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Valvular Heart Disease

Mitral Stenosis
Yerizal Karani MD Cardiology Division Faculty of Medicine Andalas University

A 75 year old woman with loud first heart sound and mid-diastolic murmur
Chronic dyspnea Class 2/4 Fatigue Recent orthopnea/pnd Nocturnal palpitation Pedal edema

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Mitral Stenosis
Etiology Symptoms Physical Exam Severity Natural history Timing of Surgery
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Mitral Stenosis: Etiology


Primarily a result of rheumatic fever
(~ 99% of MVs @ surgery show rheumatic damage )

Scarring & fusion of valve apparatus Rarely congenital Pure or predominant MS occurs in approximately 40% of all patients with rheumatic heart disease Two-thirds of all patients with MS are female.
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Mitral Stenosis:
Pathophysiology
Normal valve area: 4-6 cm2 Mild mitral stenosis:
MVA 1.5-2.5 cm2 Minimal symptoms

Mod mitral stenosis


MVA 1.0-1.5 cm2 usually does not produce symptoms at rest

Severe mitral stenosis


MVA < 1.0 cm2
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Mitral Stenosis:
Pathophysiology
Right Heart Failure: Hepatic Congestion JVD Tricuspid Regurgitation RA Enlargement Pulmonary HTN Pulmonary Congestion LA Enlargement Atrial Fib LA Thrombi LA Pressure

RV Pressure Overload RVH RV Failure


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LV Filling
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Mitral Stenosis: Symptoms


Fatigue Palpitations Cough SOB Left sided failure
Orthopnea PND

Afib Systemic embolism Pulmonary infection Hemoptysis Right sided failure


Hepatic Congestion Edema

Worsened by conditions that cardiac output.


Exertion,fever, anemia, tachycardia, Afib, intercourse, pregnancy, thyrotoxicosis
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Palpitation
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Recognizing Mitral Stenosis


Palpation:
Small volume pulse Tapping apex-palpable S1 +/- palpable opening snap (OS) RV lift Palpable S2

Auscultation:
Loud S1- as loud as S2 in aortic area A2 to OS interval inversely proportional to severity Diastolic rumble: length proportional to severity In severe MS with low flowS1, OS & rumble may be inaudible
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ECG:
LAE, AFIB, RVH, RAD
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Mitral Stenosis: Physical Exam

S1

S2 OS

S1

First heart sound (S1) is accentuated and snapping Opening snap (OS) after aortic valve closure Low pitch diastolic rumble at the apex Pre-systolic accentuation (esp. if in sinus rhythm)
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Common Murmurs and Timing (click on murmur to play)


Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve prolapse Tricuspid insufficiency Diastolic Murmurs Aortic insufficiency Mitral stenosis
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S1

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S1

AuscultationTiming of A2 to OS Interval
Width of A2-OS inversely correlates with severity The more severe the MS the higher the LAP the earlirthe LV pressure falls below LAP and the MV opens
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Say Prrr Pada Pata Papa Tuhuh

Timing Severity Other seconds of MS HSs 0.06 Severe .07-.08 .08-.09 0.10 .12 Modsevere Mod Mild PK
0.1-0.110

A2-S3
0.12-0.18

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Mitral Stenosis: Natural History


Progressive, lifelong disease, Usually slow & stable in the early years. Progressive acceleration in the later years 20-40 year latency from rheumatic fever to symptom onset. Additional 10 years before disabling symptoms
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Mitral Stenosis: Complications


Atrial dysrrhythmias Systemic embolization (10-25%) Risk of embolization is related to, age, presence of atrial fibrillation, previous embolic events Congestive heart failure Pulmonary infarcts (result of severe CHF) Hemoptysis Massive: 20 to ruptured bronchial veins (pulm HTN) Streaking/pink froth: pulmonary edema, or infection Endocarditis Pulmonary infections
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Mitral Stenosis: EKG


LAE RVH
Premature contractions Atrial flutter and/or fibrillation
freq. in pts with mod-severe MS for several years A fib develops in 30% to 40% of pts w/symptoms

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A 75 year old woman with loud first heart sound and mid-diastolic murmer

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Mitral Stenosis: Role of Echocardiography


Diagnosis of Mitral Stenosis Assessment of hemodynamic severity mean gradient, mitral valve area, pulmonary artery pressure Assessment of right ventricular size and function. Assessment of valve morphology to determine suitability for percutaneous mitral balloon valvuloplasty Diagnosis and assessment of concomitant valvular lesions Reevaluation of patients with known MS with changing symptoms or signs. F/U of asymptomatic patients with mod-severe MS
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Continuing Medical Implementation

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Mitral Stenosis:Therapy
Medical
Diuretics for LHF/RHF Digitalis/Beta blockers/CCB: Rate control in A Fib Anticoagulation: In A Fib Endocarditis prophylaxis

Balloon valvuloplasty
Effective long term improvement
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Mitral Stenosis:Therapy
Surgical
Mitral commissurotomy Mitral Valve Replacement
Mechanical Bioprosthetic

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Recommendations for Mitral Valve Repair for Mitral Stenosis


ACC/AHA Class I
Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if percutaneous mitral balloon valvotomy is not available Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if a left atrial thrombus is present despite anticoagulation Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),* and a non-pliable or calcified valve with the decision to proceed with either repair or replacement made at the time of the operation.
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Recommendations for Mitral Valve Repair for Mitral Stenosis


ACC/AHA Class IIB Patients in NYHA functional Class I, moderate or severe MS (mitral valve area <1.5 cm 2 ),* and valve morphology favorable for repair who have had recurrent episodes of embolic events on adequate anticoagulation. ACC/AHA Class III Patients with NYHA functional Class I-IV symptoms and mild MS.

*The committee recognizes that there may be a variability in the


measurement of mitral valve area and that the mean trans-mitral gradient, pulmonary artery wedge pressure, and pulmonary artery pressure at rest or during exercise should also be considered.
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Valvular Heart Disease


Mitral Regurgitation
Yerizal Karani MD Cardiology Division Faculty of Medicine Andalas University

Mitral Regurgitation
Etiology Symptoms Physical Exam Severity Natural history Timing of Surgery
...bridging the care gap

Continuing Medical Implementation

An 80 year old woman with increasing dyspnea


Longstanding heart murmur Increasing dyspnea & fatigue Recent ER visit Dx CHF

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Mitral Regurgitation: Etiology


Valvular-leaflets
Myxomatous MV Disease Rheumatic Endocarditis Congenital-clefts

Annulus
Calcification, IE (abcess)

Papillary Muscles
CAD (Ischemia, Infarction, Rupture) HCM Infiltrative disorders

Chordae
Fused/inflammatory Torn/trauma Degenerative IE

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LV dilatation & functional regurgitation Trauma...bridging the care gap

MR Etiology:Surgical series
MVP(20-70%) Ischemia (13-40%) RHD (3-40%) Infectious endocarditis(10-12%)

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MR Pathophysiology
Chronic LV volume overload - compensatory LVE initially maintaining cardiac output Decompensation (increased LV wall tension) -CHF LVE annulus dilation increased MR Backflow LAE, Afib, Pulmonary HTN
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MR Symptoms
Similar to MS Dyspnea, Orthopnea, PND Fatigue Pulmonary HTN, right sided failure Hemoptysis Systemic embolization in A Fib
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Recognizing Chronic Mitral Regurgitation


Pulse: brisk, low volume Apex:
hyperdynamic laterally displaced palpable S3 +/- thrill late parasternal lift 2 to LA filling

Murmer-Fixed MR:
pansystolic loudest apex to axilla no post extra-systolic accentuation

Murmer-Dynamic MR(MVP)
mid systolic +/- click upright

S 1 soft or normal S 2 wide split (early A2) unless LBBB


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S 3 / flow rumble if severe


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Recognizing Acute Severe Mitral Regurgitation


Acute severe dyspnea, CHF & hypotension LV size normal LV may/may not be hyperdynamic Loud S1 Systolic murmur may/may not be pan-systolic Inflow/rumble S3 present-may be only abnormality
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RV lift TTE/TEE for diagnosis Chordal or papilllary muscle rupture/tear Infarction with papillary muscle ischaemia or tear Infectious endocarditis with leaflet perforation or disruption or chordal tear Flail MV segment
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Comparing AS and MR
Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve prolapse Tricuspid insufficiency Diastolic Murmurs Aortic insufficiency Mitral stenosis
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S1

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S1

Assessing Severity of Chronic Mitral Regurgitation


Measure the Impact on the LV: Apical displacement and size Palpable S3 Longer/louder MR murmer (chronic MR) S3 intensity/ length of diastolic flow rumble Wider split S2 (earlier A2) unless HPT narrows the split
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Recognizing Mitral Regurgitation


ECG: LA enlargement Afib LVH (50% pts. With severe MR) RVH (15%) Combined hypertrophy (5%)
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CXR: LV LA pulmonary vascularity CHF Ca++ MV/MAC


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MR Echocardiography
Baseline evaluation to identify etiology, quantify severity of MR Assess and quantify LV function and dimensions Annual or semi-annual surveillance of LV function, estimated EF and LVESD in asymptomatic severe MR To establish cardiac status after change in symptoms Baseline study post MVR or repair
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MR Echocardiography
Etiology:
flail leaflets (chord/pap rupture) thick (RHD) post mvt of leaflets (MVP) vegetations(IE)

Severity:
regurgitant volume/fraction/orifice area LV systolic function increased LV/LA size, EF
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MR Echo/Doppler

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MR Pressure Tracing

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MR Stages
LV size and function defined by echo Stage 1-compensated:
End-diastolic dimension less 63mm, ESD less 42mm EF more than 60

Stage 2-transitional
EDD 65-68mm, ESD 44-45mm, EF 53-57

Stage 3-decompensated
EDD more than 70mm, ESD more than 45mm, EF less than 50
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Echo Indicators for Valve Replacement in Asymptomatic Aortic & Mitral Regurgitation
Type of LVESD mm Regurgitation EF % FS

Aortic

> 55

< 55

<0.27

Mitral

> 45

< 60

< 0.32
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RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHY IN PATIENTS WITH CHRONIC MITRAL REGURGITATION AND PRIMARY MITRAL-VALVE DISEASE.
SEVERITY OF MITRAL REGURGITATION
Mild Moderate Moderate Severe Severe

LEFT VENTRICULAR FUNCTION*


Normal ESD and EF Normal ESD and EF ESD >40 mm or EF <0.65 Normal ESD and EF ESD >40 mm or EF <0.65

FREQUENCY OF ECHOCARDIOGRAPHIC FOLLOW-UP


Every 5 yr Every 1 2 yr Annually Annually Every 6 mo

*ESD denotes end-systolic dimension and EF ejection fraction. Continuing Medical Implementation

Otto C.M. NEJM 345:10. ...bridging the care gap

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Mitral Valve Surgery


Only effective treatment is valve repair/replacement Optimal timing determined:
Presence/absence of symptoms Functional state of ventricle Feasability of valve repair Presence of Afib/PHTN Preference/expectations of patient
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Surgical Therapy - Timing


Surgery reduces morbidity and mortality from severe MR but exposes patient to risk of surgery and prosthetic valve Surgery should be performed before onset of severe symptoms or development of LV contractile dysfunction

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Symptoms
Class III or IV symptoms (even if transient) always indicate need for surgery Class II symptoms indicate need for surgery in patients with repairable valves ETT may reveal concealed symptoms

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Ejection Fraction (LVEF)


Strongest predictor of outcome following surgery Should be assessed quantitatively
MUGA or Echo

Surgery indicated if LVEF is below normal (60%) If EF normal, follow every 6 to 12 months If EF <30%, medical management (valve repair experimental in this setting)

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Load-Independent Measures of LV Function


Complex measurements:
LV dP/dT End-systolic stress-strain Myocardial Elastance Peak systolic pressure/end-systolic volume

End-systolic diameter
LVIDs >45 predicts poor outcome

End-systolic volume index


ESVI >50cc/m2 predicts poor outcome
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Other Indications
Flail mitral leaflet Left atrial dimension >45mm Paroxysmal atrial fibrillation Pulmonary hypertension

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Mitral Regurgitation ACC/AHA recommendations


Surgery Recommended in patients who are Symptomatic Asymptomatic with
Any LV dysfunction Atrial fibrillation Pulmonary hypertension Reparable valves Recurrent VT
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Indications for Surgery Isolated,Severe Chronic MR


Definite (major criteria):
NYHA Class III or IV heart failure (any duration) EF <60% EF >60% but decreasing on serial measurements LVIDs >45mm ESVI >50cc/m2
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Indications for Surgery Isolated,Severe Chronic MR


Emerging (minor criteria):
Any symptoms of heart failure or sub optimal exercise tolerance test Flail mitral leaflet Left atrial diameter >45mm Paroxysmal atrial fibrillation Abnormal exercise end-systolic volume index or ejection fraction
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MV Repair vs. Replacement


Lower operative mortality Better late outcome Curative Avoids anticoagulation unless atrial fibrillation Open Afib ablation
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MV Repair vs. Replacement (2)


Valve replacement:
Mortality 2-7% Anti-coagulation Decreased LVEF

Tissue prosthetic valve degeneration Mechanical prosthetic valve dysfunction/ thrombosis


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Valve repair Mortality 2-3% No anticoagulation (unless Afib) Preservation of LVEF Valve repair always preferable Feasible in 70-90% of patients
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Mitral Valve Replacement Other Issues


Mechanical valve thromboembolism, bleed from anticoagulation Bioprosthetic valve limited durability (degeneration) Chordal/subvalvular apparatus preservation
EF preop/postop 60% to 36% VS 63% to 61% in a comparative study
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Acknowledgment
Some slides adapted from Cardiology Rounds presentation by Stephane Moffett R1 Anesthesia

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AORTIC STENOSIS
Yerizal Karani MD Cardiology Division Faculty of Medicine Andalas University

CD

VALVULAR AORTIC STENOSIS


Congenital Acquired
Rheumatic Degenerative(age related) Atherosclerotic Calcific AS associated with Pagets Disease, end-stage renal failure, rheumatoid arthritis,

etc.

AORTIC SCLEROSIS

Irregular thickening of the valve leaflets seen on echo but without significant obstruction. May result in a systolic ejection murmur.

Approx. 25% over age 65 and over 40% over 85 Evidence suggests Ao sclerosis does progress to degenerative aortic stenosis.

AORTIC SCLEROSIS
Cosmi et al studied 2000 pts with aortic sclerosis and found 16% progressed to aortic stenosis and 10% had mild, 3% moderate, and 2% severe obstruction. The average time for progression from ao sclerosis to severe stenosis was 8 years.
Arch Int Med 2002; 62:2345

Degenerative Aortic Stenosis


Most common type of AS today and the usual cause for aortic valve replacement Shares common risk factors with mitral annular calcification Risk factors for calcific aortic stenosis are similar to those for vascular atherosclerosis

AORTIC STENOSIS
NATURAL HISTORY May be asymptomatic for many years Gradual onset and slow progression LVH allows large gradient to be tolerated for years with little or no reduction of cardiac output, left ventricular dilatation, or symptoms

AORTIC STENOSIS
Obstruction is progressive-but insidious
Rate of progression is variable so difficult to predict in an individual patient On average: AVA decreases 0.12 cm2/yr with average increase jet velocity of 0.32 m/sec per year and mean gradient increase of 7 mm Hg per year

AORTIC STENOSIS

Critical obstruction is associated with:

Peak gradient >50 mm Hg in presence of normal output Effective oriface area <0.8 cm2
Normal ao valve area=2.6-3.5 cm2

AORTIC STENOSIS

In general: Mild Aortic Stenosis=1.5-2.0 cm2 Moderate Stenosis=1-1.5 cm2 Severe Aortic Stenosis=<1.0 cm2 Critical Aortic Stenosis=<0.8 cm2

AORTIC STENOSIS
Thickening and stiffening of the LV in the face of increasing obstruction results in Increased LVEDP Result=LAH and diastolic dysfunction Left atrium becomes critical in filling the ventricle and At Fib or AV dissociation are poorly tolerated

AORTIC STENOSIS
In significant ao stenosis, the cardiac output may be fairly well maintained at rest but fails to augment with exercise Late in the course of severe AS : cardiac output, stroke volume, and the gradient itself all declinewhile the Mean LA pressure, capillary wedge pressure and P.A. pressure increase

AORTIC STENOSIS
DIAGNOSIS: Symptoms Physical exam Chest X-Ray EKG Echo-major diagnostic tool and means of follow-up. Allows measurement of gradient, LV function, associated lesions

AORTIC STENOSIS
Symptoms: Can be asymptomatic Dyspnea on exertion Angina Syncope or light spells Palpitations not listed as major symptom, but common in significant heart disease

AORTIC STENOSIS
Implications of symptoms With unrelieved obstruction survival is approx 2 years after onset of failure, 3 years after onset of syncope, and 5 years after onset of angina Recent data: symptomatic pts with severe stenosis-average survival was 2 years with only 20% survival at 5 yrs

AORTIC STENOSIS
Physical Exam Narrow pulse pressure, slow arterial upstroke, carotid shudder Sustained PMI and with failure it is displaced laterally and inferiorly S4 common, S1 soft, S2 may be single, systolic ejection murmur best at the base

AORTIC STENOSIS
MANAGEMENT
Medical: medications and careful follow-up Surgical: Valve replacement is the best approach in most cases

AORTIC STENOSIS
Medical Management Patient education Medications-patients with associated hypertension or CHF can be treated with medications if AS is mild or moderate. Caution if Severe AS, especially with beta blockers and dilator type agents Favor use of statin drugs

AORTIC STENOSIS
Management-2 Periodic echo-if mild AS: echo every 2 years; for moderate AS every year, and for severe AS echo assessment every 6-8 months Question the role of SBE prophylaxis

AORTIC STENOSIS
Management-3 (surgical and related) Non-calcified congenital AS can be managed with open commissural incision at low risk Some cases of adult AS can be managed by Balloon Valvuloplasty often will need operative care in 2 yrs Most adult calcific AS if severe or progressive-symptomatic best care is AVR

AORTIC STENOSIS
Management-4 AVA <1.0 cm2 whose symptoms are believed to result from the stenosis Asymptomatic patients if progressive LV dysfunction, or if hypotensive response to exercise Threshold for AVR will likely lower in the future

AORTIC STENOSIS
Effects of successful AVR Substantial clinical and hemodynamic improvement Ten year survival approx 85% Exertional dyspnea improved as also frequency and severity of angina Impaired LV performance improves toward normal often and LV mass decreases toward normal-not normal

AORTIC STENOSIS
SUMMARY: Aortic stenosis of varying degree is common in adults Diagnosis and management are DEPENDENT on the internist, hospitalist, and family physician Follow up involves history, physical, and especially the echo-Doppler Valve replacement=best overall Rx

Valvular Heart Disease


Aortic Regurgitation
Yerizal Karani MD Cardiology Division Faculty of Medicine Andalas University

Aortic Regurgitation
Etiology Physical Examination Assessing Severity Natural History Prognosis Timing of Surgery
...bridging the care gap

Continuing Medical Implementation

Aortic Regurgitation: Etiology


Any conditions resulting in incompetent aortic leaflets Congenital
Bicuspid valve

Acquired
Rheumatic heart disease Dilated aorta (e.g. hypertension..) Degenerative Connective tissue disorders
E.g. ankylosing spondylitis, rheumatoid arthritis, Reiters syndrome, Giant-cell arteritis )

Aortopathy
Cystic medial necrosis Collagen disorders (e.g. Marfans) Ehler-Danlos Osteogenesis imperfecta Pseudoxanthoma elasticum
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Syphilis (chronic aortitis)

Acute AI: aortic dissection, infective ...bridging the care gap endocarditis, trauma

Aortic Regurgitation: Symptoms


Dyspnea, orthopnea, PND Chest pain.
Nocturnal angina >> exertional angina ( diastolic aortic pressure and increased LVEDP thus coronary artery diastolic flow)

With extreme reductions in diastolic pressures (e.g. < 40) may see angina

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Peripheral Signs of Severe Aortic Regurgitation


Quinckes sign: capillary pulsation Corrigans sign: water hammer pulse Bisferiens pulse (AS/AR > AR) De Mussets sign: systolic head bobbing Muellers sign: systolic pulsation of uvula
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Durosiers sign: femoral retrograde bruits Traubes sign: pistol shot femorals Hills sign:BP Lower extremity >BP Upper extremity by
> 20 mm Hg - mild AR > 40 mm Hg mod AR > 60 mm Hg severe AR
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Aortic Regurgitation: Physical Exam


Widened pulse pressure
Systolic diastolic = pulse pressure

High pitched, blowing, decrescendo diastolic murmur at LSB Best heard at endexpiration & leaning forward Hands & Knee position
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S1

S2

S1

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Central Signs of Severe Aortic Regurgitation


Apex:
Enlarged Displaced Hyper-dynamic Palpable S3 Austin-Flint murmur

Aortic diastolic murmur


length correlates with severity (chronic AR) in acute AR murmur shortens as Aortic DP=LVEDP in acute AR - mitral pre-closure
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Assessing Severity of AR
Assess severity by impact on peripheral signs and LV
peripheral signs = severity LV = severity S3 Austin -Flint LVH radiological cardiomegaly
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Aortic Regurgitation: Natural History


Asymptomatic Normal LV function (~good prognosis)
Progression to symptoms or LV dysfunction Progression to asymptomatic LV dysfunction 75% 5-year survival Sudden death

%/Y
<6 < 3.5 < 0.2 25 > 10

Abnormal LV function
Progression to cardiac symptoms

Symptomatic (Poor prognosis)


TX: Medical Surgery BEFORE LV dysfunction
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Mortality

Bonow RO, et al, JACC. 1998;32:1486.

Echo Indications for Valve Replacement in Asymptomatic AR & MR

Type of LVESD mm Regurgitation

EF %

FS

Aortic

> 55

< 55

<0.27

Mitral

> 45

< 60

< 0.32
...bridging the care gap

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Indication for Valve Replacement in Aortic Regurgitation


ACC/AHA Class I
Symptomatic patients with preserved LVF (LVEF >50%) Asymptomatic patients with mild to moderate LV dysfunction (EF 25-49%) Patients undergoing CABG, aortic or other valvular surgery

ACC/AHA Class II a
Asymptomatic patients with preserved LVEF but severe LV dilatation (EDD>75 mm or ESD > 55mm)
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Indication for Valve Replacement in Aortic Regurgitation


ACC/AHA Class II b
Patients with severe LV dysfunction (EF < 25%) Asymptomatic patients with normal systolic func-tion at rest (EF >0.50) and progressi ve LV dilata-tion when the degree of dilatation is moderatelysevere (EDD 70 to 75 mm, ESD 50 to 55 mm).

ACC/AHA Class III


Asymptomatic patients with normal systolicf unction at rest (EF >0.50) and LV dilatation when the degree of dilatation is not severe (EDD <70 mm, ESD <50 mm).
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