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1. Valvular Heart Disease

2. Rheumatic fever
Rheumatic fever (RF) is generally classified as a
connective tissue or collagen-vascular disease
It is an inflammatory reaction that causes damage to
collagen fibrils and to the ground substance of
connective tissue
Involves multiple organs: primarily the heart, the
joints, and the central nervous system
Recurrent attacks of RF may cause fibrosis of heart
valves, leading to chronic valvular heart disease

3. Epidemiology
Peak incidence ages 5~15 years
Rare before age 4 years and after age 40 years
The incidence of RF and prevalence of rheumatic
heart disease (RHD) are markedly variable in
different countries:
In developed country, such as the united states,
the incidence of RF ＜ 2/100,000
In many developing countries, the incidence of
acute RF approaches or exceeds 100/100,000

4. Etiology and Pathogenesis
Multiple factors contribute to the pathogenesis,
including β-hemolytic streptococcal pharyngitis
and immunological status of the human body
Cross immune response between host and
streptococcal antigens
Streptococcal pharyngitis
↓
Abnormal reaction-autoimmunity disease

5. Pathology
Pathological characters:
Exudative and proliferative inflammatory reactions
involving connective or collagen tissue
Affects primarily the heart, joints, brain, cutaneous
and subcutaneous tissues
Pathological process ：
Exudative stage
Proliferative stage: Aschoff nodule (pathognomonic)
Fibrosis and calcification (scar formation)

6. Recurrent attacks of RF (rheumatic carditis,
valvulitis) → scar formation and deformity of
heart valves → chronic RHD
Valvular involvement:
Mitral valve: 75%~80%
Aortic valve: 30%
Tricuspid & pulmonary valves: ＜ 5%

7. Clinical findings
1 、 Major manifestations
① Carditis: pericarditis, cardiomegaly, congestive
heart
failure, and mitral or aortic regurgitation murmurs
② Migratory polyarthritis: involves large joints
lasts 1~5 weeks, subsides without residual deformity
prompt response to salicylates or nonsteroidal agents
③ Erythema marginatum: rare
④ Subcutaneous nodules: uncommon
⑤ Chorea: least common, most diagnostic

8. 2 、 Minor manifestations
① Clinical findings: fever, polyarthralgias
② Laboratory findings
Elevated acute phase reactants:
ESR (erythrocyte sedimentation rate)
CRP (C reactive protein)
③ ECG change: prolonged P-R interval
④ A history of RF
Supporting evidence of an antecedent group A
streptococcal infection:
① Positive throat culture or rapid streptococcal antigen test
② Elevated or rising titers of antistreptococcal antibodies
(anti-streptolysin O and anti-DNase B)

9. Diagnosis
Based on Jones criteria and confirmation of
streptococcal infection
Guidelines for the diagnosis of initial attacks of RF
(Jones criteria, updated 1992)
If supported by evidence of preceding group A
streptococcal infection, the presence of two major
manifestations or of one major and two minor
manifestations establishes the diagnosis of acute RF

10. Treatment
General Measures
Strict bed rest
Medical Measures
1. Control streptococcal infection
Penicillin is of choice
benzathine penicillin, 1.2 million units im once,
or procaine penicillin, 600,000 units im daily, 10 days
If allergic to penicillin, erythromycin be given

11. 2. Antirheumatic therapy
(1) Salicylates
Of choice in patients with little or no cardiac involvement;
Particularly effective in reducing fever and relieving joint
pain and swelling
Aspirin 0.6~0.9 g / 4h in adults; lower doses in children
(2) Corticosteroids
Used in patients who do not respond well to adequate
doses of salicylates
Prednisone 40~60 mg orally daily, tapering over 2 weeks

12. 3. Treatment of symptoms and complications
If heart failure is present, digitalis preparations should be
used cautiously because cardiac toxicity may occur with
conventional dosages
Prevention
Primary prevention
Early treatment of streptococcal pharyngitis
Penicillin or erythromycin
Secondary prevention
To prevent recurrence of rheumatic activity
Long-acting penicillin (benzathine penicillin)
1.2 million units im, every 4 weeks
Sulfonamides or erythromycin may be substituted

13. Mitral stenosis (MS)
Etiology
Most commonly rheumatic fever
——rheumatic heart disease （ RHD ）
Symptoms commence mostly in 2nd~4th decade
2/3 of all patients are female
25% of all patients with RHD have pure MS
40% have combined MS and mitral regurgitation (MR)

14. Other rare causes
Far less frequently, MS is congenital in etiology
observed primarily in infants and young children
Calcification of mitral annulus (when subvalvular or
intravalvular extension is extensive)
observed in old patients
Very rarely, MS is a complication of carcinoid
disease or connective tissue disease (systemic lupus
erythematosus, SLE; rheumatoid arthritis)

15. Pathology
Fibrosis, thickening, rigid and calcification of the valve
apparatus
Rheumatic fever results in four forms of fusion of the
mitral valve apparatus leading to stenosis:
Commissural, cuspal, chordal, and combined
Characteristically, mitral valve cusps fuse at their
edges, and fusion of the chordae results in thickening
and shortening of these structures

16. Commissural adherent and fusion
↓
restricted opening of mitral valve
↓
“fish mouth” shape of mitral valve orifice
Thickening, fusion and shortening of the
chordae or papillary muscles
↓
funnel-shaped change of valve apparatus

17. Secondary changes ：
Chronic MS → Dilatation of the left atrium
Fibrosis of the atrial wall
Development of mural thrombi
Hypertrophy and dilation of RV

18. Hemodynamic changes
MS involves mainly LA and RV
1. Effect of MS on left atrioventricular pressure
gradient and left atrial pressure (LAP)
MVA transvalvular gradient LAP
Normal 4 ～ 6cm2
Mild MS ＞ 1.5cm2 5-10mmHg ↑
Moderate 1.0 ～ 1.5cm2 10-20mmHg ↑↑
Severe ＜ 1.0cm2 ≥20mmHg 25mmHg

19. 2. Effect of elevated LAP on pulmonary circulation
The elevated LAP in turn raises pulmonary venous and capillary
pressures (PVP, PCP), resulting in exertional dyspnea
LAP↑ → PVP↑→ PCP↑→ Dyspnea
Lung compliance↓
Pulmonary hypertension results from:
1. Passive backward transmission of the elevated LAP
2. Reactive pulmonary arteriolar constriction, which presumably
is triggered by left atrial and pulmonary venous hypertension
3. Organic obliterative changes in the pulmonary vascular bed,
which may be considered to be a complication of longstanding and
severe MS

20. 3. Effect of pulmonary hypertension on RV
Pulmonary hypertension
↓
RV hypertrophy & dilation
（ secondary TR, PR ）
↓
Right ventricular failure

21. Clinical manifestations
Symptoms
Onset in patients with moderately severe
MS （ MVA ＜ 1.5 cm2 ）
Dyspnea: Principal symptom, appears at early stage
Precipitated by exertion, fever, AF or pregnancy
Exertional dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, acute pulmonary edema
Hemoptysis
Profuse hemorrhage: rupture of bronchial
submucosal varices
Blood-stained sputum
Pink, frothy sputum
Cough occurs frequently
respiratory infection, compression of left bronchus
Hoarseness (Ortner’s syndrome), less common
Compression of left recurrent laryngeal nerve

22. Physical examination
Cardiac signs of MS
Changes of heart sounds:
Accentuated S1
Opening snap (OS) sharp, follows A2 along left
sternal border or at apex
Both suggest MV leaflets flexible
Marked calcification or thickening of the MV leaflets
S1 becomes softer, and OS may disappear
probably because of diminished motion of the leaflets

23. Diastolic murmur of MS
A low-pitched, diastolic rumbling murmur,
localized at or near apex, with pre-systolic
accentuation in patients with sinus rhythm
Auscultation of the murmur is facilitated by
placing the patient in the left lateral position and
auscultate during expiration
When the patient is in the left lateral
recumbent position, a mid-diastolic or presystolic
thrill may be palpable at apex

24. Cardiac signs secondary to pulmonary
hypertension and RV dilation
RV pulsation is present at the left parasternal region
Accentuated or splitting of P2 may be heard in the
second left intercostal space
Other signs of pulmonary hypertension:
Pulmonic ejection sound, owing to dilation of the PA
Graham Steell murmur of PR: a decrescendo diastolic
murmur along the left sternal border
When RV dilation is companied by TR, a pansystolic
murmur may be audible in the 4th or 5th intercostal
space in the left parasternal region

25. Other signs
Mitral face: malar flush
Signs of right heart failure:
Systemic venous hypertension, hepatomegaly, edema,
and ascites are all signs of severe MS with elevated
pulmonary vascular resistance and right heart failure

26. Laboratory examination
Electrocardiography (ECG)
Left atrial enlargement
Mitral valve P wave
P-wave duration in lead II ＞ 0.12 s
Large terminal negative P force in lead V1
Right ventricular hypertrophy
Arrhythmia
Premature atrial contraction → atrial fibrillation

27. Radiological findings
“Mitral valve heart”
Marked enlargement of LA
Enlargement of RV
Dilatation of PA
Pulmonary congestion
Interstitial edema (manifested as Kerley B lines)

28. Echocardiography
The most valuable technique for diagnosing MS,
and determining its severity
M-mode echo ：
Thickened, calcified leaflets
open poorly, close slowly (EF slope↓)
The double peaks disappear
Both leaflets move anteriorly during early diastole
Two-dimensional echo:
Fusion, thickening, doming of the valve leaflets, and
poor leaflet separation in diastole; mitral orifice area↓

29. Doppler echo ：
Most accurate noninvasive technique for quantifying the
severity of MS
Spectrum Doppler: measure transvalvular gradient, MVA
Color Doppler: display high velocity color jet
Provide other important information
Cardiac chamber size (LA, RV)
Left ventricular contractility
Pulmonary arterial pressure
Other coexisted valvular or congenital abnormalities
Mural thrombi

30. Cardiac catheterization
Its value in assessment of patients with MS or
suspected MS has been largely superseded by
echocardiography
If surgery is planned, coronary angiography is
performed to ascertain whether or not bypass
grafting is indicated in patients at risk of having
coexisting coronary artery disease

31. Diagnosis and differential diagnosis
Diagnosis Diastolic rumbling murmur at apex
ECG or X ray reveals LA dilatation
Confirmed by echocardiography
Differential diagnosis Diastolic murmur at apex
Increased flow across mitral valve
Severe MR
Massive left to right shunts （ VSD, PDA ）
Hyperdynamic circulation （ hyperthyroid, anemia ）
Austin-Flint murmur （ severe AR ）
Left atrial myxoma postural change of the murmur
other signs of myxoma
Graham Steell murmur
should be differentiated from aortic regurgitation

32. Complication
Atrial fibrillation Common
↓cardiac output by about 20%
LA↑, age↑→ Incidence↑
Acute pulmonary edema Severe
Dyspnea and cyanosis; unable to lie on back
pink, frothy sputum; both lungs filled with rales
Thromboembolism
Develop in 20% of patients
About 2/3 found in the cerebral vessels
Recurrent and multiple
Risk factors: AF, LA ＞ 55mm, a history of recent
embolism or a low cardiac output

33. Right ventricular failure
Late stage, main cause of death
Dyspnea and hemoptysis↓—“protective effect”
(RV CO↓→ pulmonary circulation↓→LAP↓;
thickening of alveolus & pulmonary capillary walls)
Infective endocarditis
Occurs less frequently on rigid, thickened, calcified
valves and is therefore more common in patients
with mild than with severe MS
Respiratory infection
Common
Induce and aggregate heart failure

34. Management
General treatment
① Patients with RHD should receive penicillin
prophylaxis to prevent recurrence of RF and
prophylaxis for IE
Avoid and control anemia and infections
② Asymptomatic patients: avoid strenuous
exertion
③ Patients with dyspnea should reduce physical
activity, restrict sodium intake, and take oral
diuretics

35. Treatment of complications
Profuse hemoptysis
Measures designed to reduce pulmonary venous pressure,
including sedation, assumption of the upright posture, and
aggressive diuresis, are used to treat hemoptysis
Acute pulmonary edema
Dilate venous system, reduce preload (nitrates)
Avoid dilating small artery
Digitalis glycosides do not benefit patients with MS and sinus
rhythm, but are of great value in slowing the ventricular rate
in patients with AF and in the treatment of right-sided HF

36. Treatment of Arrhythmias
AF with rapid ventricular rate:
↓Ventricular rate (70~80 bpm) ：
Digitalis glycosides （ iv cedilanid, oral digoxin ）
β-blockers
In patients with mild MS without marked LA dilation
who have been in AF less than 6~12 months, elective
cardioversion (electrical or pharmacological) should
be considered

37. Prophylactic anticoagulant treatment
AF
Previous embolic episodes
LA thrombus revealed by echocardiography
Long term anticoagulant treatment with warfarin is
necessary in patients without contraindication
Right ventricular failure
Restriction of sodium intake
Diuretics
Nitrates

38. Indications for relieving stenosis
Symptomatic patients with moderate to severe MS
(MVA ＜ 1.5 cm2), or evidence of pulmonary
hypertension with RV hypertrophy
Recurrent systemic emboli despite anticoagulation
with moderate or severe stenosis
Percutaneous balloon mitral
valvuloplasty （ PBMV）
Procedure of choice for pure MS with pliable and
noncalcific valve

39. Surgical techniques
Open mitral commissurotomy
Indication:
Patients without significant MR
valvular calcification, involvement of chordae and
papillary muscle, left atrial thrombus or restenosis
Mitral valve replacement
Indication:
Severe distortion and extensive calcification of the
valve
and subvalvular apparatus;
Associated with significant MR or aortic valve disease

40. Mitral regurgitation (MR)
Etiology
Mitral valve apparatus and/or LV structural
and functional abnormality
RHD: common(1/3); + MS and/ or aortic valve disease
Mitral valve prolapse (MVP)
myxomatous degeneration, floppy and redundancy
Ischemic heart disease (or CAD)
papillary muscle dysfunction
Mitral annular calcification

41. Severe dilatation of LV
result in dilatation of the mitral annulus and
lateral movement of papillary muscle
Infective endocarditis
valve leaflets destruction, perforation, retraction;
valve closure interfered by vegetation
Other causes:
Rupture of the chordae
congenital abnormalities
obstructive hypertrophic cardiomyopathy

42. Hemodynamic changes
MR involves mainly LA and LV
Chronic MR
Compensation: MR→ LV volume↑→LV, LA↑→
LVEDV↑→ SV↑→ CO↑, EF↑
Decompensation:
Left HF, LAP and LVEDP↑ → pulmonary congestion,
pulmonary hypertension, right HF
(hepatomegaly, edema, and ascites)
CO↓
Acute MR
MR →LA, LV volume↑→LVEDP↑→LAP↑→
↓ pulmonary congestion, pulmonary edema
SV and CO↓

43. Clinical manifestations
Symptoms
Chronic MR
Mild— no symptom
Severe— left-sided heart failure
Weakness, fatigue (CO↓)
Dyspnea (pulmonary congestion)
RHD: symptoms occur late, once present, LV
dysfunction is usually irreversible
MVP: asymptomatic, or atypical chest pain,
palpitation, fatigue; in severe MR, left
HF occur at late stage
Acute Mild— mild exertional dyspnea
Severe— acute left HF, pulmonary edema,
or cardiac shock

44. Physical examination
Cardiac impulse at apex
Hyperdynamic
Displaced laterally, inferiorly (Chronic)
Changes of heart sounds
S1↓(RHD) or normal (MVP, CAD)
S3 (severe MR): prominent
Mid or late systolic click （ MVP ）
（ Acute: P2↑ ， S4 ）

45. Systolic murmur
RHD ： Pansystolic, blowing, high-pitched murmur
maximal at the apex
Anterior valve lesion, radiate to the axilla and back
Posterior leaflet abnormality, radiate to the base
MVP ： mid- to late-systolic murmur
Dysfunction of papillary muscles:
Variable (early, mid, late or holosystolic)
Rupture of the chordae: musical
(Acute MR: not pansystolic murmur, but lower-pitched,
decrescendo, and softer than the murmur of chronic MR )

46. Laboratory examination
ECG
Chronic (severe) MR:
LA dilation, Atrial fibrillation
LV enlargement and non-specific ST-T changes
Acute MR: sinus tachycardia
Radiological findings
Chronic (severe) MR:
Cardiomegaly with LA, LV↑; pulmonary congestion,
interstitial edema with Kerley B lines (left HF)
C-shaped calcification of mitral annulus
Acute MR:
Normal cardiac silhouette or mild LA dilation
overt pulmonary congestion, edema

47. Echocardiography
1 、 Display anatomy of the mitral valve apparatus
Useful in determining the etiology of MR (2D)
2 、 Confirm the existence of MR
Doppler (color, spectrum): reveal high-velocity jet into
LA during systole
Sensitivity~100%
Estimate the severity of MR
＜ 4 cm2 Mild
（ Color flow jet area ） 4~8 cm2 Moderate
＞ 8 cm2 Severe
3 、 Measure cardiac chamber sizes, evaluate LV
function, pulmonary artery pressure, provide
data concerning other valvular lesions

48. Radionuclide angiography and MRI
Evaluate LV function
Estimate the severity of regurgitation
The regurgitant fraction can be estimated from
the ratio of LV to RV (LV/RV) stroke volume
Cardiac catheterization
Confirm the diagnosis of MR and estimate
its severity, evaluate cardiac function and
pulmonary artery pressure
Coronary angiography is performed to
determine presence of CAD prior to surgery

49. Diagnosis
Chronic MR
Typical systolic murmur at apex associated
with enlargement of LA and LV
Acute MR
Sudden onset of dyspnea
Systolic murmur at apex
Normal cardiac silhouette, but obvious
pulmonary congestion
etiology existed
Confirmed by Echocardiography

50. Differential diagnosis
Tricuspid regurgitation (TR)
SM heard best along the left sternal border
augmented during inspiration
Ventricular septal defect (VSD)
SM loudest at the left sternal border
accompanied by a parasternal thrill
Systolic ejecting murmur at left sternal border:
aortic or pulmonic stenosis
hypertrophic obstructive cardiomyopathy
Echocardiography

51. Complication
Atrial fibrillation
seen frequently in severe cases
Infective endocarditis
more common than in MS
Systemic embolism
less common than in MS
Heart failure
occur early in acute MR
but late in chronic MR

52. Management
Chronic MR
Medical treatment
① Prevention: same as in MS
② Asymptomatic patients with normal cardiac
function ： follow-up regularly
③ Management of AF ： similar to that in MS
(slow ventricular rate, anticoagulation)
④ Treatment of heart failure ： restriction of
sodium intake, angiotensin-converting enzyme
inhibitors (ACEI), diuretics, digitalis glycosides

53. Surgical treatment
Mitral valve replacement
Indications
① Severe MR and in functional Class Ⅲ or Ⅳ
② Functional ClassⅡ associated with LV dilation
(LVESD ＞ 45mm on echocardiography)
③ Severe MR, progressive deterioration of LVEF↓,
LVESD and LVEDD↑
Mitral valve repair
Indications
MVP
Chordal rupture
Mitral annulus dilation

54. Acute MR
Principle
Reduce pulmonary venous pressure
Increase cardiac output
Correct etiology
Medical treatment
Intravenous nitroprusside
Intravenous diuretics
ACEI and other vasodilators
Surgical treatment
Mitral valve replacement
Mitral valve repair

55. Aortic stenosis (AS)
Etiology
RHD
Common, + AR and mitral valve disease
Degenerative calcific AS
Common in the elderly, accompanied by calcification of
the mitral annulus
Congenital abnormalities
Calcific stenosis of congenitally bicuspid aortic valve
Congenital aortic stenosis

56. Hemodynamic changes
Normal aortic orifice area (AOA): 3.0~4.0 cm2
AOA ≤1.0cm2, LVSP↑, with significant transvalvular
gradient
Compensation
AS→LV pressure load↑
Concentric LVH→compliance↓→LVEDP↑→LAH
Maintain systolic wall stress and CO ↑LVEDV
Decompensation
LVEDV↑→wall stress↑, myocardial ischemia, fibrosis
→ left HF

57. Clinical manifestations
Symptoms
Cardinal symptoms: dyspnea, angina and syncope
1. Dyspnea: exertional dyspnea
orthopnea
paroxysmal nocturnal dyspnea
acute pulmonary edema
(varying degrees of pulmonary venous hypertension)
2. Angina pectoris:
occurs frequently in patients with critical AS,
>1/3 associated with coronary artery disease

58. Mechanisms of ischemia ：
① Myocardial oxygen consumption↑: LVH, LVSP↑, LVET↑
② Relative decrease in myocardial capillary density
③ Subendocardial coronary artery compression: LVDP↑
④ Coronary perfusion pressure↓: AO pressure↓, LVDP↑
Imbalance between myocardial oxygen demand and supply
3. Syncope: typically exertional
Arterial pressure↓→ cerebral perfusion↓
Mechanisms:
Increase blood flow to exercising muscle without
compensatory increase in cardiac output
Severe arrhythmias

59. Physical examination
Systolic ejection murmur
Blowing, harsh, crescendo-decrescendo
Maximal at aortic area (R2 or L3, 4)
Transmitted to the neck and apex
May be associated with systolic thrill
The more severe the AS, the longer the duration
of the murmur
When the LV fails and the CO falls, the murmur
becomes softer or disappear

60. Heart sound changes
S1 normal or soft
A2 weak or absent
paradoxical splitting of S2
prominent S4
Aortic ejection sound
congenital AS or pliable valve AS
Other signs
Left ventricular heave
Systolic and pulse pressures↓
Delayed and diminished carotid pulses

61. Laboratory examination
ECG
Severe: LVH and secondary ST-T changes,
LA↑ ， arrhythmias
Radiological findings
Normal size or slightly enlarged heart
Calcification of the aortic valve
Poststenotic dilatation of the ascending aorta
Pulmonary congestion

62. Echocardiography
Establish a diagnosis, and determine the
severity of AS
M-mode and 2D echo
Observe aortic valve opening, thickening and
calcification
Helpful in determining the etiology of AS
Also invaluable in detecting associated mitral
valve disease and in assessing LV performance,
hypertrophy, and dilatation

63. Doppler echo
Allows calculation of the aortic valve gradient
Estimate the severity of the stenosis
＜ 30 mmHg Mild AS
MPG 30~50 mmHg Moderate AS
＞ 50 mmHg Severe
AS
Color Doppler flow imaging is helpful in the
detection and determination of the severity of
any accompanying aortic regurgitation

64. Cardiac catheterization
Determine the severity of AS by measuring
systolic LV and aortic pressure simultaneously,
and calculating the valve area
An average pressure gradient of ＞ 50mmHg or
peak pressure gradient of ≥ 70mmHg represent
severe AS
Coronary angiography is performed in most
adults to assess for concomitant coronary disease

65. Diagnosis and differential diagnosis
Diagnosis
Typical systolic murmur of AS
Associated with AR and/or mitral valve damage——RHD
Pure AS:
Infants and young children——unicuspid malformation
Childhood ~65 years——calcification of bicuspid AV
＞ 65 years——degenerative calcification
Confirmed by echocardiography

66. Differential diagnosis
Transmitted murmur （ MR, TR,
VSD ）
Other LVOT obstructive disease
Congenital supravalvular AS
Congenital subvalvular AS
Hypertrophic obstructive cardiomyopathy

67. Management
Medical treatment
 Treatment of Arrhythmias: prevent AF with an
antiarrhythmic agent when premature atrial
contractions are frequent; when AF does occur,
restore sinus rhythm
 Treatment of angina pectoris: nitrates
 Treatment of heart failure: diuretics must be
used with caution; vasodilators should be
avoided

68. Surgical treatment
Valve replacement
Indications:
① Repeated occurrence of syncope, angina pectoris or
significant left heart failure
② Asymptomatic patients with progressive LV dysfunction
and/or LV hypertrophy, and very high transvalvular
gradient ( ＞ 80mmHg)
③ Severe AS （ AOA≤0.7 cm2 ）
Commissural incision under direct vision
In children and adolescents with noncalcific
severe congenital AS

69. Percutaneous balloon valvuloplasty
Indications
Children and adolescents with congenital noncalcific AS
Adults with severe calcific AS who are poor candidates
for surgery or as an intermediate procedure prior to
surgery:
①Patients with cardiogenic shock due to critical AS
②Patients with critical AS who require an urgent noncardiac
operation
③Pregnant women with critical AS
④Patients with critical AS who refuse surgical treatment

70. Aortic regurgitation (AR)
Etiology
Primary disease of the aortic valves
and/ or aortic root

71. Aortic valve disease
① RHD ： most common, about 2/3
+ AS and/or mitral valve disease
② Infective endocarditis
③ Congenital deformity: bicuspid valves
④ Myxomatous degeneration of the aortic valve
Aortic root dilatation
① Marfan syndrome
② Aortic dissection (involve annulus or leaflets)
③ Syphilitic aortitis

72. Hemodynamic changes
Chronic AR
Compensation ：
AR→LV volume↑→ LV↑, LVEDV↑→ SV↑(CO)
Decompensation:
LV systolic dysfunction→ LV failure (EF↓, LVESV↑)
Acute AR
AR →LV volume↑→ LVDP↑→ LAP↑
↓ ↓
CO↓ pulmonary congestion
pulmonary edema

73. Clinical manifestations
Symptoms
Chronic AR
Asymptomatic for many years
Palpitation, precordial discomfort, head pounding
(related to SV↑)
LV failure (dyspnea, fatigue): occur at late stage
Angina pectoris or chest pain: less common
Acute AR
mild—no symptom
severe—Acute LV failure and hypotension
(pulmonary edema)

74. Physical examination
Chronic, severe AR
① Peripheral arterial signs: Owing to wide pulse pressure:
SBP↑, DBP↓
Water-hammer pulse (rapid rise and fall)
“Pistol shot sounds” (booming systolic & diastolic sounds
sounds
heard over femoral artery)
Duroziez’s sign (systolic, diastolic murmur over partially
compressed femoral artery)
Quincke’s sign (subungual capillary pulsations)
de Musset’s sign (head bobs with each heartbeat )
② Apical impulse: diffuse and forceful, displaced laterally
and inferiorly (hyperactive, enlarged LV)
③ Heart sound: An S3 gallop is common with LV failure

75. ④ Heart murmurs
Aortic diastolic murmur:
High-pitched, blowing, decrescendo pattern
When AR is due to primary valvular disease, the diastolic
murmur is best heard along the left sternal border in the
3rd and 4th intercostal spaces
However, when it is due mainly to dilatation of the ascending
aorta, the murmur is often more readily audible along the
right upper sternal border
Austin-Flint murmur:
apical mid or late diastolic low-pitched murmur:
common in severe AR, owing to partial closure of MV by
the regurgitant jet

76. Ejection systolic murmur:
common
harsh
at the base of the heart
accompanied by a systolic thrill
Acute AR
S1 soft or absent ， P2↑ ， S3 and S4
AR murmur: lower pitched and shorter than
that of chronic AR
Austin-Flint murmur: brief

77. Laboratory examination
ECG
Acute: sinus tachycardia; nonspecific ST-T changes
Chronic: LV enlargement and hypertrophy, arrhythmias
Radiological findings
Acute AR: cardiac size normal or slightly enlarged
signs of pulmonary congestion, pulmonary edema
Chronic: LV enlargement, associated with dilatation of
the ascending aorta
Severe, aneurysmal dilatation of the aorta suggests
aortic root disease （ Marfan syndrome ）
Pulmonary congestion （ LV heart failure ）

78. Echocardiography
Confirm diagnosis, estimate severity, identify the cause
2-D echo:
Structural changes of the valve leaflets and/or aortic root
M mode echo:
Diastolic fluttering of the anterior leaflet of the mitral
valve is an important echocardiographic finding in AR
Serial assessments of LV size and function
Doppler echo:
Sensitive, accurate noninvasive technique for detecting AR
LVOT diastolic regurgitant jet, estimate the severity of AR
Cardiac catheterization
Quantify the severity of AR
Evaluate the coronary and aortic root anatomy

79. Diagnosis and differential diagnosis
Diagnosis
Characteristic diastolic murmur associated with peripheral
arterial signs, make a diagnosis of AR
Combined with other information, etiology is usually found
Differential diagnosis
Graham Steell murmur (pulmonary hypertension associated
with dilatation)
Austin-Flint murmur: differentiated from that of MS

80. Management
Chronic AR
Medical treatment
① Asymptomatic patients with severe AR and LV dilation:
Vasodilators (ACEI, et al) reduce the severity of AR,
should be used to prolong the compensated period
β-blocker: slow the rate of aortic dilation in Marfan’s
② Patients with HF:
Vasodilators (ACEI), diuretics and digitalis glycosides

81. Surgical treatment
Valvular replacement
Indications:
① Symptomatic patients
② Asymptomatic patients with LV dysfunction,
with persistent or progressive LVESV↑or
EF↓at rest
Repair or replacement of the root
Aortic root disease

82. Acute AR
Medical treatment
Principle: reduce pulmonary venous pressure, increase
cardiac output, and stabilize hemodynamics
Intravenous nitroprusside
Diuretics
Positive inotropic agent
Antibiotics （ active IE ）
Surgical treatment
Urgently required
Valvular replacement or aortic valve repair