Read more about this disease, some with Classification – Types – Signs and symptoms – Genetics – Pathophysiology – Diagnosis – Screening – Prevention – Treatment and management – Cures and much more, some including pictures and video when available.
Aortic valve stenosis (AS) is a valvular heart disease caused by the incomplete opening of the aortic valve.[1]
The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle (LV) and the aorta.[2] The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.
In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.
Major causes and predisposing conditions of aortic stenosis include acute rheumatic fever and bicuspid aortic valve. As individuals age, calcification of the aortic valve may occur and result in stenosis. This is especially likely to occur in people with a bicuspid aortic valve, but also occurs in the setting of perfectly normal valves as a result of age-induced ‘wear and tear’. Typically, aortic stenosis due to calcification of a bicuspid valve occurs in the 4th or 5th decade of life, whereas that due to calcification of a normal valve tends to occur later – around the 7th or 8th decade.
Of the various forms of aortic stenosis, the calcific type is predominant. Since calcific aortic stenosis shares many pathological features and risk factors with atherosclerosis, and since atherosclerosis may be prevented and/or reversed by cholesterol lowering, there has been interest in attempting to modify the course of calcific aortic stenosis by cholesterol lowering with statin drugs. Although a number of small, observational studies demonstrated an association between lowered cholesterol and decreased progression, and even regression, of calcific aortic stenosis, a recent, large randomized clinical trial, published in 2005, failed to find any predictable effect of cholesterol lowering on calcific aortic stenosis. A 2007 study did demonstrate a slowing of aortic stenosis with the statin rosuvastatin.[3] However, what is likely to be considered the definitive trial, published in the New England Journal of Medicine in 2008, failed to find any beneficial effect of intensive cholesterol lowering on the course of aortic stenosis [4].
Aortic stenosis is a common problem. Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder. In North America and Europe, at least, the population is aging. Hence, the prevalence of aortic stenosis is increasing. Since the disease carries with it considerable morbidity and mortality, both with large personal and economic impact, aortic stenosis is a major health problem.[5]
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