Aortic stenosis is caused primarily by the narrowing of the aortic valve opening, which restricts blood flow from the left ventricle of the heart to the aorta and onward to the rest of the body. This narrowing happens when the valve leaflets, the thin flaps that open and close to regulate blood flow, become thickened, stiff, and often calcified, meaning calcium deposits build up on them, causing them to harden and stick together. This calcification and reduced mobility of the leaflets is the main physical mechanism behind aortic stenosis.
There are two broad categories of causes: congenital and acquired.
**Congenital causes** refer to abnormalities present from birth. The most common congenital cause is a bicuspid aortic valve, where the valve has two leaflets instead of the normal three. This structural difference makes the valve more prone to early wear and calcification. People with a bicuspid valve may live many years without symptoms, but they often develop aortic stenosis earlier in life, sometimes as early as their 50s or 60s. The abnormal valve structure causes turbulent blood flow, which accelerates damage and calcification of the valve leaflets. In some cases, congenital aortic stenosis can be severe enough to cause thickening of the heart muscle (left ventricular hypertrophy) and may even lead to sudden cardiac death if untreated.
**Acquired causes** develop over time, often related to aging and other health conditions. The most common acquired cause is age-related degeneration, where the valve leaflets gradually wear out and calcify as part of the natural aging process. This degeneration leads to stiffening and narrowing of the valve opening. Other acquired causes include:
– **Rheumatic fever**, a complication of untreated streptococcal infections, which can cause inflammation and scarring of the valve leaflets, leading to stenosis.
– **Infective endocarditis**, an infection of the heart valves that can damage the valve tissue and cause scarring or deformation.
– **Damage following a heart attack**, which can affect the valve or the heart muscle supporting it.
– **Diseases of the heart muscle (cardiomyopathy)**, which can alter the structure and function of the valve.
– **Uncontrolled high blood pressure**, which increases the workload on the heart and valve.
– **High cholesterol and diabetes**, which contribute to the buildup of calcium and other deposits on the valve.
– **Connective tissue diseases such as Marfan syndrome**, which affect the structural integrity of the valve.
– **Radiotherapy to the chest area**, which can cause damage and scarring to the valve tissue.
The process of calcification is central to the development of aortic stenosis. Calcium deposits accumulate on the valve leaflets, making them less flexible and impairing their ability to open fully. This calcification is similar to bone formation and is influenced by factors like inflammation, mechanical stress, and metabolic conditions. As the valve narrows, the heart must work harder to pump blood through the smaller opening, leading to thickening of the left ventricular muscle and eventually to symptoms such as chest pain, fainting, and heart failure if untreated.
In summary, aortic stenosis results from a combination of congenital valve abnormalities and acquired factors that cause the valve leaflets to become stiff, thickened, and calcified, reducing their ability to open properly and obstructing blood flow from the heart.
