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Valvular Heart Disease

Jonathan Napper, Marcus Threadcraft

Aortic stenosis

Jonathan Napper 

Etiology

  • Degenerative calcification of the aortic cusps
  • Congenital bicuspid aortic valve
  • Chronic deterioration (calcific)
  • Prior rheumatic fever/inflammation

Presentation

  • Angina, syncope, exertional dyspnea, heart failure (HF carries worse prognosis)
  • Typically aged 70 – 80 y/o; if bicuspid aortic valve expect 10-20 yrs earlier
  • Physical exam: Systolic crescendo-decrescendo murmur that radiates towards the carotids
  • Late peaking murmur, faint or absent S2, or delayed carotid upstroke suggest severe AS

Evaluation

  • TTE with doppler is test of choice
Severity   Valve Area (cm2)  Mean Gradient (mmHg) 

Velocity  

(m/s) 

 Indexed Valve Area (cm2/m2)  
Mild   >1.5  <20  2.0-2.9  >0.85 
Moderate   1.0-1.5  20-39  3.0-3.9  0.60-0.85 
Severe  <1.0  >40  >4.0  <0.6 
Critical   <0.5  --  --  -- 

AS stages

  • A: at risk of AS (those with bicuspid anatomy or calcification
  • B: Asymptomatic non-severe AS
  • C: asymptomatic AS
    • C1: normal EF
    • C2: abnormal EF
      • This stage might benefit from exercise or stress testing to elicit symptoms

  • D: Symptomatic AS

  • Some with symptomatic AS might not have enough LV reserve to produce high velocities and gradients (ex EF of 10% w/ critical valve area) = low flow/low gradient AS; consider dobutamine to unmask AS

Management

  • No proven effective medical therapy
  • Definitive treatment is valve replacement for:
    • Stage D
    • Stage C with inducible symptoms on stress testing, low EF, or undergoing other cardiac procedure
    • Rapid progression (increase in velocity >0.3m/sec per year)
  • Consult cardiac surgery for determination of SAVR vs TAVR
    • In general, high risk surgical patients benefit most from TAVR
    • At VUMC: If determined to be intermediate to high operative risk by Cardiac Surgery, they will often recommend contacting the TAVR team for evaluation
  • Avoid rapid hemodynamic shifts and aggressive changes in preload or afterload
  • Aim for normotension
    • Avoid preferential vasodilators such as hydralazine or nitroglycerin
    • Significant vasodilation may ↓ coronary filling pressures -> myocardial ischemia

Monitoring

  • Severe AS: TTE q 6-12 months
  • Moderate AS: TTE q 1-2 years
  • Mild AS: TTE q 3-5 years

Post AVR anticoagulation

  • All patients will get 3-6 months of AC s/p AVR
  • Continued duration based on type of AVR
    • Bioprosthetic (TAVR and some SAVRs): antiplatelets alone after Initial AC
    • Mechanical: lifelong AC with warfarin only

Aortic Regurgitation

Jonathan Napper 

Etiology

  • Primary valve disease (rheumatic disease, bicuspid aortic valve, infective endocarditis, syphilis)
  • Primary aortic root disease (medial degeneration, aortic dissection, Marfan’s syndrome, bicuspid aortic valve, syphilis, non-syndromic familial)

Presentation

  • Acute AR: LV cannot respond to increased volume to maintain stroke volume pulmonary edema and cardiogenic shock
  • Chronic AR: indolent presentation, often patient will develop symptoms of heart failure including DoE, orthopnea, PND
  • Physical exam: “Water-hammer” pulses, wide pulse pressure, laterally displaced PMI, high pitched “blowing” decrescendo murmur best heard at third intercostal space at left sternal border, S3

Management

  • Acute severe AR
    • Prompt surgical repair
    • Vasodilators such as nitroprusside and diuretics can be used to stabilize patient

  • Chronic severe AR

    • Medical management
    • Early symptoms of exercise intolerance can be treated with diuretics
    • Systolic BP should also be controlled with goal SBP \< 140 in chronic AR

  • Repeat imaging should be performed 3-6 month to assess for depressed LVEF or LV dilation

  • Stages of Chronic AR: Ranging from Stage (A): Asymptomatic but “At Risk” AR to Stage (D) Symptomatic Severe AR

    • If symptoms are present, automatically Stage D, otherwise Progression through stages is determined by AR Jet Width
  • Class I indications for Valve Repair:
    • Stage D (Symptomatic) or Stage C (Asymptomatic Severe AR) with LVEF \< 55%, or are undergoing other cardiac surgery
    • If LVEF > or equal 55%, patients should be considered for surgery if LV is dilated (LVESD > 50 mm (class IIa) or LVEDD > 65 mm (class IIb))
    • Any patient with progressive AR, even if they do not meet criteria for severe AR, should consider valve replacement if undergoing cardiac surgery for other reasons
    • Note: TAVI for isolated chronic AR is challenging 2/2 dilation of the aortic annulus and root

Mitral Regurgitation

Marcus Threadcraft

Etiology

  • Primary MR – caused by direct involvement of the valve apparatus (leaflets or chordae tendineae)
  • Degenerative/myxomatous mitral valve disease (mitral valve prolapse with flail leaflet, mitral annular calcification, chordal rupture)
  • Rheumatic fever
  • Infective endocarditis
  • Papillary muscle rupture following acute (inferior) MI
  • Secondary MR- caused by changes of the LV that lead to valvular incompetence
  • Dilated Cardiomyopathy
  • HOCM with systolic anterior motion
  • Coronary Artery Disease or prior MI leading to papillary muscle tethering

Presentation

  • Acute MR- sudden onset reduction in forward cardiac flow and left atrial/pulmonary vein volume overload
  • Dyspnea with flash pulmonary edema
  • Left-sided heart failure
  • Chronic MR- progressive symptoms d/t cardiac remodeling to compensate for mitral flow reversal
  • Progressively worsening heart failure: dyspnea, orthopnea, PND
  • LV dilation from volume overload
  • LA remodeling/dilation leading to afib

Auscultation

  • Holosystolic Murmur
  • Best heard at Apex
  • Radiation to the Axilla
  • Frequently associated with S3
  • Murmur may be absent in acute MR due to large regurgitant orifice/low velocity regurgitant jet
  • Increases w/ increased preload or afterload
  • Pulmonary Rales

Evaluation

  • CXR: assess for pulmonary edema, r/o other causes of acute dyspnea
  • ECG: often non-specific, LVH
  • Echocardiography: assess valve apparatus, size, and function of LA/LV, grade severity of MR

Chronic MR stages

  • A: No symptoms
  • B: >mild MR w/o hemodynamic changes or symptoms
  • C: Severe MR w/o symptoms
    • C1: preserved EF and normal LV size
    • C2: reduced EF (\<60%), dilated LV (LVESD > 40mm)
  • D: Severe/symptomatic

Management

Acute hemodynamically significant MR

  • Urgent surgical repair or replacement
  • Medical stabilization as a bridge to surgery
    • Afterload reduction is key to promote forward flow
    • Vasodilators (nitroprusside, nitroglycerin) reduce afterload
    • Diuresis to reduce preload and improve pulmonary edema
    • IABP placement can be used as mechanical afterload reduction

Chronic severe primary MR

  • Surgical repair favored over valve replacement
  • Class I:
    • Asymptomatic patients w/ LVEF 30-59% or LVESD > or equal 40mm
    • Symptomatic patients w/ EF > 30%
  • Class II:
    • A: asymptomatic patients with progressive EF decline or LV dilation on serial monitoring; or very severe MR
    • B: new onset AF
  • Secondary MR can consider MV repair with persistent class III-IV symptoms while on guideline directed medical therapy
  • In HFrEF, consider MitraClip after volume optimization (see Heart Failure section)

Mitral Stenosis

Marcus Threadcraft

Etiology

Characterized by thickened mitral valve leaflets and fused leaflet tips.

  • Rheumatic Fever (leading cause worldwide)
  • Calcification of the mitral valve annulus (common in high income countries)
  • Autoimmune Diseases: SLE, Rheumatoid arthritis

Presentation

  • Progressive symptoms: Asymptomatic Heart Failure
  • Orthopnea
  • PND
  • Hoarseness/Dysphagia (compression of recurrent laryngeal nerve/esophagus by enlarged left atrium from pressure overload)
  • Symptoms of Right Heart Failure
  • Acute Symptoms may present in settings of increased cardiac output (pregnancy, sepsis, or exercise) or tachyarrhythmias
  • Dyspnea
  • Fatigue
  • Palpitations

Physical exam

  • Low-pitched rumbling, diastolic Murmur, best heard at apex, low-pitched, rum
    • Loud S1, opening snap after S2
    • Prominent P2 if pulmonary HTN develops
  • Pulmonary Rales

Evaluation

  • CXR: LA enlargement, increased pulmonary vasculature
  • Echocardiography: thickening of mitral valve leaflets, decreased area of valve leaflets, left atrial enlargement

Management

  • Varies between rheumatic MS and calcific MS (in general, intervention of calcific MS is very challenging and high risk)
  • Severe, symptomatic rheumatic MS:
    • Percutaneous mitral balloon commissurotomy (PMBC)
    • Surgical repair/replacement if patient failed PMBC or undergoing other cardiac surgery

  • Calcific MS has a poor prognosis with 5-year survival \<50%, Intervention is higher risk and should be reserved for severely symptomatic patients

  • No role for commissurotomy with calcific MS

  • Surgical valve replacement may be considered for severely symptomatic patients (technically challenging)

Anti-Coagulation

  • Anti-coagulation is indicated if:
    • Mechanical prosthetic mitral valve
      • Warfarin, goal INR 3-4 lifelong
    • Bioprosthetic mitral valve replacement
      • Warfarin, goal INR 2-3 for first 3-6 months
    • Atrial Fibrillation regardless of CHADS2VASC score
Last update: 2022-05-29 04:05:22