Valvular Heart DiseaseValvular Heart Disease

Dept. Cardiology, 2nd Hospital,

Sun Yat-sen Univ.

YANG Li

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

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

Etiology and Pathogenesis

Multiple factors contribute to the pathogenesis, including -hemolytic streptococcal pharyngitis and immunological status of the human body

Cross immune response between host and streptococcal antigens

Streptococcal pharyngitis ↓Abnormal reaction-autoimmunity disease

Pathology

Pathological characters:Exudative and proliferative inflammatory reactions involving connective or collagen tissueAffects primarily the heart, joints, brain, cutaneous and subcutaneous tissues

Pathological process ：Exudative stageProliferative stage: Aschoff nodule (pathognomonic)Fibrosis and calcification (scar formation)

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%

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

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)

DiagnosisBased 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

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

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

3. Treatment of symptoms and complicationsIf 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

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)

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)

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

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

Secondary changes ：Chronic MS → Dilatation of the left atrium

Fibrosis of the atrial wall

Development of mural thrombi

Hypertrophy and dilation of RV

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

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

3. Effect of pulmonary hypertension on RV

Pulmonary hypertension

↓ RV hypertrophy & dilation （ secondary TR, PR ） ↓ Right ventricular failure

Clinical manifestationsSymptoms 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

Physical examination

Cardiac signs of MSChanges of heart sounds:

Accentuated S1Accentuated S1 Opening snap (OS)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

Diastolic murmur of MSDiastolic 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

Cardiac signs secondary to pulmonaryhypertension and RV dilation RV pulsation is present at the left parasternal region

Accentuated or splitting of P2 may be heard in thesecond 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 pansystolicmurmur may be audible in the 4th or 5th intercostalspace in the left parasternal region

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

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

Radiological findings

“Mitral valve heart”

Marked enlargement of LAEnlargement of RVDilatation of PA

Pulmonary congestionInterstitial edema (manifested as Kerley B lines)

EchocardiographyThe most valuable technique for diagnosing MS, and determining its severity

M-mode echoM-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:Two-dimensional echo: Fusion, thickening, doming of the valve leaflets, and poor leaflet separation in diastole; mitral orifice area↓

Doppler echoDoppler echo ：：Most accurate noninvasive technique for quantifying the severity of MS

Spectrum Doppler: measure transvalvular gradient, MVAColor Doppler: display high velocity color jet

Provide other important informationCardiac chamber size (LA, RV)Left ventricular contractilityPulmonary arterial pressureOther coexisted valvular or congenital abnormalities Mural thrombi

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

Diagnosis and differential diagnosisDiagnosis 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

ComplicationAtrial 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

Right ventricular failureLate stage, main cause of deathDyspnea and hemoptysis↓—“protective effect”(RV CO↓→ pulmonary circulation↓→LAP↓;thickening of alveolus & pulmonary capillary walls)

Infective endocarditisOccurs less frequently on rigid, thickened, calcifiedvalves and is therefore more common in patients with mild than with severe MS

Respiratory infection Common Induce and aggregate heart failure

ManagementGeneral 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

exertion③ Patients with dyspnea should reduce physical

activity, restrict sodium intake, and take oral diuretics

Treatment of complicationsProfuse hemoptysisMeasures 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

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

Prophylactic anticoagulant treatment AF Previous embolic episodes LA thrombus revealed by echocardiographyLong term anticoagulant treatment with warfarin is necessary in patients without contraindication

Right ventricular failure Restriction of sodium intake Diuretics Nitrates

Indications for relieving stenosisSymptomatic 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

Surgical techniques

Open mitral commissurotomyIndication: Patients without significant MR valvular calcification, involvement of chordae and papillary muscle, left atrial thrombus or restenosis

Mitral valve replacementIndication: Severe distortion and extensive calcification of the valve and subvalvular apparatus; Associated with significant MR or aortic valve disease

Mitral regurgitation (MR)EtiologyMitral 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

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

Hemodynamic changesMR involves mainly LA and LVChronic MRCompensation: 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 edemaSV and CO↓

Clinical manifestationsSymptomsChronic 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

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 ）

Systolic murmurRHD ： Pansystolic, blowing, high-pitched murmurPansystolic, 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 murmurDysfunction 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)

Laboratory examination

ECGChronic (severe) MR: LA dilation, Atrial fibrillation LV enlargement and non-specific ST-T changes

Acute MR: sinus tachycardia

Radiological findingsChronic (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

Echocardiography1 、 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

Radionuclide angiography and MRIEvaluate 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 catheterizationConfirm the diagnosis of MR and estimate its severity, evaluate cardiac function andpulmonary artery pressureCoronary angiography is performed todetermine presence of CAD prior to surgery

Diagnosis

Chronic MRTypical systolic murmur at apex associated with enlargement of LA and LV

Acute MRSudden onset of dyspneaSystolic murmur at apexNormal cardiac silhouette, but obvious pulmonary congestionetiology existed

Confirmed by Echocardiography

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

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

Management

Chronic MR

Medical treatment① 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

Surgical treatment

Mitral valve replacementIndications ① Severe MR and in functional Class or Ⅲ Ⅳ

② Functional Class associated with LV dilation Ⅱ

(LVESD ＞ 45mm on echocardiography)

③ Severe MR, progressive deterioration of LVEF↓,

LVESD and LVEDD↑

Mitral valve repair Indications MVP Chordal rupture Mitral annulus dilation

Acute MRPrinciple 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

Aortic stenosis (AS)

EtiologyRHD 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

Hemodynamic changesNormal aortic orifice area (AOA): 3.0~4.0 cm2AOA ≤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

Clinical manifestationsSymptomsCardinal 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

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

Physical examination

Systolic ejection murmurSystolic 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

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

Laboratory examination

ECGSevere: LVH and secondary ST-T changes,

LA↑ ， arrhythmias

Radiological findingsNormal size or slightly enlarged heart

Calcification of the aortic valve

Poststenotic dilatation of the ascending aorta

Pulmonary congestion

EchocardiographyEstablish a diagnosis, and determine the severity of AS

M-mode and 2D echo Observe aortic valve opening, thickening and calcificationHelpful in determining the etiology of AS

Also invaluable in detecting associated mitral valve disease and in assessing LV performance, hypertrophy, and dilatation

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

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

Diagnosis and differential diagnosis

DiagnosisTypical systolic murmur of ASAssociated 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

Differential diagnosis

Transmitted murmur （ MR, TR, VSD ）

Other LVOT obstructive disease Congenital supravalvular AS

Congenital subvalvular AS

Hypertrophic obstructive cardiomyopathy

ManagementMedical 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

Surgical treatment

Valve replacementIndications: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

Percutaneous balloon valvuloplasty

IndicationsChildren 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

Aortic regurgitation (AR)

Etiology

Primary disease of the aortic valves

and/ or aortic root 

Aortic valve disease① RHD ： most common, about 2/3 + AS and/or mitral valve disease

② Infective endocarditis③ Congenital deformity: bicuspid valves

④ Myxomatous degeneration of the aortic valve

Aortic root dilatation① Marfan syndrome② Aortic dissection (involve annulus or leaflets) ③ Syphilitic aortitis

Hemodynamic changes

Chronic ARCompensation ： AR→LV volume↑→ LV↑, LVEDV↑→ SV↑(CO)

Decompensation: LV systolic dysfunction→ LV failure (EF↓, LVESV↑)

Acute ARAR →LV volume↑→ LVDP↑→ LAP↑ ↓ ↓CO↓ pulmonary congestion pulmonary edema

Clinical manifestationsSymptomsChronic ARAsymptomatic for many yearsPalpitation, precordial discomfort, head pounding

(related to SV↑)LV failure (dyspnea, fatigue): occur at late stage

Angina pectoris or chest pain: less common

Acute ARmild—no symptomsevere—Acute LV failure and hypotension (pulmonary edema)

Physical examinationChronic, severe AR

① Peripheral arterial signs: Owing to wide pulse pressure: SBP↑, DBP↓

Water-hammer pulse Water-hammer pulse (rapid rise and fall)

“Pistol shot soundsPistol shot sounds” (booming systolic & diastolic sounds heard over femoral artery) Duroziez’s signDuroziez’s sign (systolic, diastolic murmur over partially compressed femoral artery) Quincke’s sign Quincke’s sign (subungual capillary pulsations)

de Musset’s sign 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

④ Heart murmurs

Aortic diastolic murmur: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

Ejection systolic murmur: common harsh at the base of the heart accompanied by a systolic thrill

Acute ARS1 soft or absent ， P2↑ ， S3 and S4AR murmur: lower pitched and shorter than that of chronic ARAustin-Flint murmur: brief

Laboratory examinationECG Acute: sinus tachycardia; nonspecific ST-T changes

Chronic: LV enlargement and hypertrophy, arrhythmias

Radiological findingsAcute 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 ）

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

Diagnosis and differential diagnosis

DiagnosisCharacteristic diastolic murmur associated with peripheral arterial signs, make a diagnosis of AR

Combined with other information, etiology is usually found

Differential diagnosisGraham Steell murmur (pulmonary hypertension associated with dilatation)

Austin-Flint murmur: differentiated from that of MS

ManagementChronic AR

Medical treatment① 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

-blocker: slow the rate of aortic dilation in Marfan’s

② Patients with HF: Vasodilators (ACEI), diuretics and digitalis glycosides

Surgical treatmentValvular 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

Acute AR

Medical treatmentPrinciple: reduce pulmonary venous pressure, increase cardiac output, and stabilize hemodynamics

Intravenous nitroprusside

Diuretics

Positive inotropic agent

Antibiotics （ active IE ）

Surgical treatmentUrgently required

Valvular replacement or aortic valve repair