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Valvular Heart Disease Mitral Stenosis

Valvular Heart Disease Mitral Stenosis

Yerizal Karani MD

Cardiology Division

Faculty of Medicine Andalas University

© Continuing Medical Implementation …...bridging the care gap

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

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


Mitral StenosisMitral Stenosis

• Etiology

• Symptoms

• Physical Exam

• Severity

• Natural history

• Timing of Surgery


Mitral Stenosis: EtiologyMitral Stenosis: Etiology

• Primarily a result of rheumatic fever

(~ 99% of MV’s @ 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.


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


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 LV Filling




Mitral Stenosis: SymptomsMitral Stenosis: Symptoms

• Fatigue • Palpitations• Cough• SOB• Left sided failure

– Orthopnea

– PND

• Palpitation

• 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


Recognizing Mitral Stenosis

Recognizing Mitral Stenosis

Palpation:• Small volume pulse

• Tapping apex-palpable S1

• +/- palpable opening snap (OS)

• RV lift

• Palpable S2

ECG:• LAE, AFIB, RVH, RAD

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 flow- S1, OS & rumble may be inaudible

Wave Sound


Mitral Stenosis: Physical ExamMitral Stenosis: Physical Exam

• 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)

S1 S2 OS S1


Common Murmurs and Timing (click on murmur to play)

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

S1 S2 S1


Auscultation-Timing of A2 to OS Interval

Auscultation-Timing 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

Say Timing seconds

Severity of MS

Other HS’s

Prrr 0.06 Severe

Pada .07-.08 Mod-severe

Pata .08-.09 Mod

Papa 0.10 Mild PK 0.1-0.110

Tu-huh

.12 A2-S3 0.12-0.18


Mitral Stenosis: Natural HistoryMitral 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


Mitral Stenosis: ComplicationsMitral 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


Mitral Stenosis: EKGMitral 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


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

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


Mitral Stenosis: Role of Echocardiography

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 determinesuitability 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


Mitral Stenosis:TherapyMitral 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


Mitral Stenosis:TherapyMitral Stenosis:Therapy

• Surgical– Mitral commissurotomy– Mitral Valve Replacement

• Mechanical

• Bioprosthetic


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.




• 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.

Valvular Heart Disease Mitral Regurgitation

Valvular Heart Disease Mitral Regurgitation

Yerizal Karani MD

Cardiology Division


© Continuing Medical Implementation ® …...bridging the care gap

Mitral RegurgitationMitral Regurgitation

• Etiology

• Symptoms

• Physical Exam

• Severity

• Natural history



An 80 year old woman with increasing dyspnea

An 80 year old woman with increasing dyspnea

• Longstanding heart murmur

• Increasing dyspnea & fatigue

• Recent ER visit Dx CHF


Mitral Regurgitation:Etiology

Mitral Regurgitation:Etiology

• Valvular-leaflets– Myxomatous MV

Disease– Rheumatic– Endocarditis– Congenital-clefts

• Chordae– Fused/inflammatory– Torn/trauma– Degenerative– IE

• Annulus– Calcification, IE (abcess)

• Papillary Muscles– CAD (Ischemia,

Infarction, Rupture)– HCM– Infiltrative disorders

• LV dilatation & functional regurgitation

• Trauma


MR Etiology:Surgical series MR Etiology:Surgical series

• MVP(20-70%)

• Ischemia (13-40%)

• RHD (3-40%)

• Infectious endocarditis(10-12%)


MR PathophysiologyMR 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


MR SymptomsMR Symptoms

• Similar to MS

• Dyspnea, Orthopnea, PND

• Fatigue

• Pulmonary HTN, right sided failure

• Hemoptysis

• Systemic embolization in A Fib


Recognizing ChronicMitral Regurgitation

Recognizing ChronicMitral Regurgitation

• Pulse:– brisk, low volume

• Apex:– hyperdynamic– laterally displaced– palpable S3 +/- thrill– late parasternal lift 2 to LA

filling

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

unless LBBB

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

accentuation

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

• S 3 / flow rumble if severe

Wave Sound


Recognizing Acute SevereMitral Regurgitation

Recognizing Acute SevereMitral 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

• 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


Comparing AS and MRComparing AS and MR

Systolic Murmurs• Aortic stenosis• Mitral insufficiency• Mitral valve prolapse• Tricuspid insufficiency

Diastolic Murmurs• Aortic insufficiency• Mitral stenosis

S1 S2 S1

Wave Sound

Wave Sound

Wave Sound

Wave Sound

Wave Sound


Assessing Severity of Chronic Mitral Regurgitation

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


Recognizing Mitral Regurgitation

Recognizing Mitral Regurgitation

• ECG:– LA enlargement– Afib– LVH (50% pts.

With severe MR)– RVH (15%)– Combined

hypertrophy (5%)

• CXR: LV LA pulmonary

vascularity– CHF– Ca++ MV/MAC


MR EchocardiographyMR 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


MR EchocardiographyMR 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


MR Echo/DopplerMR Echo/Doppler


MR Pressure TracingMR Pressure Tracing


MR StagesMR 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


Echo Indicators for Valve Replacement in Asymptomatic Aortic & Mitral Regurgitation

Echo Indicators for Valve Replacement in Asymptomatic Aortic & Mitral Regurgitation

Type of Regurgitation

LVESD mm

EF %

FS

Aortic > 55 < 55 <0.27

Mitral > 45 < 60 < 0.32


RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHYIN PATIENTS WITH CHRONIC MITRAL REGURGITATION

AND PRIMARY MITRAL-VALVE DISEASE.

RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHYIN PATIENTS WITH CHRONIC MITRAL REGURGITATION

AND PRIMARY MITRAL-VALVE DISEASE.

SEVERITY OF

MITRAL

REGURGITATION

LEFT VENTRICULAR FUNCTION*

FREQUENCY OF

ECHOCARDIOGRA-PHIC FOLLOW-UP

Mild Normal ESD and EF Every 5 yr

Moderate Normal ESD and EF Every 1 –2 yr

Moderate ESD >40 mm or EF <0.65 Annually

Severe Normal ESD and EF Annually

Severe ESD >40 mm or EF <0.65 Every 6 mo

*ESD denotes end-systolic dimension and EF ejection fraction. Otto C.M. NEJM 345:10.


Mitral Valve SurgeryMitral 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


Surgical Therapy - TimingSurgical 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


SymptomsSymptoms

• 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


Ejection Fraction (LVEF)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)


Load-Independent Measures of LV Function

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


Other IndicationsOther Indications

• Flail mitral leaflet

• Left atrial dimension >45mm

• Paroxysmal atrial fibrillation

• Pulmonary hypertension


Mitral RegurgitationACC/AHA recommendations

Mitral RegurgitationACC/AHA recommendations

Surgery Recommended in patients who are• Symptomatic• Asymptomatic with

– Any LV dysfunction– Atrial fibrillation– Pulmonary hypertension– Reparable valves– Recurrent VT


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




• 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


MV Repair vs. ReplacementMV Repair vs. Replacement

• Lower operative mortality

• Better late outcome

• Curative

• Avoids anticoagulation unless atrial fibrillation

• Open Afib ablation


MV Repair vs. Replacement (2)MV Repair vs. Replacement (2)

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

• Tissue prosthetic valve degeneration

• Mechanical prosthetic valve dysfunction/ thrombosis

• Valve repair

– Mortality 2-3%

– No anticoagulation (unless Afib)

– Preservation of LVEF

• Valve repair always preferable

– Feasible in 70-90% of patients


Mitral Valve Replacement Other Issues

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


AcknowledgmentAcknowledgment

• Some slides adapted from Cardiology Rounds presentation by Stephane Moffett – R1 Anesthesia

AORTIC STENOSIS AORTIC STENOSIS

Yerizal Karani MDCardiology Division


VALVULAR AORTIC STENOSISVALVULAR AORTIC STENOSIS

Congenital Acquired Rheumatic

Degenerative(age related) Atherosclerotic Calcific AS associated with Paget’s Disease,

end-stage renal failure, rheumatoid arthritis,

etc.

•

AORTIC SCLEROSISAORTIC 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 SCLEROSISAORTIC 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 StenosisDegenerative 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 STENOSISAORTIC 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


• 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•


• 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


• 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


• 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


• 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 decline……while the• Mean LA pressure, capillary wedge • pressure and P.A. pressure increase


• 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


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


• 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


• 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•


• MANAGEMENT

• Medical: medications and careful • follow-up

• Surgical: Valve replacement is• the best approach in most cases•


• 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


• 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


• 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


• 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


• 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 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

Valvular Heart Disease Aortic Regurgitation

Yerizal Karani MD

Cardiology Division



Aortic RegurgitationAortic Regurgitation

• Etiology

• Physical Examination

• Assessing Severity

• Natural History

• Prognosis



Aortic Regurgitation:Etiology

Aortic Regurgitation:Etiology

• Any conditions resulting in incompetent aortic leaflets

• Congenital– Bicuspid valve

• Aortopathy– Cystic medial necrosis– Collagen disorders (e.g.

Marfan’s)– Ehler-Danlos– Osteogenesis imperfecta– Pseudoxanthoma elasticum

• Acquired– Rheumatic heart disease– Dilated aorta (e.g.

hypertension..)– Degenerative– Connective tissue disorders

• E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis )

– Syphilis (chronic aortitis)

• Acute AI: aortic dissection, infective endocarditis, trauma


Aortic Regurgitation:Symptoms

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


Peripheral Signs of Severe Aortic Regurgitation

Peripheral Signs of Severe Aortic Regurgitation

• Quincke’s sign: capillary pulsation

• Corrigan’s sign: water hammer pulse

• Bisferiens pulse (AS/AR > AR)

• De Musset’s sign: systolic head bobbing

• Mueller’s sign: systolic pulsation of uvula

• Durosier’s sign: femoral retrograde bruits

• Traube’s sign: pistol shot femorals

• Hill’s sign:BP Lower extremity >BP Upper extremity by – > 20 mm Hg - mild AR

– > 40 mm Hg – mod AR

– > 60 mm Hg – severe AR

Wave Sound


Aortic Regurgitation: Physical Exam

Aortic Regurgitation: Physical Exam

• Widened pulse pressure – Systolic – diastolic

= pulse pressure

• High pitched, blowing, decrescendo diastolic murmur at LSB

• Best heard at end-expiration & leaning forward

• Hands & Knee position

S1 S2 S1

Wave Sound


Central Signs of Severe Aortic Regurgitation

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


Assessing Severity of AR

Assessing Severity of AR

• Assess severity by impact on peripheral signs and LV peripheral signs = severity LV = severity– S3– Austin -Flint– LVH– radiological cardiomegaly


Aortic Regurgitation: Natural History

Aortic Regurgitation: Natural History

Asymptomatic %/Y• Normal LV function (~good prognosis)

– Progression to symptoms or LV dysfunction < 6– Progression to asymptomatic LV dysfunction < 3.5– 75% 5-year survival– Sudden death < 0.2

• Abnormal LV function– Progression to cardiac symptoms 25

• Symptomatic (Poor prognosis)– Mortality > 10

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

TX: Medical Surgery BEFORE LV dysfunction


Echo Indications for Valve Replacement in Asymptomatic AR & MR

Echo Indications for Valve Replacement in Asymptomatic AR & MR

Type of Regurgitation

LVESD mm

EF %

FS

Aortic > 55 < 55 <0.27

Mitral > 45 < 60 < 0.32


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)




• 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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