Aortic Stenosis

Overview 

Aortic stenosis (AS) is the most common valvular heart disease requiring intervention in developed countries, with a global age-standardized prevalence of 116.3 cases per 100,000 individuals.¹ In the United States, AS affects 1–2% of adults older than 65 years and approximately 12% of those older than 75.² The global prevalence increased 124% between 1990 and 2017, and AS leads to more than 100,000 deaths annually worldwide.¹˒²

AS involves progressive narrowing of the aortic valve opening, reducing or obstructing blood flow from the left ventricle to the body. The condition is associated with exertional dyspnea, angina, and syncope. It progresses over time and may lead to heart failure.

Pathophysiology

The two principal causes of AS are calcific aortic valve disease and congenital bicuspid aortic valve. Calcific (degenerative) disease is the leading cause in older adults, involving progressive leaflet thickening and calcification, a process that begins as aortic sclerosis in approximately 25% of adults older than 65, with an approximate 2% annual rate of progression to significant stenosis.²˒³

A congenital bicuspid aortic valve is present in 1–2% of the population and is the most common predisposition to AS overall, accounting for up to 50% of all aortic valve interventions and more than 80% of valve replacements in patients younger than 60 years.²

The resulting valve obstruction increases left ventricular pressure, driving myocardial hypertrophy, diastolic dysfunction, and, if untreated, heart failure.²

Risk Factors

Established risk factors for calcific AS include older age, male sex, hypertension, smoking, diabetes, coronary artery disease, elevated serum lipoprotein(a) concentrations, and impaired kidney function. Many of these overlap with traditional cardiovascular risk factors.²˒³

Disease progression

Once mild aortic valve obstruction is established (aortic velocity > 2 m/s), hemodynamic progression occurs in nearly all patients. Many patients with severe AS remain asymptomatic for years. The first symptom is typically reduced exercise tolerance or exertional dyspnea, which can be mistaken for heart failure, COPD, asthma, or deconditioning. The classic symptomatic triad, exertional dyspnea, angina, and syncope or presyncope, represents more advanced disease.²˒⁴ Once symptoms develop, mortality rises sharply without intervention.²

Auscultation

A crescendo-decrescendo, mid-systolic ejection murmur that is heard best at the upper right sternal border, and radiates along the carotid arteries. The recommended patient position is sitting upright.⁴

ECG

There are no specific ECG changes for aortic stenosis (AS), however the high pressure load on the left ventricle can lead to ECG patterns characteristic of left ventricular hypertrophy.

Actual recording

This sound was recorded using a stethoscope powered by Eko technology.

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References

1. Small AM, Yutzey KE, Binstadt BA, et al. Unraveling the Mechanisms of Valvular Heart Disease to Identify Medical Therapy Targets: A Scientific Statement From the American Heart Association. *Circulation.* 2024;150(6):e109-e128. doi:10.1161/CIR.0000000000001254

2. Otto CM, Newby DE, Hillis GS. Calcific Aortic Stenosis: A Review. *JAMA.* 2024;332(23):2014-2026. doi:10.1001/jama.2024.16477

3. Shelbaya K, Arthur V, Yang Y, et al. Large-Scale Proteomics Identifies Novel Biomarkers and Circulating Risk Factors for Aortic Stenosis. *Journal of the American College of Cardiology.* 2024;83(5):577-591. doi:10.1016/j.jacc.2023.11.021

4. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. *Journal of the American College of Cardiology.* 2021;77(4):e25-e197. doi:10.1016/j.jacc.2020.11.018