Aortic Valvular Stenosis

Descriptive text is not available for this image BASICS

DESCRIPTION

  • Aortic stenosis (AS) is a narrowing of the aortic valve (AV) area from leaflet fibrosis or calcification, leading to obstruction of the left ventricular (LV) outflow tract.
  • AS has a long asymptomatic latency period.
  • Development of severe obstruction, syncope, angina, and symptoms of congestive heart failure (CHF) have high mortality without surgical intervention.

EPIDEMIOLOGY

  • AS is the most common acquired valve disease leading to operative intervention in Europe and North America (1).
  • Cause by age at presentation: <30 years, congenital; typically presents as bicuspid or unicuspid valve; 30 to 65 years, congenital or rheumatic fever (RF); >65 years, degenerative calcification of AV

Prevalence

  • Affects 1% of population aged 65 to 74 years, 2% of aged 75 to 84 years, 4% of aged >84 years
  • Bicuspid aortic valve present in 1–2% of population predisposes to AS at an earlier age.

ETIOLOGY AND PATHOPHYSIOLOGY

  • An increase in LV systolic pressure is required to preserve cardiac output leading to concentric LV hypertrophy (LVH), preserving ejection fraction but adversely affecting heart function. LVH impairs coronary blood flow during diastole by compressing coronary arteries and reducing capillary ingrowth into hypertrophied muscle.
    • LVH results in diastolic dysfunction by reducing ventricular compliance. Diastolic dysfunction necessitates stronger left atrial (LA) contraction to augment preload and maintain stroke volume. Loss of LA contraction by atrial fibrillation can induce acute deterioration.
  • Diastolic dysfunction may persist after AS interventions due to interstitial fibrosis.
  • Degenerative calcific changes to the AV caused by endothelial dysfunction and lipid deposition, followed by an inflammatory response, fibrosis, and calcification.
  • Congenital: unicuspid valve, bicuspid valve, tricuspid valve with fusion of commissures, hypoplastic annulus

Genetics

Bicuspid aortic valves display genetic variants leading to accelerated calcification in AS.

RISK FACTORS

  • Congenital unicommissural valve or bicuspid valve
  • RF—zost cases are associated with mitral valve disease.
  • Degenerative calcific changes
    • Most common cause of acquired AS in the US. Risk factors include hypercholesteremia, hypertension, cigarette smoking, male gender, age, diabetes mellitus, and arterial hypertension.

GENERAL PREVENTION

Optimal management of hypertension, cardiac comorbid conditions, and smoking cessation; angiotensin-converting enzyme (ACE) and ARB inhibitors decrease LV fibrosis.

COMMONLY ASSOCIATED CONDITIONS

  • Coronary artery disease (CAD) (50% of patients); hypertension (40% of patients)
  • Aortic insufficiency (common in calcified bicuspid valves and rheumatic disease)
  • Mitral valve disease: 95% of patients with AS from RF also have mitral valve disease.
  • LV dysfunction and CHF
  • Acquired von Willebrand disease: Impaired platelet function and decreased von Willebrand factor results in bleeding in 20% of AS patients. Severity of coagulopathy is directly related to severity of AS.
  • Gastrointestinal arteriovenous malformations (AVMs)
  • Cerebral or systemic embolic events due to calcium emboli.

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