Aortic stenosis pathophysiology

Aortic Stenosis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Mohammed A. Sbeih, M.D. [2], Lakshmi Gopalakrishnan, M.B.B.S. [3] Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Overview

The impedance to antegrade blood flow as a result of aortic stenosis results in chronic pressure overload of the left ventricle. The most common complication of aortic stenosis is left ventricular hypertrophy. The obstruction of flow in aortic stenosis can obviously occur at the level of the aortic valve itself, but can also occur at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) level as well.

Pathophysiology

Left Ventricular Hypertrophy

Long-standing aortic stenosis exposes the left ventricle to a sustained prolonged pressure overload state which may lead to outflow tract obstruction. Over the years, this sustained increase in systolic pressure generated by the left ventricle, results in concentric hypertrophy of the myocardium with subsequent thickening of the left ventricular wall; however, the chamber volume remains within normal limits. Although, this massive concentric hypertrophy characterized by a reduced diastolic radius-to-wall thickness ratio has shown to initially counter balance the increased systolic left ventricular pressure, if this process continued, an inverse relationship has been observed between ejection fraction and left ventricular mass.

Another factor that may contribute to reduced ventricular function is dyssynchronous contraction subsequent to regional wall motion abnormalities, fibrosis or ischemia.

Therefore, as a result of inadequate degree of hypertrophy with disproportional wall thickness an increase in systolic wall stress ensues which when coupled with reduced left ventricular contractility leads to significant reduction in the ejection fraction. Furthermore, among such patients with low ejection fraction secondary to increase afterload, Carabello et al demonstrated the lack of benefit of corrective surgery.

An increase in left ventricular end-diastolic pressure without chamber dilatation is observed subsequently to the increased left ventricular wall thickness, depressed volume/mass ratio and reduced chamber compliance thereby reflecting diastolic dysfunction

Hemodynamic Determinants

The hypertrophied left ventricle may have reduced coronary blood flow even in the absence of obstructive epicardial stenoses due to compression of the capillary network. This may lead to subendocardial ischemia during stress or exercise..

Another factor that may reduce ventricular function is dyssynchronous contraction, resulting from regional wall motion abnormalities, fibrosis or ischemia.

Pressure Gradient & Valve Area

When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta . The more constricted the valve, the bigger the gradient between the LV and the aorta. For instance, in patient with 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 into 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 and inside the LV would be considerably higher. As the left ventricle fails, however, it may no longer be able to mount the contractility necessary to generate a large gradient across the aortic valve. Therefore, absence of a large gradient across the aortic valve does not exclude the presence of critical aortic stenosis. The presence of a low gradient and low ejection results in low flow aortic stenosis. It is for this reason that the best measure of the severity of aortic stenosis is the aortic valve area, not the aortic valve gradient.

Flow Velocity

In aortic stenosis, the flow velocity across the stenosed valve is at least 2.6 m/sec. if the left ventricular function and contractility is preserved. This is based upon echocardiographic estimation of the aortic jet velocity, aortic valve area and the mean transvalvular gradient. In aortic valve sclerosis (not stenosis); the aortic valve becomes calcified but the aortic jet velocity is ≤2.5 m/sec (without a significant gradient). Aortic valve sclerosis is commonly defined as a focal or diffuse thickening of the aortic cusps with calcific nodules generally at the base of leaflets and transvalvular velocity at Doppler still in the normal range (Vmax <2 m/s). Until few years ago, it was considered a physiologic process related to aging without clinical relevance. However, aortic valve sclerosis is not observed in about 50% of people over 80 years old. Furthermore, several experimental and clinical studies have demonstrated that it could represent an active phenomenon, significantly related to risk factors for atherosclerosis and cardiovascular morbidity and mortality . .

Low Flow, Low Gradient, Low Ejection Fraction Aortic Stenosis

If there is a decline in left ventricular function due to systolic dysfunction, there may be only a moderate transvalvular gradient or low flow aortic stenosis. If there is fibrosis of the left ventricle, there may be incomplete recovery after aortic valve replacement. This scenario can also occur among patients in whom there is a history of myocardial infarction: there is insufficient contractility to mount an aortic gradient.

Definition

1. An aortic valve areas < 1.0 cm2
2. A left ventricular ejection fraction < 40%
3. A mean pressure difference or gradient across the aortic valve of < 30 mm Hg

With a dobutamine infusion, the aortic valve area should increase to > 1.2 cm2, and the mean pressure gradient should rise above 30 mm Hg. If there is a failure to acheive these improvements, early surgical mortality is 32-33%, but it is only 5–7% in those patients who can augment their contractility and gradient. Survival at five years was 88% after surgery if the patient can augment their contractility, but only 10–25% if the patient cannot augment their contractility.

ACC/AHA Guidelines- Low-Flow/Low-Gradient Aortic Stenosis

“

Class IIa 1. Dobutamine stress echocardiography is reasonable to evaluate patients with low-flow/low-gradient aortic stenosis and left ventricular dysfunction. (Level of Evidence: B) 2. Cardiac catheterization for hemodynamic measurements with infusion of dobutamine can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and left ventricular dysfunction. (Level of Evidence: C)

”

Progression of Aortic Stenosis

The rate of progression of aortic stenosis occurs at an average rate of reduction in aortic valve area of 0.1 cm2 in valve area per year . Unfortunately, there is a large interpatient variability in the rate of progression. Furthermore, multiple factors are associated with more rapid progression which include the following:

1. Left ventricular function
2. Bicuspid aortic valve stenosis
3. Initial severity of stenosis
4. Risk factors for atherosclerosis, such as age, smoking, hypertension, obesity and diabetes, lipid abnormalities, chronic renal failure and dialysis, and atherosclerotic disease itself, such as concomitant coronary artery disease

Relationship of Hemodynamic Severity to Symptoms of Aortic Stenosis

In general, symptoms in patients with aortic stenosis and normal left ventricular systolic function usually occur when:

• The valve area is <1.0 cm2.
• The jet velocity is over 4.0 m/sec.
• The mean transvalvular pressure gradient exceeds 40 mm Hg.

However, many patients develop symptoms only when more severe valve obstruction is present, other patients become symptomatic at less severe degree of stenosis, particularly if there is coexisting aortic regurgitation.

ACC/AHA Guidelines- Severity Classification

Indicator	Mild	Moderate	Severe
Jet velocity (m per s)	Less than 3.0	3.0–4.0	Greater than 4.0
Mean gradient (mm Hg)†	Less than 25	25–40	Greater than 40
Valve area (cm2)	Greater than 1.5	1.0–1.5	Less than 1.0
Valve area index (cm2 per m2)			Less than 0.6

† Valve gradients are flow dependent and when used as estimates of severity of valve stenosis should be assessed with knowledge of cardiac output or forward flow across the valve.

Guideline Resources

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons