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.

Pathophysiology

When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle (LV) and the aorta. 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.

Etiology

Causes of aortic stenosis include acute rheumatic fever, bicuspid aortic valve and congenital anomalies. As individuals age, calcification of the aortic valves may occur and result in stenosis.

Physical examination

It is most often diagnosed when it is asymptomatic. It is found on routine examination of the heart. A fairly loud systolic, crescendo-decrescendo murmur is heard loudest at the upper right sternal border, and radiates to the carotid arteries. The murmur increases with squatting, decreases with standing and isometric muscular contraction, which helps distinguish it from hypertrophic obstructive cardiomyopathy (HOCM). Respiration has no effect on the loudness of the murmur. The more severe the degree of the stenosis, the later the peak occurs in the crescendo-decrescendo of the murmur. Due to increases in left ventricular pressure from the stenotic aortic valve, over time the ventricle may hypertrophy, resulting in a diastolic dysfunction. As a result, one may hear a 4th heart sound due to the stiff ventricle. With continued increases in ventricular pressure, dilatation of the ventricle will occur, and a 3rd heart sound may be manifest.

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Can statins slow the progression of aortic stenosis? - Tips from Other Journals
From American Family Physician, 4/15/03 by Karl E. Miller

No proven medical treatment is currently available that can delay or reverse the progression of aortic stenosis. New insight into the development and progression of aortic stenosis has resulted in the hypothesis that cholesterol may play a role, implying that lipid-lowering agents may slow progression of the disease. This association between aortic stenosis and hyperlipidemia has been inconsistent in the literature, with some studies reporting a positive correlation and others reporting little or no correlation. Bellamy and associates conducted a community-based study to analyze the effect of hyperlipidemia on the progression of aortic stenosis and to evaluate the impact of lipid-lowering agents, particularly statins, on this progression.

Participants in the study were obtained by screening all adults with aortic stenosis in one county from January 1987 to March 2000. Aortic stenosis was defined as an aortic mean gradient of at least 10 mm Hg and an aortic valve area of 2.0 [cm.sup.2] or less. Additional information assessed included cholesterol level, age, gender, etiology of valvular stenosis, smoking history, and diagnosis of other chronic diseases such as hypertension, diabetes, and coronary disease. A second echocardiogram of the aortic valve was obtained at least six months after the initial measurement, and the value used for the study was the most recent measurement or last performed before the aortic valve replacement surgery. In addition, all drug treatments given to the subjects who participated in the study were recorded. A total of 156 subjects were enrolled in the study, of which 38 subjects received lipid-lowering treatment during the follow-up period.

In the 118 participants who did not receive any statin therapy, the aortic valve mean gradient increased from 22 mm Hg to 39 mm Hg and the aortic valve area decreased from 1.20 [cm.sup.2] to 0.92 [cm.sup.2]. The annualized decrease in the aortic valve area was 0.09 [cm.sup.2] per year. No correlation was found between the total cholesterol or low-density cholesterol levels and the progression of aortic stenosis. Progression of aortic stenosis was significantly slower in patients receiving statin therapy when compared with those who did not receive this class of medications, even when controlling for other variables. The association between statin therapy and slower progression of aortic stenosis was confirmed when the analysis was restricted to patients presenting for systematic follow-up.

The authors conclude that in a community-based population, the progression of aortic stenosis is not correlated with cholesterol levels. The authors add that patients who are receiving statin therapy experience slower progression of aortic stenosis. The results of this study suggest that there is a promise of safe and effective medical treatment for aortic stenosis.

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