Simultaneous left ventricular and aortic pressure tracings demonstrate a pressure gradient between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generates higher pressures than what is transmitted to the aorta.  The pressure gradient, caused by aortic stenosis, is represented by the green shaded area. (AO = ascending aorta; LV = left ventricle; ECG = electrocardiogram.)
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Aortic valve stenosis

Aortic valve stenosis (AS) is a heart condition caused by the incomplete opening of the aortic valve. more...

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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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Impact of myocardial hypertrophy and preoperative left ventricular ejection fraction on post operative complications after aortic valve replacement for
From CHEST, 10/1/05 by Jean-Louis Mariage

PURPOSE: Patients (pts) with aortic stenosis (AS) have a good prognosis after aortic valve replacement (AVR). Morbidity and mortality of AS pts with severe septal hypertrophy (SSH, [greater than or equal to] 16mm) or supranormal ([greater than or equal to] 70%) left ventricular ejection fraction (LVEF) have been poorly investigated. We retrospectively analysed complications and outcome of such pts after surgery.

METHODS: Between 10/98 and 03/03, 280 pts underwent AVR. Only pure AS pts were included; excluding aortic regurgitation, ischaemic cardiomyopathy, associated coronary or thoracic aortic surgery, or mitral disease. Eighty seven pts met the criteria. Analysis was performed on 2 criteria: preoperative LVEF and septal thickness (ST). For LVEF analysis, pts were divided in 2 groups: GA: LVEF 50 to 69% (n=29) and GB: LVEF [greater than or equal to] 70% (n=44); and in 3 for the ST criteria: G1: ST<13mm (n=18); G2: 13 [less than or equal to] ST<16mm (n=31); and G3: ST [greater than or equal to] 16mm (n=11). We analysed length of ICU and hospital stay; duration of ventilation; use of vasoactive drugs, calcium channel's blockers or b-blockers; arrhythmia events, occurrence of renal failure or need for haemodialysis, and mortality. Usually pts after AVR stay at least 2 nights in our ICU.

RESULTS: In LVEF analysis, 17% of pts in GB were ventilated [greater than or equal to] 24 hours in comparison with 0% in GA [p=0.036]. In ST analysis, 27.8% of pts in G1, 35.5% in G2, and 54.5% in G3 stayed >2 nights in the ICU (NS). Two pts from G3 required haemodialysis [p=0.032]. There were no difference in the length of ICU and hospital stay, use of vasoactive or vasodilator drugs, and occurrence of arrhythmia in group GA vs. GB, or in group G1 vs. G2 vs. G3. No patient died during hospital stay.

CONCLUSION: Using selective criteria, pure AS pts have an excellent prognosis after AVR; however pts with LVEF [greater than or equal to] 70% have a higher risk of prolonged ventilation, and SSH pts have a higher incidence of haemodialysis.

CLINICAL IMPLICATIONS: Diastolic dysfunction consecutive to SSH or supranormal LVEF pts could be improved by pharmacological intervention. Further studies are necessary to confirm this hypothesis.

DISCLOSURE: Jean-Louis Mariage, None.

Jean-Louis Mariage MD * Pierre Bulpa MD Isabelle Michaux MD Manuel Gonzalez MD Jacques Jamart MD Etienne Installe MD Patrick Evrard MD Mont-Godinne Hospital, Cliniques Universitaires de MontGodinne, Yvoir, Belgium

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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