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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When should patients with asymptomatic aortic stenosis be evaluated for valve replacement? - Clinical Inquiries: from the Family Practice Inquiries Network
From Journal of Family Practice, 9/1/02 by Michelle Colen

EVIDENCE-BASED ANSWER For patients whose echocardiograms show advanced calcification of the aortic valves, a jet velocity of > 4.0 m/s, or a progression in jet velocity of 0.3m/s/year; and for patients who have an abnormal exercise response or an impaired functional status, consider referral for valve replacement prior to the onset of symptoms (Grade of Recommendation: C).

EVIDENCE SUMMARY Aortic stenosis is a narrowing of the aortic valve. Degree of severity is judged by vane area: mild (1.5-2.0 [cm.sup.2]), moderate (1.0-1.5 [cm.sup.2]), severe (< 1.0 [cm.sup.2]). Alternatively, stenosis may be classified by transvalvular gradient or jet velocity, the latter being the easier quantity to measure by echocardiogram. Prevalence of aortic stenosis increases with age; one series of 1243 elderly women (mean age of 82) found mild stenosis in 10%, moderate stenosis in 6%, and severe stenosis in 2%. (1) Natural history studies show that once classic symptoms develop, average survival decreases to 5 years with the onset of angina, 3 years after cardiac syncope, and 2 years after heart failure. (2) The incidence of sudden death increases from < 1% annually among asymptomatic patients to 15% to 20% among symptomatic patients. (3,4)

Aortic stenosis is suggested by such findings as a harsh systolic murmur at the right upper sternal border, pulsus parvus et tardus, and a sustained point of maximal impulse. Exercise stress testing may provide additional information. In one prospective study of 123 patients, those who had a greater increase in valve area, cardiac output, and blood pressure and a smaller decrease in stroke volume on stress echocardiogram were more likely to remain asymptomatic for the entire length of their time in the study, an average of 2.5 year. (5)

Asymptomatic patients with aortic stenosis who undergo coronary artery bypass grafting (CABG) often have their aortic valve replaced at the same time; the timing of aortic valve replacement in patients nor requiring CABG is controversial. One prospective study found the severity of stenosis at baseline to be the strongest prognostic predictor. Patients with a jet velocity, of < 3.0 m/s were unlikely to develop symptoms within 5 years; those with a jet velocity of [greater than or equal to] 4.0 m/s had a > 50% likelihood of developing symptoms or dying within 2 years. (5) Another study followed 128 patients for 4 years and found that moderate to severe valvular calcification and an increase in jet velocity of [greater than or equal to] 0.3 m/s/year were the best prognostic predictors. (6) Almost 80% of those with both calcification and a rapid change in jet velocity underwent surgery or died within 2 years (6) (Table).

RECOMMENDATIONS FROM OTHERS The American College of Cardiology/American Heart Association Task Force on Practice Guidelines recommends echocardiograms every 5 years for mild stenosis, every 2 years for moderate stenosis, and annually for severe stenosis. (4) There is no guideline for exercise testing. Aortic valve replacement is recommended for symptomatic patients and patients with severe stenosis undergoing CABG or other valvular or aortic surgery.

REFERENCES

(1.) Aronow WS, Ahn C, Kronzon I. Am J Cardiol 1997; 79:379-80.

(2.) Ross J Jr., Braunwald E., Circulation 1968; 38(1 Suppl):61-7.

(3.) Balentine J, Eisenhart A. Aortic Stenosis EMedicine Journal 2002; 3:1.

(4.) Bonow RO, Carabello B, deLeon AC Jr., et al. Circulation 1998; 98:1949-84.

(5.) Otto CM, Burwash IG, Legget ME, et al Circulation 1997; 93:2262-70

(6.) Rosenhek R, Binder T. Porenta G, et al. N Engl J Med 2000; 343:611-7

Members of the Family Practice Inquiries Network answer clinical questions with the best available evidence in a concise, reader-friendly format. Each peer-reviewed answer is based on a standard search of resources, including MEDLINE, the Cochrane Library, and InfoRetriever, and is graded for level of evidence (http://cebm.jr2.ox.ac.uk/docs/levels.html). The collected Clinical Inquiries can be found at http://www.jfponline.com and http://www.fpin.org; the latter site also includes the search strategy used for each answer.

Clinical Commentary by Ken Grauer, MD; and search strategy, at www.fpin.org.

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