Epidemiology


Etiology

Tip

  • <60-65 years: Congenital bicuspid aortic valve is the most common cause. The altered hemodynamics across two leaflets instead of three leads to premature fibrosis and calcification.
  • >65-70 years: Degenerative (senile) calcific stenosis of a previously normal tricuspid valve is the most common cause.
  • Aortic valve sclerosis: calcification and fibrosis of aortic valve leaflets
    • Most common cause of aortic stenosis
    • Occurs at an increasing rate as patients age (prevalence is 35% in those aged 75–85 years)
    • Similar pathophysiology to Atherosclerotic cardiovascular disease
  • Bicuspid aortic valve (BAV): fusion of two of the three aortic-valve leaflets in utero
    • Most common congenital heart valve malformation, predominantly affects males (3:1)
    • Predisposes the valve to dystrophic calcification and degeneration
    • Bicuspid Aortic Valve can cause both Aortic Stenosis (AS) and Aortic Regurgitation (AR), though AS is the most common complication overall. c
    • AR often presents earlier than AS (e.g., 20s or 30s) if due to prolapse, or acutely if secondary to IE.

Pathophysiology


Clinical features

  • Symptoms (SAD Triad)Syncope (exertional), Angina, Dyspnea (HF).
    • Prognosis post-symptom onset: HF (2 yrs) < Syncope (3 yrs) < Angina (5 yrs, severe phase). c
    • Due to increased LV oxygen demand and reduced coronary flow reserve
  • Signs and symptoms
  • Physical Exam
    • Pulses: Pulsus parvus et tardus (weak and delayed carotid upstroke) + narrow pulse pressure t
    • Harsh crescendo-decrescendo (diamond-shaped), late systolic ejection murmur that radiates bilaterally to the carotids
      • Best heard in the 2nd right intercostal space
      • Handgrip decreases the intensity of the murmur.
      • Valsalva and standing from squatting decreases or does not change the intensity of the murmur (in contrast to hypertrophic cardiomyopathy).
      • Late-peaking” murmur in severe AS, because as the valve becomes more stenotic, the Left Ventricle requires more time to build up sufficient pressure to overcome the obstruction and eject blood. t
    • Soft, single S2
      • A soft S2 results from a delay in the aortic component (A2) and softer closing of the aortic valve due to reduced mobility.
    • S4 is best heard at the apex.
      • Because of decreased compliance of the LV
    • Early systolic ejection click
      • Results from the abrupt stop of the valve leaflets upon opening

Diagnostics

  • Initial/Screening: Transthoracic Echocardiogram (TTE).
    • Determines severity. Severe AS: Valve area ≤ 1.0 cm², mean gradient ≥ 40 mm Hg, peak velocity ≥ 4 m/s. t
  • Key Labs/Imaging:
    • ECG: Shows LVH w/ strain pattern, LA enlargement.
    • CXR: Aortic valve calcification, post-stenotic aortic dilation, LV prominence.
    • BNP/pro-BNP: Elevated in decompensated HF.
  • Confirmatory/Gold Standard: Cardiac catheterization (only if TTE is inconclusive or discrepancies exist b/w clinical exam and echo).

Treatment

  • Asymptomatic (LVEF > 50%): Observation and serial TTEs (every 6-12 months for severe AS).
  • Symptomatic OR Asymptomatic w/ LVEF < 50% OR undergoing other cardiac surgery: Aortic Valve Replacement (AVR).
    • Surgical AVR (SAVR): Preferred in pts with low surgical risk. (Mechanical valve if < 50-65 yrs; Bioprosthetic if > 65 yrs).
    • Transcatheter AVR (TAVR): Preferred in pts with high/prohibitive surgical risk or older age (> 80 yrs).
  • Medical Management: AS pts are highly preload dependent. Use diuretics, nitrates, and vasodilators with extreme caution to avoid severe hypotension.