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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Valve Replacement in Patients with Aortic Stenosis
From American Family Physician, 6/1/02 by Bill Zepf

Aortic stenosis is an important health issue because it is the most common cardiac valve problem, yet there is no effective medical therapy. Because of the increasing age of the U.S. population, this is a condition that family physicians will have to deal with more frequently in the future. Carabello reviews the management of aortic stenosis using the case history of a 60-year-old man with a loud systolic murmur noted on examination.

The author mentions other physical examination features that may be noted while aortic stenosis is progressing to at least moderate severity. These features include later peaking of the murmur in systole, palpable delay of the carotid upstroke, and a softening of the second heart sound as the aortic component is lost.

Hemodynamic disturbance ensues as the aortic valve area drops from the normal 3 to 4 cm2 to 1.5 to 2.0 cm2. The mean pressure gradient across the valve rises rapidly as the stenosis progresses to less than 1.0 cm2. The author's cutoff for severe aortic stenosis is a mean aortic-valve gradient above 50 mm Hg, although he notes that there is no universally accepted definition relying on valve area or gradient.

The review emphasizes that clinical symptoms of decompensated left heart function (angina, syncope, or congestive heart failure symptoms) are much more crucial than the echocardiographic measures of gradient and valve area in determining whether to proceed with valve replacement. Asymptomatic patients are generally best served by observation; fewer than one third of patients with symptomatic severe stenosis are alive in two years without surgical intervention. Clearly, symptomatic patients and patients with suggestive symptoms and gradients greater than 50 mm Hg or valve areas less than 1.0 cm2 should proceed to valve replacement, according to the author. Exercise testing may reveal occult ventricular dysfunction in seemingly asymptomatic patients with severe stenosis by echocardiography.

Aortic stenosis that progressed to ventricular dysfunction with a low ejection fraction has traditionally been cited as a contraindication to valve surgery. The author recommends that patients with low ejection fractions who still have an elevated valve gradient (greater than 40 mm Hg) should be considered for surgery because it appears to improve their survival. A low ejection fraction with a low gradient is usually an ominous sign of highly decompensated left heart function that does not improve with valve surgery.

Return to Aortic valve stenosis

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