Valvular Heart Disease

Valvular Heart Disease – Benjamin Palmer

Background

  • Aortic Stenosis: Degenerative calcification of the aortic cusps, usually due to congenital disease (bicuspid), chronic deterioration, or previous rheumatic inflammation
  • Aortic Insufficiency: Primary valve disease (rheumatic disease, bicuspid aortic valve, infective endocarditis, syphilis) or primary aortic root disease (medial degeneration, aortic dissection, Marfan’s syndrome, bicuspid aortic valve, syphilis, non-syndromic familial)
  • Mitral Regurgitation:
    • Acute: endocarditis, papillary muscle rupture post-MI, trauma, chordal rupture/leaflet flail in the setting of mitral valve prolapse
    • Chronic: myxomatous degeneration, rheumatic fever, healed endocarditis, mitral annular calcification, HOCM with systolic anterior motion, dilated cardiomyopathy
    • Secondary (aka “functional”): 2/2 LV dilation/dysfunction w/ structurally normal MV
  • Mitral Stenosis: Rheumatic fever is the leading cause of mitral stenosis worldwide
    • Calcific MS is more common in high income countries

 

Aortic stenosis

Presentation

  • Angina, syncope, exertional dyspnea, heart failure
  • 70 – 80 y/o symptoms; 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, delayed carotid upstroke (suggest severe AS)

Management

  • Definitive treatment is valve replacement, with the most common indication being symptomatic, severe aortic stenosis
    • Consult cardiac surgery for determination of SAVR vs TAVR (often a multidisciplinary decision between cardiac surgery and TAVR team)
    • In general, high risk surgical patients benefit most from TAVR
  • VUMC:  If the pt is 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

 

 

Aortic Regurgitation

Presentation

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

Management

  • Acute severe AR should be treated with prompt surgical repair
  • Vasodilators such as nitroprusside and diuretics can be used to stabilize patient
  • Chronic severe AR should undergo replacement if:
    • Class I indications: Symptomatic, LVEF < 50%, or are undergoing other cardiac surgery
    • If LVEF > or equal 50%, patients should be considered for surgery if 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
    • Quick mnemonic: 50/50 rule
  • Early symptoms of exercise intolerance can be treated with diuretics
  • Systolic BP should also be controlled with goal SBP < 140 in chronic AR
  • Monitor over time for development of depressed LVEF and/or LV dilation

 

Mitral regurgitation

Presentation

  • Isolated chronic mild to moderate MR is typically only minimally symptomatic
  • Pts w/ severe chronic MR develop progressively worsening dyspnea, orthopnea, and PND
  • Palpitations may develop in the setting of new atrial fibrillation due to LA remodeling/dilation
  • Acute severe MR typically presents with flash pulmonary edema
  • Holosystolic murmur most prominent at the apex and radiating towards the axilla, frequently associated with S3
  • In acute severe MR, pulmonary congestion is typically present
  • Murmur may be absent due to large regurgitant orifice/low velocity regurgitant jet

Management

  • Acute severe MR should be treated with surgery
    • Utilize diuretic therapy and vasodilators such as nitroprusside as means to stabilize patient; Afterload reduction is key to promote forward flow
  • Chronic severe primary MR, surgical repair (favored over valve replacement)
    • Performed if patient develops symptoms (EF > 30% class I, EF < 30% class IIb)
    • Asymptomatic patients if LVEF 30-59% or LVESD > or equal 40 mm (class I) 
    • If EF > or equal 60% and LVESD < 40 mm, or new onset AF or PASP > 50, can also consider repair in low-risk patient (class IIa). Quick mnemonic: 60/40
  • Secondary MR can consider MV repair with persistent class III-IV symptoms while on guideline directed medical therapy
  • If HFrEF, consider MitraClip after volume optimization (see HF section)

 

Mitral Stenosis

Presentation

  • Dyspnea and cough typically occur with activities that increase the flow and pressure gradient across the valve, such as tachy-arrhythmias
  • As the stenosis worsens, symptoms of PND and orthopnea develop 
  • Physical exam: Accentuated S1, prominent P2 if pulmonary hypertension develops, opening snap heard at cardiac apex followed by low-pitched rumbling diastolic murmur

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 pt failed PMBC or undergoing other cardiac surgery
  • Intervention for calcific MS is higher risk and should be reserved only for severely symptomatic patients (in general, prognosis is poor: 5-year survival <50%)
    • No role for commissurotomy with calcific MS, surgical valve replacement may be considered for severely symptomatic patients (technically challenging)