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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Listening to the aortic valve: novel acoustic analysis predicts aortic valve calcification and cardiovascular events
From CHEST, 10/1/05 by Kian Keong Poh

PURPOSE: Aortic valve calcification (AVC) measured by multislice computed tomography (MSCT) has previously been shown to be of prognostic importance. We aimed to determine if a novel acoustic method of evaluating heart sounds in pts with valvular aortic stenosis (AS) or sclerosis is a useful alternative.

METHODS: ECG-gated acoustic data recorded from the precordial aortic area using an electronic stethoscope were subjected to energy-based continuous wavelet transformation by a laptop software program, which extract the dominant systolic frequency (DF). These were compared to AVC quantified in Agatston units (AU) by MSCT and echocardiographic indices of AS severity, determined independently. Patients were prospectively followed up for occurrence of cardiac death and symptom-driven aortic valve replacement.

RESULTS: Of 50 pts (age 68 [+ or -] 11 yrs, 58% males), 35 had lone AS of varying severity and 15 with aortic valve sclerosis. Mean aortic valve area indexed to body surface area (AVAI), AVC, DF and left ventricular ejection fraction (EF) were 0.94 [+ or -] 0.50 cm2/m2, 1037 [+ or -] 1476 AU, 103 [+ or -] 69 Hz and 62 [+ or -] 14% respectively. DF correlated significantly with AVC, maximal pressure gradient across the aortic valve (Pmax), AVAI and aortic valve resistance (r=0.62, 0.61, -0.51 and 0.60 respectively, all P<0.001). In a multivariate linear regression model incorporating AVC, AVAI and Pmax, the only independent predictor of DF was AVC (13=0.37, P=0.03). Over 15 [+ or -] 7 months, 7 pts reached the composite endpoint. Pts with events had higher DF (170 [+ or -] 65 vs 93 [+ or -] 64 Hz, P=0.005). For prediction of the endpoint, the areas under receiver characteristic curves for DF, AVC, AVAI, age and EF were 0.82(P=0.007), 0.79(P=0.013), 0.88(P=0.001), 0.50(P=NS) and 0.65(P=NS) respectively. A threshold of 145 Hz for DF provided optimal sensitivity of 86% and specificity of 81% of predicting an event.

CONCLUSION: DF derived from novel acoustic analysis of aortic valve stenosis or sclerosis correlates well with AVC by MSCT and offers prognostic information in these patients.

CLINICAL IMPLICATIONS: Acoustic analysis of heart sound may provide a simple and useful non-invasive adjunct in the management of patients with aortic valve calcification.

DISCLOSURE: Kian Keong Poh, Grant monies (from sources other than industry) National Healthcare Group (Singapore) and Singapore Heart Foundation grants.

Kian Keong Poh MB, BCh * Mark Y. Chan MBBS Hong Yang MD Lieng H. Ling MBBS National University Hospital, Singapore, Singapore

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