1. ACQUIRED VALVULAR HEART DISEASE
Iwona Świątkiewicz
Katedra i Klinika Kardiologii i Chorób Wewnętrznych
Collegium Medicum w Bydgoszczy

2. AVHD – acquired valvular heart disease
LV – left ventricle
LA – left atrium
RV – right ventricle
RA – right atrium
HF – heart failure
AF – atrial fibrillation
AV – aortic valve
MV – mitral valve
EF – ejection fraction
MR - mitral regurgitation
TR – tricuspid regurgitation
LVEDP – LV end-diastolic pressure
LVED(S)V(D) – LV end-diastolic (systolic)volume (diameter)
SV – stroke volume
CO – cardiac output

3. Left ventricular end-diastolic volume (LVEDV): 110-120 ml
Left ventricular end-systolic volume (LVESV): ml
Left ventricular stroke volume (LVSV): ml
Left ventricular ejection fraction (LVEF): 58-73%
Cardiac output (CO): at rest about 5 l (on exertion l)

4. Left ventricular end-diastolic pressure (LVEDP): 6-12 mm Hg
Left ventricular end-systolic pressure (LVESP): mm Hg
Left atrial pressure (mean): 6-11 mm Hg
Right atrial pressure (mean): 1-5 mm Hg
Right ventricular end-diastolic/end-systolic pressure : 2-7 / mm Hg
Pressure in pulmonary artery (diastolic/peak systolic/mean): 4-13/16-30/9-18 mm Hg
Pulmonary wedge pressure: 5-12 mmHg
Aortic pressure (diastolic/peak systolic/mean): 70-90/90-140/ mmHg
Pulmonary load: 0,8-1,1 (0,3-1,6) acc. Wood’s

5. Acquired valvular heart disease - definition
The dysfunction of heart due to the presence of acquired abnormal structure and/or function of the valve

6. Acquired valvular heart disease – primary (structural)
- due to the changes in the structure of valve

7. Acquired valvular heart disease – secondary (functional)
- due to the changes in the function of valve caused by abnormalities in the structure of other elements of the heart

20. Causes of death in acquired valvular heart disease
Congestive heart failure
Sudden cardiac death
Arrythmia
Stroke
Infective endocarditis
Death in the periintervention period (because of the complications of interventional/surgical treatment)

21. Left ventricle in acquired valvular heart diseases
Volume and/or pressure overload
Remodelling
Dysfunction – decides about prognosis

22. Remodelling of left ventricle
Left ventricular hypertrophy (LVH)
Left ventricular enlargement
Spheric shape of left ventricle
Increased wall stress of left ventricle

23. Left ventricular hypertrophy
Left ventricular eccentric hypertrophy (volume overload)
Left ventricular concentric hypertrophy (pressure overload)

24. T = p X R² / Th T – LV wall stress p – LV pressure R – LV radius Th – LV wall thickness

25. AORTIC STENOSIS

26. Aortic valve replacement
Aortic stenosis
the third most frequent cardiovascular disease
Aortic valve replacement
– the second most frequent cardiosurgical procedure

27. Aortic valve - physiology
Aortic valve area (AVA): 2–4 cm2
Peak velocity of aortic flow: 1,0–1,7 m/s
Left ventricular pressure:
end-systolic ( mm Hg)
end-diastolic (do 12 mm Hg)
Peak pressure gradient across aortic valve
< 20 mmHg

29. Bicuspid aortic valve Most frequent congenital defect in adults
More frequent in male (4x)
Positive family history
With other cardiovascular defects (CoA, PDA)
30% patients – cardiovascular complications (valvular and/or vascular)

30. Bicuspid aortic valve Valvular complications Vascular complications
Aortic stenosis
Aortic regurgitation
Infective endocarditis – prevention !!!
Vascular complications
Dilatation/aneurysma
Dissecting aneurysm

31. Aortic stenosis - patophysiology
Aortic valve area < 1 cm2
Left ventricular outflow obstruction during systole
LV systolic pressure
LV pressure overload ↓
LV concentric hypertrophy → normalisation of LV wall stress

32. Aortic stenosis - patophysiology
Compensation preventing cardiac output decrease:
 LV systolic pressure ,
 antegrade velocity across the narrowed valve,
 systolic pressure gradient across aortic valve (between LV and aorta),
LV concentric hypertrophy ,
 LV contractility,
 LV ejection time.
Unchanged cardiac output at rest
Decreased cardiac output on exertion  symptoms (angina, syncope)
 LV end-diastolic pressure caused by LVH  symptoms on exertion (dyspnea, fatigue)

33. Aortic stenosis - patophysiology
LV contractility (caused by increased wall stress) 
↓ LV cardiac output  symptoms (syncope, angina)
LV end- systolic volume
LV end-diastolic pressure  symptoms (dyspnea, fatigue)
LV heart failure  symptoms (dyspnea in rest)

34. Aortic stenosis - history
Asymptomatic for many years
First symptoms in calcified bicuspid valve at age of years, and in degenerative tricuspid valve at age of years
First symptoms associated with exertion,
Angina (5 years to death),
Syncope (3 years),
Dyspnea (2 years).

35. Aortic stenosis Symptoms: - angina - exertional lightheadedness
- syncope
- heart failure
- sudden cardiac death

36. Aortic stenosis - angina
Reasons:
- Coronary artery disease
Inadequate oxygen supply/demand
LV hypertrophy
coronary microciculation not increased
increase of vascular thickness and load
perivascular fibrosis
LV EDP increase
subendocardial ischaemia

37. Aortic stenosis - syncope
Reasons:
Inadequate brain perfusion:
- acute drop in blood pressure due to an inappropriate LV baroreceptor response
- ventricular arrhythmias
Podwyższone LV ciśnienie aktywuje baroreceptory które mediują wazodilatację a w obwcności zwężenia AV CO nie daje rady adekwatnie wzrastać

38. Aortic stenosis – reasons of death
Heart failure %
Infective endocarditis %
SUDDEN DEATH %
65-80% pt - symptomatic
3-5% pt - asymptomatic

39. Aortic stenosis – physical examination (key features)
Apex beat displaced laterally and down
Loud single second heart sound (severe AS) or reverse splitting of second heart sound (moderate AS)
S4 gallop
Systolic murmur: timing - crescendo-decrescendo during systole; location - the loudest at the base (over the right second intercostal space); systolic thrill (in severe AS); radiation - to the carotides; typically AS first diagnosed based on the finding on a murmur on auscultation
Palpation of the carotid pulse contour and amplitude: pulsus tardus (peak aortic pressure later in systole) and parvus (decreased pulse amplitude)
Typical signs of heart failure (if hemodynamic decompensation occured)
Crescendo-decrescendo pattern of amplitude corresponding to the shape of pressure between LV and A during the ejection period
Aortic component of the second heart sound is inaudible due to impaired motion of thickened valve leaflets
Reverse splitting with respiration due to prolonged LV ejection time

40. Aortic stenosis –diagnostic approaches
- ECG (LVH)
Chest radiograph (poststenotic dilatation
of ascending aorta, calcifications of
aortic valve)
- Echocardiography

41. Aortic stenosis – echocardiography
- morphology and mobility of AV leaflets
- calcifications of AV
- maximum velocity of aortic jet (vmax)
- peak pressure gradient
- mean pressure gradient
- AV area (AVA)
- contractility and LV ejection fraction
- LV hypertrophy
- assessment of other valves!!!
Patient with known or suspected aortic stenosis
With an experienced examiner diagnostic data are obtained on transthoracic echo in nearly all (>99%) patients, even when ultrasound penetration tissue is poor
TEE does allow planimetry of aortic orifice
Accurate Doppler data acquisition requires trained and experience examiners (ultrasound beam parallel to aortic jet)

42. Severe aortic stenosis – echocardiographic criteria
v max MeanPG AVA
>4,0 m/s >40 mmHg <1,0 cm AVAI
<0,6cm2/m2
ESC, 2012

43. Predictors of survival in adult patients with symptomatic aortic stenosis are stenosis severity expressed as jet velocity or transaortic gradient, functional status and LV systolic function.

44. Aortic stenosis -prognosis
50% increase of cardiovascular risk
5-year survival in symptomatic patients15-50%

45. MITRAL STENOSIS

46. Mitral valve - physiology
Mitral valve area
4 – 6 cm2
Diastolic pressure gradient between LA and LV
1 – 3 mmHg
Maximal velocity of mitral flow
0,6 – 1,3 m/s

47. Mitral stenosis - ethiology
- rheumatic
(fibrosis and thickening of leaflets; fusion of leaflet edges along commissures; fusion, thickening and shortening of chordae; superimposed calcific changes)
- myxoma in LA
massive calcifications in mitral annulus
poreumatyczna

48. Mitral stenosis - pathophysiology
Presence of mechanical obstruction at MV level
(significant if MVA < 2,0 cm²) 
 diastolic transmitral pressure gradient between LA and LV
 LA pressure
normal LV filling but  LA pressure

49. Mitral stenosis - pathophysiology
MVA 1–1,5 cm² 
  transmitral gradient and LA pressure 
LA enlargement
Pulmonary venous pressure  dyspnea
Pulmonary arterial pressure
RV pressure overload  RV hypertrophy 
RV dilation + tricuspid functional regurgitation
Right heart failure

50. Mitral stenosis – clinical history
Acute rheumatic fever episode in past medical history (rare finding)
Slow but progressive decline in exercise capacity, fatigue
Symptoms of pulmonary congestion: dyspnea on exertion, shortness of breath, paroxysmal nocturnal dyspnea, pulmonary oedema
Symptoms of right heart failure: peripheral oedema, abdominal distention, decreased appetite
Hoarseness (Ortners’ s. – due to compression of the left recurrent laryngeal nerve by the enlarged LA)
Recurrent pulmonary infections, hemoptysis
In many patients the disease process is so slow that pts deny symptoms, as expectations and lifestyle are gradually modified to accomodate the decreased cardiac reserve

51. Mitral stenosis – clinical history
Atrial fibrillation: may be the first symptom, may cause pulmonary oedema
Systemic embolic event due to LA thrombus formation: may be the first symptom in 20% of patients

52. Mitral stenosis – physical examination: auscultation
Loud S1
Opening snap in early diastole
Diastolic murmur („mitral rumbling”) with presystolic accentuation (when?): using the bell of stethoscope positioned near the apex with the patient in a left lateral decubitus position, murmur quite localized
Prominent pulmonic closure sound (when?)
Graham-Steell murmur
RV S3
Holosystolic tricuspid functional regurgitation murmur
Loud S1 due to increased amplitude of mitral closing click

53. Mitral stenosis – physical examination
Pulmonary congestion signs
Right heart failure signs: elevated jugular venous pressure, peripheral oedema, hepatosplenomegaly
Loud S1 due to increased amplitude of mitral closing click

54. Mitral stenosis – echocardiography
Evaluation of MV morphology
Evaluation of mitral stenosis severity
Evaluation of LA and RV sizes and RV hypertrophy
Evaluation of the presence of LA thrombi
Evaluation of pulmonary hypertension

55. Mitral stenosis – echocardiography
Mitral valve area:
1,5 – 2 cm² mild stenosis
1 – 1,5 cm² moderate stenosis
< 1 cm² severe stenosis

56. Mitral stenosis – prognosis
10-year risk of HF 60%
5-year survival of symptomatic patients 44%

57. Reasons of death in mitral stenosis
CHF (60-70%)
Systemic embolic events (20-30%)
Pulmonary embolic events (10%)
Infections (1-5%)

58. MITRAL REGURGITATION

59. Mitral regurgitation
Onset
acute chronic

60. Mitral regurgitation
primary (structural) secondary (functional)

61. Mitral regurgitation - etiology
Rheumatic fever
- Degenerative changes (60%)
Coronary artery disease
- papillary muscle dysfunction
- papillary muscle rupture
Left ventricular dilation
- coronary artery disease
- dilated cardiomyopathy
Mitral leaflet prolapse (myxomatosus mitral valve disease)

62. Mitral regurgitation - etiology
Rupture of chordeae tendineae
Infective endocarditis
- leaflet perforation
vegetation on mitral leaflet
Mitral annulus calcification
degenerative, end-stage renal disease
Hypertrophic cardiomyopathy

63. Chronic mitral regurgitation - pathophysiology
Increased volume flow entering LA in systole  LA dilation (> 500 mL) as a compensatory mechanism
 LA pressure and pulmonary pressure
 pulmonary hypertension

64. Chronic mitral regurgitation – pathophysiology: compensation (isolated volume overload)
Increased volume flow entering LV in diastole:
„normal” mitral inflow + regurgitant volume (30-50%)
dilation of LV in diastole
eccentric LVH
 LV contraction (Frank-Starlings’ law)
Increased volume pumped by the ventricle being ejected into the low-impedance LA – the backflow of blood across MV provides afterload reduction

65. Chronic mitral regurgitation – pathophysiology: decompensation (isolated volume overload)
→  LV wall stress (Laplace law)
 LV contractility ( LVEF)
 LVEDP → heart failure

66. Immediate cardiosurgery!
Acute mitral regurgitation
Abrupt increase volume flow entering LA
Severe  LA pressure
 Pulmonary pressure
Pulmonary oedema
Immediate cardiosurgery!

67. Chronic primary mitral regurgitation – clinical history
Asymptomatic for many years
Exertional dyspnea/exercise intolerance
Overt symptoms of heart failure
AF (new onset of AF may be the first symptom, AF increases the symptoms of LVHF)
RVHF

68. Chronic mitral regurgitation – physical examination
Precordial palpation: diffuse or displaced LV apical impulse, appreciated RV heave
Auscultation: loud S3, soft S1, increased pulmonary S2 (in pulmonary hypertension)
Auscultation: holosystolic murmur loudest at the apex and radiates to the axilla, midsystolic click (MV prolapse), the loudness of murmur correlates with regurgitant severity
Overt signs of pulmonary congestion and LVHF
RVHF signs
S3 may be present due to the increased rate and velocity of early diastolic filling

69. Acute mitral regurgitation – physical examination
Signs of pulmonary oedema
Protomesosystolic murmur crescendo-decrescendo, radiates to the base: severe MR may be present despite a soft murmur (up to 50% of patients have no audible murmur) S4

70. Echocardiography in mitral regurgitation
Evaluation of etiology
Evaluation of severity
Evaluation of mechanisms
Evaluation of LV size and function, LA size, pulmonary artery pressure
Determination of timing of intervention and evaluation the possibilities of correction without valve replacement

71. AORTIC REGURGITATION

72. Aortic regurgitation
acute chronic

73. Aortic regurgitation
primary secondary

74. Aortic regurgitation - etiology
degenerative changes
bicuspid aortic valve
rheumatic etiology
infective endocarditis
dissecting aortic aneurysm
dilation of ascending aorta/aortic annulus

75. Aortic regurgitation – pathophysiology Left ventricular volume and pressure overload
Regurgitant stroke volume besides forward stroke volume ↓
LV volume overload in diastole
Increased LV end-diastolic and end-systolic volumes (↑↑LV but normal LVEF)
Eccentric LV hypertrophy
Increased wall stress → Decompensation (↑LVEDP, ↓ LVEF)
In systole increased antegrade flow velocity due to increased volume flow rate across valve
In diastole aortic pressure deceases more rapidly than normal

76. Chronic aortic regurgitation – clinical history
Asymptomatic for many years
Exertional dyspnea, than dyspnea at rest, paroxysmal nocturnal dyspnea, orthopnea (left heart failure)
Angina
Headaches (pulsatile)
Palpitations
Increased forward systolic flow and retrograde diastolic flow in ascending aorta

77. Chronic aortic regurgitation – physical examination
LV apex is typically enlarged, hyperdynamic, laterally displaced, apical heave may be appreciated
Holodiastolic murmur, loudest at the left sternal border, decrescendo (with the patient sitting and leaning slightly forward) S3
Systolic murmur of aortic stenosis (organic or functional)
Austin-Flint murmur (echo!),
Widened pulse pressure
Carotid pulse is typically bounding („waterhammer”)

78. Acute aortic regurgitation – physical examination
Rapid increase in LVEDP
Pulmonary oedema
Cardiogenic shock
Very short diastolic murmur, crescendo-decrescendo
MR diastolic
Drop in DBP to 0 mmHg!

79. Aortic regurgitation - echocardiography
Evaluation of aortic valve and root anatomy
Evaluation of LV size and function
Evaluation of aortic regurgitation severity