AORTIC STENOSIS


Pathophysiology:

  1. Typically caused by atherosclerotic deposits on the valve, though can be congenital
  2. Highest LV systolic pressure of any condition (massive hypertrophy)
  3. Causes LV hypertrophy which in turn leads to decreased ventricular compliance end diastolic kick, marked increase in 'a' wave, and increased LV oxygen requirements
  4. Aortic pressure rises more gradually than normal, leading to longer systole
  5.  
  6. Risk factors for progression of Aortic Stenosis:
    1. In a prospective study of 170 pts with AS undergoing echocardiography twice, vg. 23mos apart, rapid progression (valve area reduction > 7%/yr) ass'd with large initial valve area, small initial valve gradient, higher serum Cr level, chol. > 200 mg/dL, current smoking, and high serum Ca levels (Circ. 101:2497, 2000--JW)
  7. Generally classified in severity according to aortic jet velocity (in m/sec) or valve area; both estimated on echocardiography

Clinical features:

  1. Symptoms tend to occur late in disease (valve area <1 cm2) and can consist of angina, exertional syncope or presyncope, or nonspecific fatigue
  2. Heart Sounds: Classic murmus is harsh, crescendo-decrescendo midsystolic murmur heard best in the 2nd intercostal space; possibly radiating to right side of neck; See also see under "Cardiac Murmurs".
  3. Pts need increased coronary blood flow but longer systole impedes flow. Can cause angina even with nl arteries
  4. Pulsus parvus and tardus
  5. Cardiac output usually remains normal until very late in course
  6. Onset of LV failure associated with rapid deterioration, death
  7. Generally no pulmonary congestion (because mean LA pressure is normal)
  8. Diagnosis usually by echocardiography
  9. Median survival 2-3y once symptomatic if valve replacement not performed

Management:

  1. Monitoring with echocardiography Q1y with severe disease, Q 1-2 years with moderate disease, and Q3-5 years with mild disease
  2. Aortic valve replacement is the mainstay of treatment
    1. Generally recommended with disease accompanied by LV systolic dysfunction or symptoms
    2. Requires prophylaxis for thromboembolism
      1. In a non-randomized prospective study of 149 pts undergoing aortic valve replacement with a biograft, some of whom received warfarin x the first 3mos, and ther est of which received only aspirin, the 3mo incidence of cerebral ischemic events, major bleeding, and mortality were not sig. diff. between the two groups (Circ. 110:496, 2004--abst)
    3. Types of AVR
      1. Bioprosthetic (doesn't require lifelong anticoagulation but shorter-lived)
      2. Mechanical (requires lifelong anticoagulation-and antimicrobial prophylaxis with certain procedures-but longer-lived)
  3. Self-expanding aortic valve prosthesis (CoreValve)
  4. Balloon valvuloplasty has had disappointing results
  5. Statins for aortic stenosis
    1. Use of statins was ass'd with significantly slower progression of aortic stenosis in a non-randomized trial in 156 pts with aortic stenosis (mean gradient > 9mm Hg and aortic valve area < 2.1 cm2) (J. Am. Coll. Cardiol. 40:1723, 2002--AFP)
    2. In a study in 155 pts with calcific aortic stenosis randomized to atorvastatin 80mg/d vs. placebo, over median 25mo f/u, there were no sig. differences in change in aortic jet velocity or aortic-valve calcium scores (NEJM 352:2389, 2005--abst)
  6. ACE Inhibitors for aortic stenosis
    1. In a non-randomized prospective study of 211 pts 60-80yo with aortic stenosis (peak velocity > 2.5 m/s) and normal LVEF at baseline, hemodynamic progression of the AS occurred sig. less frequently in pts treated with statins than those who were not; ACEI use was not ass'd with a change in progression incidence (Circ. 110:1291, 2004--abst)

n.b. Aortic valve sclerosis (thickening & calcification w/o obstruction of outflow) ass'd with elevation in cardiovascular and all-cause mortality (5y RR of 1.52 and 1.35 in one prospective study--NEJM 341:142, 1999--JW)

(Sources include Core Content Review of Family Medicine, 2012)