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Valvular Heart Disease

Susan Schima MD September 29, 2015

Cardiac Physical Exam

n  S1=mitral valve closure (can’t really hear tricuspid component)

n  S2=Aortic valve closure, pulmonic n  S3=Very healthy or very sick LV

n  Children and young athletes, CHF n  Healthy=suckers Sick=pushers

n  S4=Stiff LV, incr LVEDP, HTN, hypertrophy n  Cannot hear in afib. Occurs during atrial

contraction

Physiologic Splitting

n  S1 S2 n  Expiration M1,T1 A2,P2

n  Inspiration M1,T1 A2 P2

Persistent Splitting RBBB, Pulm HTN

n  S1 S2 n  Expiration M1,T1 A2 P2

n  Inspiration M1 ,T1 A2 P2

n  Delayed activation of the RV, so delayed closure of P2

Fixed Splitting ASD

n  S1 S2 n  Expiration M1,T1 A2 P2

n  Inspiration M1, T1 A2 P2

n  Increased venous return balanced by reciprocal decr flow through shunt

Paradoxical Splitting LBBB

n  Expiration S1 P2 A2

n  Inspiration S1 P2A2

n  Delayed LV activation, ejection and AV closure

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Paradoxical Splitting

n  Delayed LV activation n  LBBB n  RV pacing

n  Delayed LV outflow n  LV systolic failure n  AS, HOCM

Summary- Splitting of S2

n  Physiologic Splitting=respiratory flow variation

n  Paradoxical=LBBB, AS n  Persistent=RBBB, pulm HTN, MS n  Fixed=ASD

Murmurs

n  Innocent/functional murmur n  Short, soft n  <grade 2 n  Right sternal border n  No increase with valsava n  Normal S2 n  No other abnormal sounds n  No LV enlargement on exam or ecg

Stages of Progression of VHD

Stage Definition Description

A At risk Risk factors for development of VHD

B Progressive Mild to moderate, asymptomatic

C Asymptomatic Severe C1: LV or RV remains compensated C2: LV or RV decompensated

D Symptomatic Severe Symptoms due to VHD

Frequency of Echo in Asymptomatic pts with VHD and

Normal EF

Stage AS AR MS MR Progressive (stage B)

3-5 yr if mild, 1-2 y if mod

3-5 yr if mild 1-2 y if mod

3-5 yr (MVA >1.5 cm2)

3-5 yr if mild 1-2 y if mod

Severe (Stage C)

6-12 m 6-12 m Dilating LV- more frequently

1-2 y (MVA 1-1.5cm2) Every yr (MVA < 1 cm2)

6-12 m Dilating LV- more frequently

Medical Therapy

n  Most valve disease is ultimately surgical, however benefit to ACE inhibitor or ARB and beta blockers if LV dysfunction

n  Care taken not to abruptly lower BP in pts with stenotic lesions

n  Rheumatic fever and IE prophylaxis n  Maintenance of optimal oral health n  Influenza and pneumococcal vaccines to

appropriate pts

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Medical Therapy

n  All patients should be optimized with goal directed medical therapy

n  Safety and efficacy of exercise programs in VHD not established n  Pts benefit from regular aerobic exercise

program to ensure CV fitness n  Heavy isometric repetitive training may

increase AL, but resistive training with small free weights or repetitive isolated muscle training may be used

Exercise Testing

n  Class IIa n  Reasonable in selected patients with

asymptomatic severe VHD to n Confirm absence of symptoms n Assess hemodynamic response to exercise n Determine prognosis

Rheumatic Fever

n  Important cause of VHD, slight increase in cases since 1987

n  Group A strep-prompt recognition and rx for primary prevention

n  Pts with prior episodes of RF or those with evidence of RHD, long-term antistreptococcal prophylaxis is indicated for secondary prevention

Secondary Prevention of Rheumatic Fever

Agent Dosage

PCN G benzathine 1.2 million units IM q 4 wks

PCN V potassium 200 mg po BID

Sulfadiazine 1g po daily

Macrolide or azalide abx (PCN/sulfa allergic)

Varies

Duration of Secondary Prophylaxis for RF

Type Duration after Last Attack

RF with carditis and persistent VHD 10y or until pt is 40 yo (whichever longer)

RF with carditis but no residual VHD 10 yr or until pt is 21 yo (whichever longer)

RF without carditis 5 y or until pt 21 yo (whichever longer)

IE Prophylaxis

n  IIa : Reasonable for the following pts at highest risk for adverse outcomes from IE before dental procedures that involve manipulation of gingival tissue, manipulation of the periapical region of teeth, or perforation of the oral mucosa

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IE Prophylaxis

n  Prosthetic cardiac valves n  Previous IE n  Cardiac transplant recipients with valve regurgitation due

to structurally abnormal valve n  Congenital heart disease with:

n  Unrepaired cyanotic CHD, incl palliative shunts n  Repaired CHD with prosthetic material or device

during first 6 m after procedure n  Repaired CHD with residual defects at site or adjacent

to site of prosthetic patch or prosthetic device

IE Prophylaxis No Benefit

n  Class III Not recommended in patients with VHD who are at risk of IE for nondental procedures (eg TEE, EGD, colonoscopy or cystoscopy) in the absence of active infection

Aortic Stenosis Etiology

n  Senile degenerative (calcific)

n  > 70 n  Most common

n  Rheumatic n  40-60

n  Calcified bicuspid n  40-60

n  Congenital n  <30 n  Unicuspid, bicuspid

Bicuspid

n  Associated with other abnormalities (aortic disease)

n  1-2% of all live births n  Familial-AD with low

penetrance n  DNA transcription

error, defective myofibrils

n  Screen relatives of patients with bicuspid valve

Clinical Presentation: Physical Exam

-Loud, late peaking systolic murmur that radiates to carotids, crescendo-decrescendo

-Single or paradoxically split S2 -Delayed and diminished carotid upstroke

(parvus et tardus) -Only reliable sign to exclude severe AS is

normally split S2

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Clinical Presentation

n  Symptoms n  Syncope n  CHF (worst prognosis) n  Angina

Medical Therapy AS

n  Control of blood pressure in those at risk for AS and those with asymptomatic AS (stages A,B,C). Start at low dose and titrate up

n  Avoid diuretics if small LV chamber size because may result in fall in CO.

n  Statins have no role in AS (although many have CAD)

Evaluation of Severity

AVA AREA MEAN GRADIENT

JET VELOCITY

MILD >1.5 cm2 <25mmHg <3 m/s

MODERATE 1-1.5 cm2 25-40mmHg

3-4 m/s

SEVERE <1 cm2 >40mmHg >4 m/s

When to operate

n  Class I n  Symptomatic with Severe AS n  Severe AS and undergoing CABG, aorta or

other valve surgery n  Severe AS and LV systolic dysfunction (EF <

50%)

Surgical Treatment of AS

n  Surgical AVR for patients with low or intermediate surgical risk

n  TAVR if prohibitive surgical risk and predicted post-TAVR survival greater than 12 months (Class I)

n  TAVR is reasonable alternative to surgical AVR in those with high surgical risk (Class IIa)

Evaluation of Surgical and Interventional Risk

n  Individualized n  Operative mortality estimated from

different risk scoring systems (STS risk estimate or Euroscore)

n  http://www.euroscore.org/) n  Fraility should be considered

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Low Risk (all)

Intermed. Risk (any 1)

High Risk (any 1)

Prohibitive Risk (Any 1)

STS PROM <4% AND 4-8% OR >8% OR Risk of death or major morbidity > 50% at 1 yr

Fraility None AND 1 Index (mild) OR

> Or = 2 Indices (mod to severe) OR

Major Organ System Compromise not to be improved postop

None AND

1 Or

No more than 2

Ø  Or= 3 OR

Pre-op Coronary Angiogram

n  Males > 35 yo n  Premenopausal women > 35 with risk

factors n  Postmenopausal women

Aortic Regurgitation Etiology

n  Congenital, calcific, rheumatic, IE, HTN, Marfans, RA, syphilis, anorectic drugs, inflammatory (psoriatic arthritis, ankylosing spondylitis)

n  Trauma, MI

n  Acute and Chronic

Acute Severe AI

n  Sudden large regurgitant volume on unprepared LV.

n  Abrupt increase in LVEDP and LAP, LV can’t compensate quickly and get decrease in forward SV.

n  Tachycardia is compensatory but insufficient

Presentation

n  Pulmonary congestion n  S3 and S4 n  AR murmur may be absent n  Pulse pressure may not be increased

because systolic pressure is reduced and aortic diastolic pressure equilibrates with elevated LV diastolic pressure

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Treatment

n  Urgent surgery n  IABP contraindicated n  Beta-blockers contraindicated (unless

dissection) because increase diastolic filling time and worsen the AI, blunt compensatory tachycardia

n  Nitroprusside is an option (augment forward flow and reduce LVEDP)

Chronic AI

n  Compensatory increase in ED volume, increase in chamber compliance to accommodate increased volume without increase in filling pressures- concentric and eccentric hypertrophy

n  Greater diastolic volume allows LV to eject large total SV to maintain forward CO

n  Pressure and Volume overload

Chronic AI

n  Preload reserve can be exhausted and hypertrophic response may be inadequate, so that further increase in afterload results in reduced EF.

n  May have prolonged asymptomatic interval n  Dyspnea and exertional angina

Physical Exam

n  Most consistent finding is wide pulse pressure (if don’t have, not severe)

n  Head nodding (de Mussets) n  Capillary pulsations (Quinke’s) n  Rapid carotid upstroke, rapid collapse

(Corrigan’s pulse) n  “Pistol shot” femoral pulse (Duroziez’s)

Physical Exam

n  Diastolic decrescendo murmur n  May also have short SEM with ejection

click (if bicuspid)

n  Displaced LV impulse n  Austin-Flint murmur specific for severe AI

Evaluation

n  Severe n  AR jet/LVOT diameter

> 60% n  Flow reversal in

proximal desc thoracic aorta

n  Regurgitant volume > 60ml

n  Regurgitant fraction > 55%

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Surgical Treatment of AR

n  Symptomatic pts with severe AR regardless of LV systolic function

n  Asymptomatic n  EF < 50% n  Nl EF but LVESD > 50 mm, stage C2 n  Nl EF but LVEDD > 65 mm if surgical risk is

low

Medical Treatment of AR

n  Treat hypertension, ideally with CCB or ACEI/ARB. Reduced HR with BB may cause higher stroke volume, which contribute to elevated SBP in pts with chronic severe AR

n  If LV dysfunction/symptoms and surgery not option, treat with vasodilators (CCB, ACEI/ARB,BBL). Not needed if LV function normal and asymptomatic

Mitral Stenosis Etiology

n  Almost always Rheumatic! n  W:M 2:1

Pathophysiology

Diastolic transmitral gradient is the fundamental expression of MS

Results in increased LA pressure, which is reflected back to pulmonary circulation atrial arrhythmias Right sided heart failure

Clinical Presentation

n  First symptoms usually precipitated by exercise, emotional stress, infection, pregnancy or afib with RVR (increase in transmitral flow or decr in diastolic filling period – rise in LAP)

n  Dyspnea, PND, orthopnea n  Hemoptysis n  Palpitations n  Emboli

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Physical Exam

n  Accentuated S1, opening snap, low pitched mid diastolic rumble, and presystolic murmur

n  Shorter A2-os interval and longer diastolic rumble indicate more severe MS n  S2-OS interval <70msec severe, >110 mild n  AS MS worsens, pressure increases, leading to

earlier opening of MV and shortening of A2-Os interval

Evaluation

n  Echo for severity Mean Gradient MVA PASP

Mild <5mmHg >1.5 cm2

<30mmHg

Moderate 5-10mmHg 1-1.5 30-50 mmHg

Severe >10 mmHg <1 >50 mmHg

Treatment

n  Anticoagulation if AF n  Intervention if symptoms

Percutaneous Mitral Balloon Valvotomy

n  Success rate depends on morphology of MV (pliable)

n  Absent 0s, soft S1- probably calcified and won’t do well

n  Crisp OS and loud S1- should do well n  Contraindications- MR > 2+, LA thrombus

Mitral Balloon Valvotomy Severe MS and non-pliable Valve

n  Class I or II: Observe n  Class III or IV: MVR

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Severe MS, pliable Valve,

n  Class II, III, IV : Consider PMBV n  Asymptomatic

n  PAP > 60mmHg n  New onset Afib

Mitral Regurtiation

Acute MR

n  Etiology n  Chordal rupture n  IE n  Ischemic heart disease

Acute MR

n  Consider if hyperdynamic LV function and shock

n  Pulmonary congestion/edema n  S3 and S4 n  MR murmur may be absent or soft

Acute MR

n  Sudden volume overload on unprepared LA and LV. Increased preload and increased SV. Without time to develop LVH, forward SV and CO are reduced

Management

n  Papillary mm rupture- poor prognosis without surgery

n  IE- depends on response to abx (if CHF- OR)

n  Chordal rupture-depends on tolerance of severe MR

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Treatment

Unstable: IV nitroprusside, IABP, Surgery Stable: IV vasodilators, diuretics, abx. IE- OR if progressive CHF, no response to

abx, abscess or recurrent emboli

Chronic MR

n  Etiology n  Most is degenerative (MVP) n  Ischemic n  IE n  Rheumatic

Pathophysiology

n  Compensatory increase in LVEDV to increase SV and restore forward CO.

n  Eventually, prolonged burden of volume overload results in LV dysfunction, reduced forward output and pulm congestion.

n  By the time symptoms develop, LV dysfunction may have already occurred

n  Once there is LV dysfunction, prognosis poor

Presentation

n  Physical Exam n  Displaced of LV apical impulse n  S3 n  Holosystolic murmur n  May also have diastolic rumble without MS

due to early diastolic filling (sign of severity)

Assessment of Severity

n  Regurgitant volume > 60 mL n  Regurgitant fraction > 50% n  ERO >.4 cm2 n  LV gram n  If normal sized LA and LV- can’t be

severe

Management

Surgery for- Symptoms (Class II-IV) LV dysfunction (EF < 60%, ESD > 40mm) Prophylactic?

Reasonable in asymptomatic pt if low operative mortality (<1%) and high chance of successful repair