stroke
volume leaking back from the aorta into the left ventricle
 The added volume of regurgitant blood produces an increase in left
ventricular end-diastolic volume;
 According to Laplace's law, the increase in left ventricular end-
diastolic volume causes an elevation in wall stress.
 Chronic AR is thus a state in which LV preload and afterload are
both increased
 The heart responds with compensatory myocardial hypertrophy,
which returns wall stress toward normal
41

42. MANAGEMENT OF AS
 Medical
 surgery
42

43. CONT’D…… In patients with acute severe AR:
 The LV is unprepared for the regurgitant volume load
 LV compliance is normal or reduced, and LV diastolic pressures
rise rapidly, occasionally to levels >40 mmHg.
 The LV pressure may exceed the LA pressure toward the end of
diastole, and this reversed pressure gradient closes the mitral valve
prematurely
43

44. PATHOPHYSIOLOGY OF AR
44

45. SYMPTOMS OF AR
 Patients with AR may remain asymptomatic for decades (as long as
10–15 years), even if there is progressive ventricular dilatation.
 If, however, there is a large regurgitant volume, the patient may
complain of symptoms related to the increased mass of the
enlarged left ventricle. These include:
 A sense of pounding and an uncomfortable awareness of the
heartbeat.
 Atypical chest pain induced by a mechanical interaction between
the heart and the chest wall
 Palpitations due to tachycardia or premature beats
 Symptoms of left-sided heart failure occur in the presence of left
ventricular dysfunction
45

46. CONT’D… Angina pectoris is uncommon with isolated AR, since the coronary
arteries are typically dilated
 In patients with acute severe AR, as may occur in infective
endocarditis, aortic dissection, or trauma, the LV cannot dilate
sufficiently to maintain stroke volume, and LV diastolic pressure
rises rapidly with associated marked elevations of LA and PA wedge
pressures.
 Pulmonary edema and/or cardiogenic shock may develop rapidly
46

47. SIGN OF AR
 palpation
 There is an elevation of the systolic pressure, sometimes
to as high as 300 mmHg, and a depression of the
diastolic pressure( approach zero in severe case)
 This wide pulse pressure manifest on examination as
“Water-hammer" or Corrigan's pulse
 best appreciated by palpation of the radial or brachial
arteries (exaggerated by raising the arm) or the carotid
pulses.
 The level of cuff pressure at the time of muffling of the
Korotkoff sounds (Phase IV) generally corresponds fairly
closely to the true intraarterial diastolic pressure
47

48. CONT’D…… Other findings are associated with a hyperdynamic pulse:
 DeMusset's sign — A head bob occurring with each heart beat
 Traube's sign — A pistol shot pulse (systolic and diastolic sounds)
heard over the femoral arteries
 Duroziez's sign — A systolic and diastolic bruit heard when the
femoral artery is partially compressed
 Quincke's pulses — Capillary pulsations in the fingertips or lips
 Mueller's sign — Systolic pulsations of the uvula
 Becker's sign — Visible pulsations of the retinal arteries and pupils
 Hill's sign — Popliteal cuff systolic pressure exceeding brachial
pressure by more than 60 mmHg
 Mayne's sign — More than a 15 mmHg decrease in diastolic blood
pressure with arm elevation from the value obtained with the arm in
the standard position
 Rosenbach's sign — Systolic pulsations of the liver
 Gerhard's sign — Systolic pulsations of the spleen
48

49. CONT’D…….
 The LV(apical) impulse is and displaced laterally and inferiorly
 Apical heave
 A diastolic thrill is often palpable along the left sternal border, and
 prominent systolic thrill may be palpable in the suprasternal notch
and transmitted upward along the carotid arteries. This systolic
thrill and the accompanying murmur do not necessarily signify the
coexistence of AS
49

50. SIGN OF AR
AUSCULTATION
 A2 is usually absent
 An S3 and systolic ejection sound are frequently audible, and occasionally
an S4 also may be heard
 The murmur of chronic AR:
 is typically a high-pitched, blowing, decrescendo diastolic murmur,
 heard best in the third intercostal space along the left sternal border
 it can be heard best with the diaphragm of the stethoscope and with the
patient sitting up, leaning forward, and with the breath held in forced
expiration
 Other murmurs :
 A mid-systolic ejection murmur is frequently audible
 The Austin Flint murmur,
 In acute severe AR, the elevation of LV end-diastolic pressure may lead to
early closure of the mitral valve, an associated mid-diastolic sound, a soft
or absent S1, a pulse pressure that is not particularly wide, and a soft,
short diastolic murmur of AR
50

51. INVESTIGATIONS
 ECG: LVH,strain pattern and left axis deviation and/or QRS
prolongation denote diffuse myocardial disease, generally associated
with patchy fibrosis, and usually signify a poor prognosis
 CXR:
 the apex is displaced downward and to the left in the frontal
projection
 In the left anterior oblique and lateral projections, the LV is
displaced posteriorly and encroaches on the spine
 When AR is caused by primary disease of the aortic root,
aneurysmal dilatation of the aorta may be noted, and the aorta may
fill the retrosternal space in the lateral view
• ECHO: (see severity assessment on next slide)
• Cardiac catheterization and angiography 51

52. CONT’D……..
 AR severity grading by ECHO
52

53. MANAGEMENT OF AR
 Medical
 Surgery
53

54. OTHER VALVULAR LESION
 Less common
 TR
 PR
 TS
 PS
54

55. GENERAL TREATMENT FOR VHD
Treatment of valvular heart disease
Prophylaxis for :
 Sub acute bacterial endocarditis
 CRHD
 Avoid strenuous exercise
 aortic stenosis
 salt, diuretics
 Special treatment
 AF
 Embolic events
 Valve repair or replacement 55