Valvular heart disease


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Valvular heart disease

  1. 1. Valvular Heart Disease
  2. 2. Rheumatic feverRheumatic fever (RF) is generally classified as aconnective tissue or collagen-vascular diseaseIt is an inflammatory reaction that causes damage tocollagen fibrils and to the ground substance ofconnective tissueInvolves multiple organs: primarily the heart, thejoints, and the central nervous systemRecurrent attacks of RF may cause fibrosis of heartvalves, leading to chronic valvular heart disease
  3. 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 rheumaticheart disease (RHD) are markedly variable indifferent countries: In developed country, such as the united states,the incidence of RF < 2/100,000 In many developing countries, the incidence ofacute RF approaches or exceeds 100/100,000
  4. 4. Etiology and Pathogenesis Multiple factors contribute to the pathogenesis,including β-hemolytic streptococcal pharyngitisand immunological status of the human body Cross immune response between host andstreptococcal antigens Streptococcal pharyngitis ↓ Abnormal reaction-autoimmunity disease
  5. 5. PathologyPathological characters:Exudative and proliferative inflammatory reactions involving connective or collagen tissueAffects primarily the heart, joints, brain, cutaneous and subcutaneous tissuesPathological process :Exudative stageProliferative stage: Aschoff nodule (pathognomonic)Fibrosis and calcification (scar formation)
  6. 6. Recurrent attacks of RF (rheumatic carditis,valvulitis) → scar formation and deformity ofheart valves → chronic RHDValvular involvement: Mitral valve: 75%~80% Aortic valve: 30% Tricuspid & pulmonary valves: < 5%
  7. 7. Clinical findings 1 、 Major manifestations ① Carditis: pericarditis, cardiomegaly, congestiveheart 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. 8. 2 、 Minor manifestations① Clinical findings: fever, polyarthralgias② Laboratory findings Elevated acute phase reactants: ESR (erythrocyte sedimentation rate) CRP (C reactive protein)③ ECG change: prolonged P-R interval④ A history of RFSupporting evidence of an antecedent group A streptococcal infection:① Positive throat culture or rapid streptococcal antigen test② Elevated or rising titers of antistreptococcal antibodies (anti-streptolysin O and anti-DNase B)
  9. 9. Diagnosis Based on Jones criteria and confirmation ofstreptococcal infection Guidelines for the diagnosis of initial attacks of RF(Jones criteria, updated 1992) If supported by evidence of preceding group Astreptococcal infection, the presence of two majormanifestations or of one major and two minormanifestations establishes the diagnosis of acute RF
  10. 10. TreatmentGeneral Measures Strict bed restMedical Measures1. 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. 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. 12. 3. Treatment of symptoms and complications If heart failure is present, digitalis preparations should beused cautiously because cardiac toxicity may occur withconventional 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. 13. Mitral stenosis (MS)EtiologyMost commonly rheumatic fever——rheumatic heart disease ( RHD )Symptoms commence mostly in 2nd~4th decade2/3 of all patients are female25% of all patients with RHD have pure MS40% have combined MS and mitral regurgitation (MR)
  14. 14. Other rare causesFar less frequently, MS is congenital in etiology observed primarily in infants and young childrenCalcification of mitral annulus (when subvalvular or intravalvular extension is extensive) observed in old patientsVery rarely, MS is a complication of carcinoiddisease or connective tissue disease (systemic lupuserythematosus, SLE; rheumatoid arthritis)
  15. 15. PathologyFibrosis, thickening, rigid and calcification of the valveapparatusRheumatic fever results in four forms of fusion of themitral valve apparatus leading to stenosis:Commissural, cuspal, chordal, and combinedCharacteristically, mitral valve cusps fuse at theiredges, and fusion of the chordae results in thickeningand shortening of these structures
  16. 16. Commissural adherent and fusion ↓restricted opening of mitral valve ↓“fish mouth” shape of mitral valve orificeThickening, fusion and shortening of thechordae or papillary muscles ↓funnel-shaped change of valve apparatus
  17. 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. 18. Hemodynamic changes MS involves mainly LA and RV1. Effect of MS on left atrioventricular pressuregradient and left atrial pressure (LAP) MVA transvalvular gradient LAPNormal 4 ~ 6cm2Mild MS > 1.5cm2 5-10mmHg ↑Moderate 1.0 ~ 1.5cm2 10-20mmHg ↑↑Severe < 1.0cm2 ≥20mmHg 25mmHg
  19. 19. 2. Effect of elevated LAP on pulmonary circulationThe elevated LAP in turn raises pulmonary venous and capillarypressures (PVP, PCP), resulting in exertional dyspnea LAP↑ → PVP↑→ PCP↑→ Dyspnea Lung compliance↓Pulmonary hypertension results from:1. Passive backward transmission of the elevated LAP2. Reactive pulmonary arteriolar constriction, which presumablyis triggered by left atrial and pulmonary venous hypertension3. Organic obliterative changes in the pulmonary vascular bed,which may be considered to be a complication of longstanding andsevere MS
  20. 20. 3. Effect of pulmonary hypertension on RV Pulmonary hypertension ↓ RV hypertrophy & dilation ( secondary TR, PR ) ↓ Right ventricular failure
  21. 21. 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 edemaHemoptysis Profuse hemorrhage: rupture of bronchial submucosal varices Blood-stained sputum Pink, frothy sputumCough occurs frequently respiratory infection, compression of left bronchusHoarseness (Ortner’s syndrome), less common Compression of left recurrent laryngeal nerve
  22. 22. Physical examinationCardiac signs of MSChanges 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. 23. Diastolic murmur of MS A low-pitched, diastolic rumbling murmur,localized at or near apex, with pre-systolicaccentuation in patients with sinus rhythm Auscultation of the murmur is facilitated byplacing the patient in the left lateral position andauscultate during expiration When the patient is in the left lateralrecumbent position, a mid-diastolic or presystolicthrill may be palpable at apex
  24. 24. 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
  25. 25. Other signsMitral face: malar flushSigns of right heart failure:Systemic venous hypertension, hepatomegaly, edema,and ascites are all signs of severe MS with elevatedpulmonary vascular resistance and right heart failure
  26. 26. Laboratory examinationElectrocardiography (ECG)Left atrial enlargement Mitral valve P wave P-wave duration in lead II > 0.12 s Large terminal negative P force in lead V1Right ventricular hypertrophyArrhythmia Premature atrial contraction → atrial fibrillation
  27. 27. Radiological findings“Mitral valve heart”Marked enlargement of LAEnlargement of RVDilatation of PAPulmonary congestionInterstitial edema (manifested as Kerley B lines)
  28. 28. EchocardiographyThe most valuable technique for diagnosing MS,and determining its severityM-mode echo : Thickened, calcified leaflets open poorly, close slowly (EF slope↓) The double peaks disappear Both leaflets move anteriorly during early diastoleTwo-dimensional echo: Fusion, thickening, doming of the valve leaflets, andpoor leaflet separation in diastole; mitral orifice area↓
  29. 29. Doppler echo :Most accurate noninvasive technique for quantifying theseverity of MSSpectrum Doppler: measure transvalvular gradient, MVAColor Doppler: display high velocity color jetProvide other important informationCardiac chamber size (LA, RV)Left ventricular contractilityPulmonary arterial pressureOther coexisted valvular or congenital abnormalitiesMural thrombi
  30. 30. Cardiac catheterization Its value in assessment of patients with MS orsuspected MS has been largely superseded byechocardiography If surgery is planned, coronary angiography isperformed to ascertain whether or not bypassgrafting is indicated in patients at risk of havingcoexisting coronary artery disease
  31. 31. Diagnosis and differential diagnosisDiagnosis Diastolic rumbling murmur at apex ECG or X ray reveals LA dilatation Confirmed by echocardiographyDifferential diagnosis Diastolic murmur at apexIncreased 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 myxomaGraham Steell murmur should be differentiated from aortic regurgitation
  32. 32. ComplicationAtrial fibrillation Common↓cardiac output by about 20% LA↑, age↑→ Incidence↑Acute pulmonary edema SevereDyspnea and cyanosis; unable to lie on backpink, frothy sputum; both lungs filled with ralesThromboembolismDevelop in 20% of patientsAbout 2/3 found in the cerebral vesselsRecurrent and multipleRisk factors: AF, LA > 55mm, a history of recent embolism or a low cardiac output
  33. 33. 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 patientswith mild than with severe MSRespiratory infectionCommonInduce and aggregate heart failure
  34. 34. 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 exertion ③ Patients with dyspnea should reduce physical activity, restrict sodium intake, and take oral diuretics
  35. 35. Treatment of complicationsProfuse hemoptysisMeasures designed to reduce pulmonary venous pressure,including sedation, assumption of the upright posture, andaggressive diuresis, are used to treat hemoptysisAcute pulmonary edema Dilate venous system, reduce preload (nitrates) Avoid dilating small arteryDigitalis glycosides do not benefit patients with MS and sinusrhythm, but are of great value in slowing the ventricular ratein patients with AF and in the treatment of right-sided HF
  36. 36. Treatment of ArrhythmiasAF with rapid ventricular rate:↓Ventricular rate (70~80 bpm) : Digitalis glycosides ( iv cedilanid, oral digoxin ) β-blockersIn patients with mild MS without marked LA dilationwho have been in AF less than 6~12 months, electivecardioversion (electrical or pharmacological) shouldbe considered
  37. 37. Prophylactic anticoagulant treatment AF Previous embolic episodes LA thrombus revealed by echocardiographyLong term anticoagulant treatment with warfarin isnecessary in patients without contraindicationRight ventricular failure Restriction of sodium intake Diuretics Nitrates
  38. 38. Indications for relieving stenosisSymptomatic patients with moderate to severe MS(MVA < 1.5 cm2), or evidence of pulmonaryhypertension with RV hypertrophyRecurrent systemic emboli despite anticoagulationwith moderate or severe stenosisPercutaneous balloon mitralvalvuloplasty ( PBMV)Procedure of choice for pure MS with pliable andnoncalcific valve
  39. 39. Surgical techniquesOpen mitral commissurotomyIndication: Patients without significant MR valvular calcification, involvement of chordae and papillary muscle, left atrial thrombus or restenosisMitral valve replacementIndication: Severe distortion and extensive calcification of thevalve and subvalvular apparatus; Associated with significant MR or aortic valve disease
  40. 40. Mitral regurgitation (MR)EtiologyMitral valve apparatus and/or LV structural and functional abnormalityRHD: common(1/3); + MS and/ or aortic valve diseaseMitral valve prolapse (MVP) myxomatous degeneration, floppy and redundancyIschemic heart disease (or CAD) papillary muscle dysfunctionMitral annular calcification
  41. 41. Severe dilatation of LV result in dilatation of the mitral annulus and lateral movement of papillary muscleInfective endocarditis valve leaflets destruction, perforation, retraction; valve closure interfered by vegetationOther causes: Rupture of the chordae congenital abnormalities obstructive hypertrophic cardiomyopathy
  42. 42. 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 MRMR →LA, LV volume↑→LVEDP↑→LAP↑→↓ pulmonary congestion, pulmonary edemaSV and CO↓
  43. 43. 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 stageAcute Mild— mild exertional dyspnea Severe— acute left HF, pulmonary edema, or cardiac shock
  44. 44. Physical examinationCardiac 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. 45. Systolic murmurRHD : Pansystolic, blowing, high-pitched murmur maximal at the apex Anterior valve lesion, radiate to the axilla and back Posterior leaflet abnormality, radiate to the baseMVP : 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 )
  46. 46. Laboratory examinationECGChronic (severe) MR: LA dilation, Atrial fibrillation LV enlargement and non-specific ST-T changesAcute MR: sinus tachycardiaRadiological findingsChronic (severe) MR: Cardiomegaly with LA, LV↑; pulmonary congestion, interstitial edema with Kerley B lines (left HF) C-shaped calcification of mitral annulusAcute MR: Normal cardiac silhouette or mild LA dilation overt pulmonary congestion, edema
  47. 47. 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 Severe3 、 Measure cardiac chamber sizes, evaluate LV function, pulmonary artery pressure, provide data concerning other valvular lesions
  48. 48. Radionuclide angiography and MRIEvaluate LV functionEstimate the severity of regurgitation The regurgitant fraction can be estimated from the ratio of LV to RV (LV/RV) stroke volumeCardiac catheterizationConfirm the diagnosis of MR and estimateits severity, evaluate cardiac function andpulmonary artery pressureCoronary angiography is performed todetermine presence of CAD prior to surgery
  49. 49. DiagnosisChronic MRTypical systolic murmur at apex associatedwith enlargement of LA and LVAcute MRSudden onset of dyspneaSystolic murmur at apexNormal cardiac silhouette, but obvious pulmonary congestionetiology existedConfirmed by Echocardiography
  50. 50. Differential diagnosisTricuspid regurgitation (TR) SM heard best along the left sternal border augmented during inspirationVentricular septal defect (VSD) SM loudest at the left sternal border accompanied by a parasternal thrillSystolic ejecting murmur at left sternal border: aortic or pulmonic stenosis hypertrophic obstructive cardiomyopathy Echocardiography
  51. 51. ComplicationAtrial fibrillation seen frequently in severe casesInfective endocarditis more common than in MSSystemic embolism less common than in MSHeart failure occur early in acute MR but late in chronic MR
  52. 52. ManagementChronic MRMedical treatment① Prevention: same as in MS② Asymptomatic patients with normal cardiac function : follow-up regularly③ 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. 53. Surgical treatmentMitral valve replacementIndications 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 repairIndications MVP Chordal rupture Mitral annulus dilation
  54. 54. Acute MRPrinciple Reduce pulmonary venous pressure Increase cardiac output Correct etiologyMedical treatment Intravenous nitroprusside Intravenous diuretics ACEI and other vasodilatorsSurgical treatment Mitral valve replacement Mitral valve repair
  55. 55. Aortic stenosis (AS)EtiologyRHD Common, + AR and mitral valve diseaseDegenerative calcific AS Common in the elderly, accompanied by calcification of the mitral annulusCongenital abnormalities Calcific stenosis of congenitally bicuspid aortic valve Congenital aortic stenosis
  56. 56. Hemodynamic changesNormal aortic orifice area (AOA): 3.0~4.0 cm2AOA ≤1.0cm2, LVSP↑, with significant transvalvulargradientCompensation AS→LV pressure load↑ Concentric LVH→compliance↓→LVEDP↑→LAH Maintain systolic wall stress and CO ↑LVEDVDecompensation LVEDV↑→wall stress↑, myocardial ischemia, fibrosis→ left HF
  57. 57. Clinical manifestationsSymptomsCardinal symptoms: dyspnea, angina and syncope1. 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. 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 supply3. Syncope: typically exertional Arterial pressure↓→ cerebral perfusion↓ Mechanisms: Increase blood flow to exercising muscle without compensatory increase in cardiac output Severe arrhythmias
  59. 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. 60. Heart sound changes S1 normal or soft A2 weak or absent paradoxical splitting of S2 prominent S4Aortic ejection sound congenital AS or pliable valve ASOther signs Left ventricular heave Systolic and pulse pressures↓ Delayed and diminished carotid pulses
  61. 61. Laboratory examinationECGSevere: LVH and secondary ST-T changes, LA↑ , arrhythmiasRadiological findingsNormal size or slightly enlarged heartCalcification of the aortic valvePoststenotic dilatation of the ascending aortaPulmonary congestion
  62. 62. EchocardiographyEstablish a diagnosis, and determine theseverity of ASM-mode and 2D echoObserve aortic valve opening, thickening andcalcificationHelpful in determining the etiology of ASAlso invaluable in detecting associated mitralvalve disease and in assessing LV performance,hypertrophy, and dilatation
  63. 63. Doppler echoAllows calculation of the aortic valve gradientEstimate the severity of the stenosis < 30 mmHg Mild AS MPG 30~50 mmHg Moderate AS > 50 mmHg SevereASColor Doppler flow imaging is helpful in thedetection and determination of the severity ofany accompanying aortic regurgitation
  64. 64. Cardiac catheterizationDetermine the severity of AS by measuringsystolic LV and aortic pressure simultaneously,and calculating the valve areaAn average pressure gradient of > 50mmHg orpeak pressure gradient of ≥ 70mmHg representsevere ASCoronary angiography is performed in mostadults to assess for concomitant coronary disease
  65. 65. Diagnosis and differential diagnosisDiagnosisTypical systolic murmur of ASAssociated with AR and/or mitral valve damage——RHDPure AS: Infants and young children——unicuspid malformation Childhood ~65 years——calcification of bicuspid AV > 65 years——degenerative calcificationConfirmed by echocardiography
  66. 66. Differential diagnosisTransmitted murmur ( MR, TR, VSD )Other LVOT obstructive disease Congenital supravalvular AS Congenital subvalvular AS Hypertrophic obstructive cardiomyopathy
  67. 67. 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
  68. 68. Surgical treatmentValve replacementIndications:① Repeated occurrence of syncope, angina pectoris or significant left heart failure② 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 noncalcificsevere congenital AS
  69. 69. Percutaneous balloon valvuloplastyIndicationsChildren and adolescents with congenital noncalcific ASAdults 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. 70. Aortic regurgitation (AR)EtiologyPrimary disease of the aortic valves and/ or aortic root
  71. 71. Aortic valve disease① RHD : most common, about 2/3 + AS and/or mitral valve disease② Infective endocarditis③ Congenital deformity: bicuspid valves④ Myxomatous degeneration of the aortic valveAortic root dilatation① Marfan syndrome② Aortic dissection (involve annulus or leaflets)③ Syphilitic aortitis
  72. 72. Hemodynamic changesChronic 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
  73. 73. Clinical manifestationsSymptomsChronic ARAsymptomatic for many yearsPalpitation, precordial discomfort, head pounding (related to SV↑)LV failure (dyspnea, fatigue): occur at late stageAngina pectoris or chest pain: less commonAcute AR mild—no symptom severe—Acute LV failure and hypotension (pulmonary edema)
  74. 74. Physical examinationChronic, severe AR① 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. 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. 76. Ejection systolic murmur: common harsh at the base of the heart accompanied by a systolic thrillAcute ARS1 soft or absent , P2↑ , S3 and S4AR murmur: lower pitched and shorter than that of chronic ARAustin-Flint murmur: brief
  77. 77. Laboratory examinationECGAcute: sinus tachycardia; nonspecific ST-T changesChronic: LV enlargement and hypertrophy, arrhythmiasRadiological findingsAcute AR: cardiac size normal or slightly enlarged signs of pulmonary congestion, pulmonary edemaChronic: 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. 78. EchocardiographyConfirm diagnosis, estimate severity, identify the cause2-D echo: Structural changes of the valve leaflets and/or aortic rootM 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 functionDoppler echo: Sensitive, accurate noninvasive technique for detecting AR LVOT diastolic regurgitant jet, estimate the severity of ARCardiac catheterizationQuantify the severity of AREvaluate the coronary and aortic root anatomy
  79. 79. Diagnosis and differential diagnosisDiagnosisCharacteristic diastolic murmur associated with peripheralarterial signs, make a diagnosis of ARCombined with other information, etiology is usually foundDifferential diagnosisGraham Steell murmur (pulmonary hypertension associatedwith dilatation)Austin-Flint murmur: differentiated from that of MS
  80. 80. ManagementChronic ARMedical 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 β-blocker: slow the rate of aortic dilation in Marfan’s② Patients with HF: Vasodilators (ACEI), diuretics and digitalis glycosides
  81. 81. Surgical treatmentValvular replacementIndications:① Symptomatic patients② Asymptomatic patients with LV dysfunction, with persistent or progressive LVESV↑or EF↓at restRepair or replacement of the root Aortic root disease
  82. 82. Acute ARMedical treatmentPrinciple: reduce pulmonary venous pressure, increase cardiac output, and stabilize hemodynamicsIntravenous nitroprussideDiureticsPositive inotropic agentAntibiotics ( active IE )Surgical treatmentUrgently requiredValvular replacement or aortic valve repair