Valvular Heart Disease

    .

     

    Introduction/Review

    • Valve dysfunction can be:
      • Stenotic lesions --> overload of chamber proximal.
      • Regurgitation --> overload of both chambers proximal and distal. 
      • Both
    • Often associated with chamber remodeling to adapt to pressure or volume overload (or both).
    • Two types of hypertrophy:
      • Eccentric hypertrophy
        • Elongation of cells due to new sarcomeres layed down in series rather than in parallel. > myocytes become longer > LV dilates without thickening walls.
        • Progressive dilation leads to systolic dysfunction.
      • Concentric hypertrophy
        • Sarcomeres layed down in parallel -> thickening of LV wall -> causing smaller chamber. 
    • Combined regurgitation and stenosis develop both concentric and eccentric hypertrophy (i.e. aortic regurg and stenosis)
      • Dominant abnormality dictates predominant remodeling. 
    • Compensatory changes maintain heart function, and are asymptomatic for a long time.
    • Acute valve changes lack compensatory remodeling, can can present as severe symptoms. and hemodynamically unstable
      (i.e. sudden volume overload)
      • I.e. acute papillary muscle rupture causing severe MR.

     

     

    Diagnostic Tests

    • Indication for echocardiography in incidentally discovered murmur:
      • Symptomatic
      • Systolic grade 3 or louder, extending from S1 to S2 or longer, or diastolic murmurs..
    • DO NOT investigate Grade ≤2 systolic non-radiating murmurs with no other abnormalities or reasons to investigate.

     

    • Transthoracic Echo: LV size/function, pulmonary pressures, other disease and severity.
      • If image quality is poor --> TEE recommended.
    • CT/MRI if echo not helpful, along with stress testing and BNP levels.
    • Other indications for TEE for valve assessment:
      • Endocarditis, prosthetic valves, etc..

     

    Aortic Stenosis

    • Cause:
      • 1st most common: Calcific degeneration of trileaflet aortic valve is the most common cause.
        • Along with mitral annular calcification, this is often regarded as an atherosclerotic process.
      • 2nd most common: Congenital bicuspid valve disease.
        • Younger presentation, earlier need for intervention.
      • 3rd most common: Rheumatic heart disease (uncommon)
    • Initially get aortic "sclerosis", thickening of aortic leaflets without obstruction or stenosis (25% of pts >65yo).
      • Often early-peaking systolic murmur is detected.  Echo: thickening of aortic leaflets, but no elevated pressure gradient.
      • In minority, can progress to aortic stenosis.
    • Multiple RCT's using statins, but did not find slowed rate of progression AS.
    • In aortic stenosis: increased LV afterload, results in concentric LV hypertrophy.  Pattern is adaptive to increased wall stress and helps maintain systolic function.  However as it progresses, diastolic dysfunction occurs, causing increased filling pressures and symptoms of angina/dyspnea.
      • High endocardial pressures and hypertrophy can cause subendocardial ischemia and angina.
    • Symptoms
      • Reduced exercise tolerance and exertional dyspnea are earliest symptoms.
      • Onset of cardinal symptoms: (avg. survival 2-3y without intervention.)
        • Angina
        • Syncope
        • Heart failure 

     

    • Physical Exam:

     

    Classic Murmur

    Associated Features

    Severity / Notes:

    Location: RUSB

     

    Quality: Mid-systolic; crescendo-decrescendo

     

    Radiates:

    - Right clavicular, carotid, apex

    - Enlarged, nondisplaced apical impulse;

    - S4;

    - bicuspid valve without calcification will have

    systolic ejection click

    followed by murmur

    Severe aortic stenosis may include:

    - decreased A2;

    - low amplitude, high pitched,

    - late peaking murmur;

    - diminished and delayed carotid upstroke

    NOTE: Radiation of murmur down the descending

    thoracic aorta may mimic mitral regurgitation


    • Consequences:
      • Due to strict outlet size, fixed output, cardiac output limited with exertion.
        • syncope during exercise.
      • Loss of atrial kick, or decrease in diastolic filling time (i.e. exercise or Afib) can lead to deterioration.
      • BUT! asymptomatic patients have same survival time as those without AS.
    • Some patients have low gradient (or moderate) but have small calculated valve area = "low gradient AS"
      • Dobutamine stress echo useful to differentiate from true AS (persists stenosis) vs. pseudo-stenosis (calc. valve area increases in response to dobutamine-induced increased contractility.
      • Replacement is indicated for patients with severe aortic stenosis: valve gradient > 40 mmHg and
        • Symptoms such as dyspnea, chest discomfort, syncope.
        • LVEF is abnormal < 50%
        • Poor response to exercise (hypotension, symptoms).
        • Rapid AS progression (i.e. mean gradient > 60 mmHg).
        • Other cardiac surgery is planned.
      • If patient is asymptomatic: repeat physical exam in 6 months, repeat echo in 12 months. 
    • AVRindications.png
    • Source: AHA guidelines
       
    •  ETT: exercise treadmill test;

     

    • Surgical valve repair/replacement is the only definitive treatment.
    • Workup:
      • If systolic dysfunction and moderate AS --> do dobutamin stress echo to find the true severity of AS. (low flow, low gradient AS)
      • Cardiac catheterization to assess CAD.
    • AS and heart failure
      • Cautious diuresis can improve symptoms.
        • Acute reduction in preload by diuresis can reduce stroke volume and BP drops.
      • Diuresis can be effective, but does not change indication for surgery.
      • Afterload reduction can be used in acute pulmonary edema (in systolic dysfunction), but titrate carefully to avoid hypotension. 
    • Treatment options:
      • No pharmacologic therapy know to decrease progression of AS.
        • Treat concominant risk factors for CAD (high prevalence of CAD).
        • Only surgery offers survival benefit and durable symptom relief.
      • Balloon aortic valve replacement
        • Indicated for severe AS with hemodynamic compromise. (bridges to aortic valve repair).
        • Only mild improvement, and high rate of restenosis at 6mo.
        • High complications (stroke, MI, death)
      • Transcatheter aortic valve replacement (TAVI)
        • Reserved for very high predicted operative mortality.
        • Superior to medical therapy.
        • Mortality equivalent to surgical replacement.
        • Extends indications for patients who are not operative candidates.
      • ***Surgical valve repair*** (3-4% operative mortality?)
        • Recommended therapy.

     

    TAVR

    • Candidates carefully selected
    • Surgical Risk Assessed: Society of Thoracic Surgeons adult cardiac risk score (STS Score)
    • Not approved for:
      • Concomitant valve disease (such as AR, or Mitral disease)
      • Bicuspid Aortic Valve

    Aortic Regurgitation

    • Acute AR relatively uncommon.. can be due to:
      • dissection
      • endocarditis
      • trauma
    • More commonly chronic, gradually progressive due to :
      • Bicuspid valve
      • Calcific degeneration
      • Myxomatous degeneration
      • Ascending Aortic pathology (Marfans, ascending aortic dilation, aortitis (AnkSpond or giant cell aortitis)).
      • Subvalvular abnormalities (subaortic stenosis, VSD causing aortic valve leafelet damage).
    • Leads to volume and pressure overload of LV.
      • (Eccentric hypertrophy is due to increased preload, and concentric due to increased afterload/wall stress).
    • Symptoms:
      • Dyspnea, angina, presyncope/syncope => mortality rate 10-20%/year.
      • (Most pts have symptoms)
    • Complications:
      • LV systolic dysfunction (EF < 50%)
        • Progressive LV dilation -> contractility impairment -> global LV dysfunction 
      • LV dilation progressive, annual risk of symptoms increases + LV dysfunction, death up to 19% with LV end-systolic diameter >50mm. = marker of aortic vavel surgery in asymptomatic pt.
    • Physical Exam:
      • Vitals: Wide pulse pressure
    • Classic Murmur

      Associated Features

      Severity / Notes:

      Location: LLSB (valvar) or

                  RLSB (dilated aorta)

       

      Quality: Diastolic; decrescendo

       

      Radiates: NONE

      - Enlarged, displaced apical impulse; 

      - S3 or S4; increased pulse pressure; 

      - bounding carotid and peripheral pulse

       

      Chronic AR (many features! will list later)

      - Acute, severe regurgitation murmur 

      may be masked by tachycardia, short 

      duration of murmur

      - Severity difficult to assess by physical

        exam

     

    • Echocardiogram
      •  
    • Management:
      • Surgery required to reverse LV dysfunction (early stage).
      • Pharmacology
        • Vasodilators theortically reduce regurgitant volume, decrease symptoms, and reduce remodeling.
          • Indications for vasodilator therapy in AR:
            • Acute severe AR for short term hemodynamic improvement (before surgery)
            • AR with LV dysfunction in non-surgical candidates and concominant HTN.
            • Intra-aortic balloon counter-puslation is counterindicated in moderate/severe AR (increase back-flow and AR volume).
        • However, results from small trials did not show benefit on rate of progression. 
      • Surgical valve replacement is the only definitive management.  (see indication below)
        • The BEST management option.
        • Indications when symptoms or evidence of LV systolic dysfunction or severe dilation develops.
    • chronicAI.png

     

    Bucuspid aortic valve

    - most common form of congenital heart lesion (1% of people)

    • Mechanism:
      • Intrinsically abnormal connective tissue.
      • High association with dilation of the ascending aortic arch (require serial screening with TTE, or CT/MR if poor TTE imaging.
        • Indication for replacement of ascending arch:
          • If replacing bicuspid valve, the arch is replaced if >4.5cm (otherwise continues dilating)
          • When no plans to replace the bicuspid valve, then surgery indicated for an aortic root >5.0cm.
        • Post-replacement, serial evaluation of ascending aorta is still needed.
    • High risk of congenital lesions (coarctation of aorta, interrupted arch, turner's syndome).
    • 70% of pts will require surgery for stenotic or regurgitant valve.  
    • Predisposition to calcification leads to stenosis (intervention required at earlier age).
    • 50% of excised valve specimens have bicuspid valve.
    • Also high risk of infective endocarditis!
    • NOTE: Acquired valve disease do not require abx prophylaxis for dental procedures.
    • Ascending aortic dilation can occur in bicuspid valves.
    • Management
      • Balloon valvotomy for young patients <30yo without calcification.
        • This offers intermediate term benefit to delay repair/replacement of the valve. 
        • Often done to wait until valve technology improves.

    Mitral Regurgitation

    • Causes:
      • Organic (Primary)
        • Mitral valve prolapse
        • Rheumatic heart disease
        • Infective endocarditis
        • Collagen vascular disease
      • Functional (Secondary)
        • LV systolic dysfunction causing mitral annular dilation +/- restricted leaflet mobility.
        • CAD/ischemia can cause acute degeneration such as papillary muscle rupture/dysfunction.
        • chronic functional changes in the setting of LV dilatation and systolic dysfunction causing mitral valve leaflet tethering and malcoaptation
    • Pathophysiology:
      • MR causes an increase in ventricular preload, whereas afterload is unchanged or reduced due to low impedance of flow into the LA.
      • Eccentric hypertrophy occurs to accommodate increased LV filling volume initially with normal diastolic filling pressure and maintain full stroke volume.  Eventually increased LA pressure results in dyspnea and pulmonary hypertension and progressive LA dilation results in AFib.
      • Volume overload to LV, ventricle adapts through eccentric hypertrophy/remodeling.
        • This compensatory mechanism maintains ventricular compliance... increases LV volume without increasing filling pressures.
        • With progression of regurgitation, and regurgitation, LV contractility is impaired.
      • Typicaly present in combination with AS due to mitral annular calcification and increased LV systolic pressures, can contribute to dyspnea when MR is moderate or severe.
      • MR ventricle is usually in a hyperdynamic state, so LVEF <60 = indication for surgery.
    •  
    • Physical Exam
    • Classic Murmur

      Associated Features

      Severity / Notes:

      Location: Apex

       

      QualitySystolic; holo- or late systolic

       

      Radiates: To axilla or back

      - Systolic click in mitral valve prolapse;

      - S3;

      - apical impulse hyperdynamic and may be

      displaced if dilated left ventricle;

      - handgrip increases murmur intensity

      - in mitral valve prolapse, Valsalva maneuver

      moves onset of murmur closer to S1

      - Acute, severe regurgitation may have

      soft or no holosystolic murmur, mitral

      inflow rumble, S3

     

    • Echocardiography
      • Regurgitant Flow = 2piR^2 x Va
      • Effective Regurgitant Area (EROA)
      • Regurgitant Volume = EROA x VTI
      • Vena Contracta (where flow convergence happens - smallest diameter of stream - measure perpendicular to flow)
      • Severe =
        • Vena contracta ≥ 0.7cm
        • Regurg volume ≥ 60 mL
        • Regurg fraction ≥ 50%
        • ERO ≥ 0.40 cm^2
    • Management
      • Organic: medical therapy is limited.
        • Acute symptomatic MR  --> CV surgery.
          • Afterload reduction with vasodilators with IV nitroprusside and stroke volume enhanacement with inotropic agents may stabilize patients pre-op.  Aortic balloon pumps can help mechanical ventricular unloading.
        • Chronic severe MR
          • No studies demonstrated clinical benefit with medical therapy.
          • Chronic ischemic MR with LV systolic dysfunction treatment of underlying heart failure with ACEi, beta-blocker witll decrease severity of MR, improve LV function, CV events.
          • Benefit of surgery unclear for functional MR.
          • Mitral valve repair: preferred alternative.  Better preservation of LV systolic function.
            • Improved outcomes with repair vs. replacement.
            • Valve repair has a benefit => no need for anticoagulation.  (replacement involves mechanical valve requiring anticoagulation). 
      • Indications for Mitral Valve Surgery:

           1. Symptomatic Severe MR + LVEF > 30% (Gr I)

         

        OR if Asymptomatic:

         

           1.  LVEF < 60% (asymptomatic) 

           2.  LV End-Systolic Diameter > 40 mm (asymptomatic)

         

           Gr IIA Indications

           3.  Severe pulmonary HTN at rest (PASP >50 mm Hg) or during exercise (>60 mm Hg)

           4.  New onset of atrial fibrillation

         

           Gr IIB Indications

            Severe Symptomatic MR and  LVEF < 30% can consider

          

      • Medical therapy:
        • Preload reduction
        • Treat low EF medically
        • Avoid vasodilator therapy (can affect LV) - can still use for hypertension?
      • Secondary MR
        • Worse outcomes (worsening LV dysfunction and adverse remodeling). 
        • Sparse data that correcting secondary MR improves mortality/sx.
          • Worse outcomes with repair (replacement recommended)
          •  

     

    Mitral Valve Prolapse

    • Decreasing preload (valsalva, or squat-to-stand) cause earlier initiation and longer duration of systolic murmur.
    • Diagnosed on the echo
      • Seen displaced coaptation level of the anterior and/or posterior leaflets leading to 2mm or more displacement above mitral annulus. 
    • Benign prognosis, similar survival to general.
    • "Mitral Prolapse Syndrome"
      • Palpitations, non-anginal chest pain, fatigue, dyspnea. 
      • Link between symptoms and valvular abnormality is unclear.
    • Flail leaflets = lack of coaptation
      • The annual mortality rate is higher than mitral prolapse with regurgitation.
      • Earlier intervention needed than prolapse.

    Mitral Stenosis

    • Causes:
      • Often due to rheumatic heart disease. (can affect other valves, but mostly mitral).
        • Often women in 4-5th decades of life.
      • Rarely calcific disease can cause MS, most often mitral annular calcification in elderly
    • Loading conditions are not significantly altered.
    • Progressive stenosis of mitral valve, stenosis increases LA, pulmonary vein, and pulmonary artery pressures.
    • Symptoms:
      • Exertional dyspnea.
      • Pulmonary edema in states of high flow (i.e. pregnancy), or impaired LV flow (afib/tach)
    • Complications
      • Atrial fibrillation is the most common complication (30% of pts) and thromboembolism.
      • Pulmonary Hypertension
    • Echo Parameters
      • Mean trans-mitral gradient: >10 mm Hg and < 1.0 cm^2 = severe mitral stenosis,
      • Mitral valve area:
        • ≤ 1.5 cm2 in severe mitral stenosis
        • ≤ 1.0 cm2 in very severe mitral stenosis.
    • Physical Exam:
    • Classic Murmur

      Associated Features

      Severity / Other Notes:

      Location: Apex (best heard in left

                  lateral decubitus position)

       

      Quality: Diastolic; 

                   low pitched, decrescendo

       

      Radiates: NONE

      - Opening snap after S2 if leaflets mobile;

      - irregular pulse if atrial fibrillation present

      - Interval between S2 and opening snap is 

         short in severe mitral stenosis

      - Intensity of murmur correlates with transvalvar 

        gradient

      - P2 may be loud if pulmonary hypertension 

        present

       

     

     

    • Management
      • Negative chronotropic drugs (B-blockers etc..)
        • Allow increased diastolic filling time and can improve symptoms.
        • Rate control of AFib is VERY important
      • Anticoagulation required if develop afib, risk is higher than in non-valvular afib.
      • Rhythm control unlikely to be successful unless MS is treated (large LA).
      • Diuretic therapy can improve pulmonary congestion. 
      • Indication for surgery (see below)
        • Must measure PA pressures with exercise echo (indication for surgery if elevated)
        • Mostly presence  of symptoms or pulmonary HTN.
      • Percutaneous balloon valvotomy often a procedure of choice (must r/o LA thrombus with TEE).
        • HIGH success rates.
    • Balloon valvotomy is a possibility, but re-stenosis can occur.
      • Timing is crucial 

        - if done too early, miss asymptomatic period

        - if too late = pulmonary HTN + sx

      • Percutaneous balloon mitral valvuloplasty (PBMV) Indications:
        • Symptomatic (New York Heart Association [NYHA] functional class II, III, or IV)
        • AND severe mitral stenosis
        • AND valve morphology favorable for PBMV
        • AND absence of left atrial thrombus
        • AND absence of moderate to severe mitral regurgitation.
      • Complications:
        • MR, L-R shunt, perforation, embolism, MI
      • Surgery reserved for: (if cannot do percutaneously)
        • Open commisurotomy
        • Valve Reaplacement (last considered, higher mortality)

    Tricuspid Regurgitation

    • Two main causes:
      • Functional TR - due to processes like:
        • Pulmonary hypertension, which increases RV pressure leading to functional TR.
        • Pulmonic regurgitation
        • Left-sided disease
        • Cardiomyopathy (RV dilation)
      • Due to leaflet or myocardial dysfunction
        • Often RV systolic pressure would be < 30.
    • Physical Exam
    • Classic Murmur

      Associated Features

      Severity / Other Notes:

      Location: LLSB

       

      Quality: Holosystolic

       

      Radiates: LUSB

      Merged and prominent c and v waves

      in jugular venous pulse;

      - Murmur increases during inspiration

      - Right ventricular impulse below sternum

      - Pulsatile, enlarged liver with possible ascites

      - May be higher pitched if associated with

        severe pulmonary hypertension

       

     

    • Treatment:
      • Indication for surgery:
        • Severe, symptomatic TR
        • RV enlargement/dysfunction??
      • Surgical options:
        • Tricuspid annuloplasty
        • Replacement

     

    Valve Prophylaxis For Dental Procedures

     

     

    Murmur Maneuvers

    • Decrease Preload:
      • Valsalva
      • Squat-To-Stand
      • Cause decrease in preload.
      • Louder (earier initiation and longer duration of murmur in:
        • hypertrophic cardiomyopathy, mitral valve prolapse.
      • LVOT obstructions: Fixed valvular or subvalvular stenosis
        • If fixed, thse maneuvers decrease intensity of systolic murmur.
    • Increase in afterload
      • Hand squeeze.
      • Increase LV systolic pressure and intensity of mitral valve regurgitation murmur.
    • Other features:
      • Enlarged/displaced apical impulse.
      • S3/S4, systolic ejection click.

     

    Echo Evalutation

    Generally, follow-up echo evaluation

    • Mild: q3-5y
    • Moderate: q1-2y
    • Severe: yearly.

    Serial Evaluation of Asymptomatic Patients with Left-Sided Valvular Conditions

    (Source: MK--SAP16)

    Factors Considered

    Lesion Severity

    Frequency

    Aortic Stenosis

    Stenosis severity; rate of progression

    Mild (mean gradient <25 mm Hg, Vmax <3 m/s, AVA >1.5 cm2)

    Clinical eval yearly; echo every 3-5 y

     

    Moderate (mean gradient 25-40 mm Hg, Vmax 3-4 m/s, AVA 1.0-1.5 cm2)

    Clinical eval yearly; echo every 1-2 y

     

    Severe (mean gradient >40 mm Hg, Vmax >4 m/s, AVA <1.0 cm2)

    Clinical eval yearly; echo yearly

    Mitral Stenosis

    Stenosis severity; rate of progression

    Mild (MVA >1.5 cm2, MPG <5 mm Hg, PASP <30 mm Hg)

    Clinical eval yearly; echo every 3-5 y

     

    Moderate (MVA 1.0-1.5 cm2, MPG 5-10 mm Hg, PASP 30-50 mm Hg)

    Clinical eval yearly; echo every 1-2 y

     

    Severe (MVA <1.0 cm2, MPG >10 mm Hg, PASP >50 mm Hg)

    Clinical eval yearly; echo yearly

    Aortic Regurgitation

    Regurgitation severity; rate of progression; EF; LV chamber size; ascending aorta dilation

    Mild (VC <0.3 cm, ROA <0.10 cm2, RV <30 mL/beat); normal EF

    Clinical eval yearly; echo every 2-3 y

     

    Moderate (VC 0.3-0.6 cm, ROA 0.10-0.29 cm2, RV 30-59 mL/beat, RF 30%-49%)

    Clinical eval yearly; echo every 1-2 y

     

    Severe (VC >0.6 cm, ROA ≥0.3 cm2, RV ≥60 mL/beat, RF >50%)

     

     

    EF >50%; LV size normal

    Clinical eval every 6-12 mo; echo yearly

     

    EF >50%; LV size increased

    Clinical eval every 6 mo; echo every 6-12 mo

    Mitral Regurgitation

    Regurgitation severity; rate of progression; EF; LV chamber size; pulmonary pressure

    Mild (VC <0.3 cm, ROA <0.20 cm2, RV <30 mL/beat; RF <30%)

    Clinical eval yearly; echo only if symptomatic

    (PISA - proximal isovelocity surface area) - way to

    calculate size of orifice or regurgitant jet.

    Moderate (VC 0.3-0.69 cm, ROA 0.20-0.39 cm2, RV 30-59 mL/beat, RF 30%-49%)

    Clinical eval yearly; echo every 1-2 y

     

    Severe (VC ≥0.7 cm, ROA ≥0.4 cm2, RV ≥60 mL/beat, RF >50%)

    Clinical eval every 6-12 mo; echo every 6-12 mo

    AVA = aortic valve area; echo = echocardiography; EF = ejection fraction; eval = evaluation; LV = left ventricle; MPG = mean pressure gradient; MVA = mitral valve area; PASP = pulmonary artery systolic pressure, RF = regurgitant fraction; ROA = regurgitant orifice area; RV = regurgitant volume; VC = vena contracta width; Vmax = maximum aortic jet velocity.

    Recommendations based on American College of Cardiology/American Heart Association Task Force on Practice Guidelines; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons, Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation. 2006;114(5):e84-e231. PMID: 16880336

     

     

    Management

    Indications for Interventions for Valvular Heart Conditions

    • Generally development of LV systolic dysfunction = poor prognostic factor.
    • However, sometimes fixing reversible ischemia by stenting, can improve papillary function and help MR.
    • Generally medical therapy helps acute management, but no effect on progression of disease and mortality.
      • Acute valve dysfunction (i.e. mitral valve proplase) is a surgical emergency.  Afterload reduction and inotropes can help stabilize the patient, but surgery is often needed for definitive management.

    Source: MK-SAP16

    Valve Lesion

    Indications to Intervene

    Intervention

    Aortic stenosis

    Symptoms

    LVEF <50%

    Moderate stenosis at time of other cardiac surgery

    Abnormal blood pressure response (decrease in systolic blood pressure) during exercise

    Rapidly progressive stenosis

    Aortic valve replacement

    Aortic regurgitation

    Symptoms

    LVEF <50%

    LV dilatation (end-systolic dimension >55 mm or end-diastolic dimension >75 mm)

    Aortic valve replacement with ascending aorta graft replacement if enlarged

    Mitral stenosis

    Symptoms

    Pulmonary hypertension (PA systolic pressure ≥50 mm Hg at rest or ≥60 mm Hg during exercise)

    Percutaneous balloon valvotomy (if anatomy favorable by echocardiography with less than moderate mitral regurgitation and no left atrial thrombus)a

    Mitral valve replacement

    Mitral regurgitation

    Symptoms

    LVEF <60% (generally ventricle is in 

                         hyperdynamic state)

    LV end-systolic diameter >40 mm

    Pulmonary hypertension (PA systolic pressure ≥50 mm Hg at rest or ≥60 mm Hg during exercise)

    New-onset atrial fibrillation

    Mitral valve repair if anatomy favorable (presence of annular dilation, mitral leaflet prolapse, or myxomatous changes without calcification or stenosis)

    Mitral valve replacement

    Tricuspid regurgitation

    Refractory right-sided heart failure

    Right ventricular enlargement, systolic dysfunction

    Moderate or severe regurgitation at time of mitral valve surgery

    Tricuspid valve repair if anatomy favorable

    Tricuspid valve replacement (bioprosthetic)

    LV = left ventricle; LVEF = left ventricular ejection fraction; PA = pulmonary artery.

    aAll patients considered for percutaneous balloon mitral valvotomy should undergo transesophageal echocardiography to assess for left atrial appendage clot and mitral regurgitation severity regardless of whether patient has sinus rhythm or atrial fibrillation.

    Recommendations from: Bonow RO, Carabello BA, Chatterjee K, et al; 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118(15):e523- e661. PMID: 18820172

     

     

    Physical Exam Findings Summary

    Valvular and Other Cardiac Lesions and Their Associated Examination Findings

    Cardiac Condition

    Characteristic Murmur

    Location

    Radiation

    Associated Findings

    Severity and Pitfalls

    Aortic stenosis

    Mid-systolic; crescendo-decrescendo

    RUSB

    Right clavicular, carotid, apex

    Enlarged, nondisplaced apical impulse; S4; bicuspid valve without calcification will have systolic ejection click followed by murmur

     

    - Often has diastolic rumble @ apex

    Severe aortic stenosis may include decreased A2; high-pitched, late peaking murmur; diminished and delayed carotid upstroke

    Radiation of murmur down the descending thoracic aorta may mimic mitral regurgitation

    Aortic regurgitation

    Diastolic; decrescendo

    LLSB (valvar) or RLSB (dilated aorta)

    None

    Enlarged, displaced apical impulse; S3 or S4; increased pulse pressure; bounding carotid and peripheral pulse

    Acute, severe regurgitation murmur may be masked by tachycardia, short duration of murmur

    Severity in chronic regurgitation is difficult to assess by murmur

    Bicuspid Aortic Valve Soft systolic ejection murmur @ RUSB with an early systolic click at the apex    

    Mitral stenosis

    Diastolic; low pitched, decrescendo

    Apex (heard best in left lateral decubitus position)

    None

    Opening snap after S2 if leaflets mobile; irregular pulse if atrial fibrillation present

    Interval between S2 and opening snap is short in severe mitral stenosis

    Intensity of murmur correlates with transvalvar gradient

    P2 may be loud if pulmonary hypertension present

    Mitral regurgitation

    Systolic; holo- or late systolic

    Apex

    To axilla or back; occasionally anteriorly to precordium

    Systolic click in mitral valve prolapse; S3; apical impulse hyperdynamic and may be displaced if dilated left ventricle; in mitral valve prolapse, Valsalva maneuver moves onset of murmur closer to S1; handgrip increases murmur intensity

    Acute, severe regurgitation may have soft or no holosystolic murmur, mitral inflow rumble, S3

    Tricuspid stenosis

    Diastolic; low pitched, decrescendo; increased intensity during inspiration

    LLSB

    Nonradiating

    Elevated central venous pressure with prominent awave, signs of venous congestion (hepatomegaly, ascites, edema)

    Low-pitched frequency may be difficult to auscultate, especially at higher heart rate

    Tricuspid regurgitation

    Holosystolic

    LLSB

    LUSB

    Merged and prominent c and v waves in jugular venous pulse; murmur increases during inspiration

    Right ventricular impulse below sternum

    Pulsatile, enlarged liver with possible ascites

    May be higher pitched if associated with severe pulmonary hypertension

    Pulmonary stenosis

    Systolic; crescendo-decrescendo

    LUSB

    Left clavicle

    Pulmonic ejection click after S1 (diminishes with inspiration)

    Increased intensity of murmur with late peaking

    Pulmonary regurgitation

    Diastolic; decrescendo

    LLSB

    None

    Loud P2 if pulmonary hypertension present

    Murmur may be minimal or absent if severe due to minimal difference in pulmonary artery and right ventricular diastolic pressures

    Innocent flow murmur

    Midsystolic; grade 1/6 or 2/6 in intensity

    RUSB

    None

    Normal intensity of A2; no radiation to left clavicle

    May be present in conditions with increased flow (e.g., pregnancy, fever, anemia, hyperthyroidism)

    Hypertrophic obstructive cardiomyopathy

    Systolic; crescendo-decrescendo

    LLSB

    None

    Enlarged, hyperdynamic apical impulse; bifid carotid impulse with delay; increased intensity during Valsalva maneuver or with squatting to standing

    Harsh murmur with increased intensity; murmur may not be present in nonobstructive hypertrophic cardiomyopathy

    Atrial septal defect

    Systolic; crescendo-decrescendo

    RUSB

    None

    Fixed, split S2; right ventricular heave; rarely, tricuspid inflow murmur

    - Often no change with respiration

    May be associated with pulmonary hypertension, including increased intensity of P2 heart sound, pulmonary valve regurgitation

    Ventricular septal defect

    Holosystolic

    LLSB

    None

    Palpable thrill; murmur increases with hand-grip, decreases with amyl nitrite

    - Often no change with respiration

    Murmur intensity and duration decrease as pulmonary hypertension develops (Eisenmenger syndrome)

    Cyanosis if Eisenmenger syndrome develops

     

     

    References

    • MKSAP 16

    • MKSAP 17

    • ACC/AHA Guidelines 2014 (attached)

    • JACC valvular heart disease review

    •  

      Cardiac auscultation: rediscovering the lost art.  (Chizner, 2008)

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