Aortic stenosis is abnormal narrowing of the aortic valve. A number of conditions cause disease resulting in narrowing of the aortic valve. When the degree of narrowing becomes significant enough to impede the flow of blood from the left ventricle to the arteries, heart problems develop.
In the most severe cases, aortic valve stenosis occurs before a baby is born, and may affect the baby shortly after birth.
Less severe forms of the disease may be “silent”—causing no visible symptoms—until later in life.
Aortic valve stenosis can occur by itself, or as part of a group of abnormalities affecting the left side of the heart. Rarely, children can develop aortic stenosis as a complication of rheumatic fever. Although a physical exam and an electrocardiogram may suggest a possible diagnosis of aortic valve stenosis, an echocardiogram is the definitive test to confirm the condition. Echocardiograms are painless, do not require an IV and only take about an hour.
In adults, three conditions are known to cause aortic stenosis.
Progressive wear and tear of a bicuspid valve present since birth (congenital).
Wear and tear of the aortic valve in the elderly.
Scarring of the aortic valve due to rheumatic fever as a child or young adult.
The most common cause of aortic stenosis in patients 65 years of age and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Turbulence across the valve increases causing scarring, thickening, and stenosis of the valve once valve leaflet mobility is reduced by calcification. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is unknown. The progressive disease causing aortic calcification and stenosis has nothing to with healthy lifestyle choices, unlike the calcium that can deposit in the coronary artery to cause heart attack.
It is far less clear whether a similar effect can be achieved by oral long term vasodilator treatment in asymptomatic patients with AS. Furthermore, the best drug for lowering blood pressure in the presence of an AS has not been established. A specific potential benefit has been suggested for inhibitors of the angiotensin converting enzyme (ACE), since ACE activity has been involved not only in an unfavourable left ventricular remodelling response, but also in the progression of valve degeneration.
However, use of vasodilators has been classically considered contraindicated in AS, because of their potentially hazardous effect related to the risk of decreasing coronary perfusion pressure in this population. Although there are no empirical data to support it, this hypothesis definitely cannot be overlooked. Patients with AS are known to have a diminished coronary flow reserve, as do patients with ischaemic heart disease. It is remarkable that lowering diastolic pressure below 80 mm Hg has been shown to increase the risk of myocardial infarction in ischaemic patients. Consequently, the particular “J shaped” curve of the blood pressure–risk relation needs to be specifically clarified for AS. Until the results of randomised placebo controlled studies become available, the role of these drugs should not be generalised.
