Criterion for Haemodynamically Severe Aortic Stenosis

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Summary

Criterion for Haemodynamically Severe Aortic Stenosis

Management of the AS patient is critically dependent on an accurate evaluation of the patient’s symptomatic status and the haemodynamic severity of the valve disease.^9,10 Haemodynamic severity is used to decide whether symptoms are likely attributable to the valve and dictate the frequency of follow-up evaluations. Numerous haemodynamic indices have been proposed for this purpose; however, transvalvular velocity (VAS), transvalvular mean gradient (MG) and aortic valve area (AVA) derived by the continuity equation are the parameters recommended for routine clinical use due to their ability to predict clinical outcome.^9–11 Haemodynamically severe AS has been defined by VAS≥4 m/s, MG≥40 mmHg and AVA≤1.0 cm², because these findings are associated with a poor prognosis.^9–11 The fulfilment of all three criteria essentially confirms the presence of severe AS; however, discordant findings occur in at least 30 % of AS patients with a normal LVEF, casting doubt about the disease severity.^12–14 In patients with a reduced LVEF, discordant findings are even more common.^15–19 In both groups, the VASt majority of the discordance relates to an AVA in the severe range, but MG or VAS in the non-severe range. In only a small minority of cases (<10 %), AVA is in the non-severe range, but MG or VAS is severe.^12,14

Sorting Out Discrepant Haemodynamic Data – Aortic Valve Area is Severe, but the Mean Gradient is Not!
The Normal Left Ventricular Ejection Fraction Patient
Technical Reasons (Measurement Error)

Accurate measurement of the left ventricular outflow tract (LVOT) velocity, LVOT diameter and VAS are critical to the calculation of AVA using the continuity equation. Underestimation of the LVOT time velocity integral or diameter can lead to an erroneously small stroke volume (SV) and underestimation of AVA. Optimal LVOT velocity signals require the ultrasound beam to be aligned parallel to left ventricular (LV) outflow, the sample volume to be positioned immediately inferior to the aortic valve (5–10 mm) and the signal to show laminar flow with minimal spectral dispersion.¹¹ The LVOT diameter measurement should be acquired on a zoomed parasternal long-axis image in mid-systole and measured 5 mm below cusp insertion.¹¹ While measurements obtained at the annulus improve reproducibility, they tend to result in a larger AVA. The circular assumption used to derive the LVOT area from the diameter measurement is an important cause for underestimation of AVA as many patients have an elliptically shaped LVOT.20 The LVOT long-axis diameter often approximates the minor axis diameter and can lead to a 26 % underestimation of SV and AVA^.21,22 Identification of the highest VAS is required to accurately measure MG and AVA, and Doppler interrogation of the aortic valve should be performed from the apical, right parasternal and suprasternal windows.²³ Failure to identify the highest VAS will lead to an underestimation of MG, an overestimation of AVA and an underestimation of AS severity that tends to have a concordant rather than discordant MG and AVA.

When discrepant data are encountered, the initial approach should be to rule out measurement error. Echocardiographic images should be carefully reviewed for proper data acquisition and repeated if improper technique was used. The SV measurement should be confirmed by using another technique such as three-dimensional (3D)-echocardiography, or corroborating the continuity equation AVA by planimetry of the anatomic orifice using two-dimensional (2D) or preferably 3D-transoesophageal echocardiography.^22,24 An AVA≤1.0 cm² on planimetry confirms the presence of severe AS. However, an AVA slightly greater than 1.0 cm² does not definitively exclude severe AS since the effective orifice area derived by continuity equation is usually slightly smaller than the anatomic AVA.

Patient Body Size
Cardiac output and AVA requirements are dependent on body size. In a small individual, an AVA≤1.0 cm² may be relatively adequate for the cardiac output and generate a VAS<4 m/s or MG<40 mmHg. Conversely, an AVA>1.0 cm² may be inadequate for a large individual, resulting in severe obstruction and a VAS≥4 m/s or MG≥40 mmHg. Current guidelines suggest that indexing AVA for body surface area (aortic valve area index [AVAi]) to account for different body sizes may be helpful and propose an AVAi≤0.6 cm²/m² to identify severe AS.^9–11 However, prognostic studies supporting this approach are limited.²⁵ Indexing AVA to body surface area increases the prevalence of severe AS, but also increases the prevalence of discrepant haemodynamic data.^12,14,26,27 In the SimVAStatin and Ezetimibe in Aortic Stenosis (SEAS) trial, AVAi did not improve the prediction of aortic valve events or cardioVAScular death compared to AVA.^26,27 A linear relationship between AVA and body surface area may not be the optimal correction factor and likely oversimplifies the different implications of body size, overweight status and obesity that might require different correction factors.^14,28 Nevertheless, body size should be considered when confronted with discordant haemodynamic data.

Inconsistencies Between Different Criteria for Severe Aortic Stenosis in the Valve Guidelines

Inherent in the definition of severe AS is that a MG of 40 mmHg equates to an AVA of 1.0 cm². However, the relationship between MG and AVA is a function of cardiac output, heart rate and systolic ejection period. A patient with a cardiac output of 6 l/min, a heart rate of 70 bpm and a systolic ejection period of 330 msec would have a MG of 34 mmHg if AVA was 1.0 cm², not 40 mmHg as suggested by the guidelines. Potentially, MG could be as low as 26 mmHg with an AVA of 1.0 cm² despite a normal cardiac output.²⁹

Low Flow State

MG is directly proportional to the squared function of transvalvular flow and can be small (<40 mmHg) despite an AVA≤1.0 cm² if transvalvular flow is significantly reduced.^16,18,19 Low flow is usually considered when the LVEF is reduced, but should not be excluded when the LVEF is normal. Low flow has been defined as an indexed stroke volume (SVi)<35 ml/m²;^19,30 however, measures that account for the systolic ejection period (i.e. mean transvalvular flow rate <200–250 ml/s) are theoretically likely more appropriate. Hypertension, significant mitral or tricuspid valve disease, pulmonary artery hypertension and atrial fibrillation are clinical entities often co-existing with AS and associated with low flow despite a normal LVEF. Elevated blood pressure can reduce transvalvular flow and result in a smaller MG, smaller AVA and discordant measurements.³¹ In patients with uncontrolled hypertension, low flow and discordant data, blood pressure should be corrected and the echocardiogram repeated as normalisation of flow may resolve the discrepancy.

Low transvalvular flow can also be present in AS patients without concomitant valve disease or pulmonary artery hypertension, a clinical entity often referred to as paradoxical low flow AS, because of the paradoxical association of a low flow state despite a preserved LVEF.³⁰ These patients tend to be older, female and have associated hypertension, metabolic syndrome, diabetes or atrial fibrillation.^{19,30,32–34} They also tend to have smaller left ventricular cavities with concentric remodeling, myocardial fibrosis, reduced compliance and restrictive physiology.^19,34,35 Despite the preserved LVEF, they have evidence of intrinsic systolic dysfunction with impaired longitudinal shortening.^34–37

The Reduced Left Ventricular Ejection Fraction Patient

The presence of a low flow state is often the first assumption when encountering discrepant haemodynamic data in the AS patient with a reduced LVEF. However, not all patients with a reduced LVEF have a low flow state. SVi or mean transvalvular flow rate (<35 ml/m2 and <200–250 ml/s, respectively) should be calculated to confirm the presence of low flow and measurement error excluded.

Additional Complementary Investigations

Discordant measurements can usually be resolved by systematically considering the above issues. However, multi-detector computed tomography (MDCT), magnetic resonance imaging (MRI) and cardiac catheterisation can be helpful when the cause for the discrepancy is not apparent and the patient has symptoms or unexplained left ventricular dysfunction. AVA, LVOT area and SV can be obtained non-inVASively using MDCT or MRI and compared with the echocardiography data.^22,38–40 Aortic valve calcification (AVC) can be quantified using MDCT and may help clarify discordant data. AVC>~1,250 Agatston units (AU) in women and >~2,050 AU in men suggests the presence of severe AS.⁴¹ Cardiac catheterisation provides a direct measurement of MG or AVA by Gorlin equation, and can evaluate for coronary artery disease as an alternate explanation for symptoms or left ventricular dysfunction.³⁹