Atielogy and Pathophysio of Aortic Stenosis

Atielogy

Congenital:
• Congenital Bicuspid Valve: Usually asymptomatic in the event of the early life. Usually diagnosed during routine physical check-up. 4 times likely to get the more compared to normal individuals in later life. Predominantly men.
• Congenital Aortic Stenosis: Usually develops congestive heart failure in the first week of life due to the incompatibly of the small left ventricle to sustain life.

Aquired
• Aortic sclerosis: Degenerative aortic valve disease with thickening of the aortic valves with fibrosis and calcification. Over the years it progresses to aortic stenosis in 15% of the patients. Resemblance to atherosclerosis with deposition of lipoproteins and active inflammation. Patients with risk factors for atherosclerosis have a higher chance to develop aortic stenosis.
• Rheumatic Fever: Patients have a fibrous contracture with shortening of the cusps due to recurrent inflammation from rheumatic carditis. Adjacent cusps tend to fuse at commissures. This causes a form of bicuspid or unicuspid valve. Calcification can occur but primary cause of stenosis is the adhesions that form the cusps. Incidence decreases with the decrease in rheumatic fever. Developing contries.
• Other less common causes of aortic stenosis include homozygous hypercholesterolemia, and radiation heart disease.

Pathophysiology
When the aortic valve becomes stenotic, resistance to systolic ejection increases as the lumen between the ventricular and aortic compartments becomes smaller. This creates a systolic gradient between the left ventricle and the aorta. This leads to pressure overload in the left ventricle to meet the demands of the cardiac output and causes left ventricle hypertrophy. At this stage, the ventricle chamber is not dilated, although diastolic compliance may be affected.
Eventually, the chamber will dilate, coupled with increase compliance, increase in end systolic pressure and rise in atrial systolic pressure will result in an overload in pressure. This eventually leads to myocardial decompensation. The contractility of the myocardium diminishes causing a drop in cardiac output. The increase in end systolic pressure causes an increase in left atrium pressure in which involving the pulmonary circuit, also decrease in ejection fraction. In the end, it sums up to Congestive Heat Failure (CHF).