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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Aortic stenosis: complications in noncardiac surgery
From American Family Physician, 11/1/04 by Karl E. Miller

Aortic stenosis, one of the most common valvular heart diseases in patients 65 years and older, occurs in approximately 2 to 9 percent of persons in this age group and may be a risk factor for perioperative cardiac complications in noncardiac surgery. Results from recent studies have been inconsistent as to whether aortic stenosis increases perioperative cardiac complications after surgery. In one recent study, increased peak aortic gradients were found to be associated with increased cardiovascular morbidity. Kertai and associates evaluated perioperative mortality and nonfatal myocardial infarction (MI) over time in patients with moderate to severe aortic stenosis who were undergoing noncardiac surgery.

The study was a retrospective examination of charts from patients who underwent noncardiac surgery between January 1991 and December 2000 at one medical center. All patients with moderate (mean gradient of 25 to 49 mm Hg) and severe (mean gradient of at least 50 mm Hg) aortic stenosis were included in the study. Patients without aortic stenosis undergoing noncardiac surgery during the study period were selected as control patients. Mortality and nonfatal MIs were recorded if they occurred before discharge from the hospital or within 30 days after the procedure. Data collected included clinical risk factors, type of surgery, and perioperative management.

There were 108 patients who met the criteria for moderate or severe aortic stenosis during the period. These patients were compared with 216 control patients. Patients with aortic stenosis were significantly more likely than control patients to die or have an acute MI during the perioperative period. Patients with severe aortic stenosis also were more likely than patients with moderate stenosis to die or have an acute MI. After adjusting for cardiac risk factors, aortic stenosis remained a strong predictor for perioperative acute MI or death (odds ratio, 5.2).

The authors conclude that aortic stenosis is a risk factor for acute myocardial infarction and mortality during the perioperative period of noncardiac surgery. In addition, the more severe the aortic stenosis, the more predictive of complications it is. These findings must be considered when assessing patients before noncardiac surgery.

KARL E. MILLER, M.D.

Kertai MD, et al. Aortic stenosis: an underestimated risk factor for perioperative complications in patients undergoing noncardiac surgery. Am J Med January 1, 2004;116:8-13.

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