Changes in the peripheral vasculature occur in patients with aortic stenosis (AS). The aims of the present study were to characterize peripheral arterial waveforms and aortic pulsewave velocity (PWV) in patients with AS and to determine their relationship to exercise time.
The study included 101 patients with a median age of 68 years (range, 27–84 years) with at least moderate AS. Patients underwent transthoracic echocardiography, an assessment of the radial artery waveform and PWV using a SphygmoCor device, and a treadmill exercise stress test.
The mean brachial systolic blood pressure was 143 ± 23 mm Hg in patients with severe AS and 135 ± 15 mm Hg in patients with moderate AS ( P = .04). The mean radial augmentation index was 102 ± 20% in patients with severe AS and 89 ± 16% in those with moderate AS ( P < .001). The radial augmentation index was related to the effective valve orifice area ( R = −0.45, P = .001), the peak transvalvular pressure difference ( R = 0.33, P = .001), and the mean transvalvular pressure difference ( R = 0.33, P = .001). On univariate analysis, exercise time was related to systemic arterial compliance ( R = 0.312, P = .008) and PWV ( R = −0.44, P < 0.001). On multivariate analysis, after adjusting for age, AS severity, and PWV, only age was a significant predictor of exercise time (β = −0.46; P = .006; 95% confidence interval, −15 to −3).
In patients with asymptomatic moderate to severe AS, exercise capacity is influenced only by age, not by resting measures of aortic valve stenosis or aortic stiffness.
The echocardiographic assessment of aortic stenosis (AS) includes effective valve orifice area (EOA), peak velocity and mean gradient, and also left ventricular (LV) function. However, these may underestimate the total outflow impedance, especially in the presence of systemic hypertension, which coexists in up to 32% of patients with AS. Accordingly, there is now increasing recognition that any assessment of AS must take into account the impedance imposed not only by AS but also the aorta and peripheral vasculature (valvuloarterial impedance [ Z va ]).
Previous studies have demonstrated that energy loss formulas that incorporate aortic root anatomy and geometry into the assessment of AS, and combined measures of Z va , better predict cardiac events than measures of valve function alone. However, few studies have investigated the independent effects of arterial stiffness on exercise capacity in patients with AS.
The current gold-standard assessment of aortic stiffness is pulsewave velocity (PWV). This represents the velocity of a propagated pressure over a fixed measured distance (typically between the carotid and femoral arteries). The major determinants of PWV are the elastic properties of the blood vessel, the geometry of the artery, and the blood viscosity. An alternative but complementary measure of assessing arterial stiffness is pulsewave analysis. This uses applanation tonometry of the radial artery to generate a waveform from which a number of parameters pertaining to arterial function can be obtained. Of these, radial augmentation provides a measure of the magnitude of wave reflectance, which is caused primarily by impedance mismatch at branching points of the arterial circulation. These measures of arterial stiffness have not previously been investigated in patients with AS.
The primary aim of the present study was to determine whether measures of arterial stiffness are independent determinants of exercise time in asymptomatic patients with at least moderate AS.
Consecutive patients with at least moderate AS were recruited from a specialist valve clinic. None admitted to symptoms on detailed examination including a symptom questionnaire. All patients had normal transverse systolic function, defined by a combination of fractional shortening ≥ 28%, visual ejection fraction ≥ 55%, and no regional wall motion abnormalities. None had more than mild mitral regurgitation, mitral stenosis, or aortic regurgitation per the American College of Cardiology and American Heart Association guidelines for valvular heart disease. Patients were excluded if they had (1) significant peripheral vascular disease (confirmed diagnosis, prior treatment for peripheral vascular disease, or leg cramps on exertion), (2) significant pulmonary disease (confirmed diagnosis of chronic obstructive airway disease, restrictive lung disease, or regular use of bronchodilators), (3) rheumatologic disease (confirmed diagnosis or mobility limiting rheumatoid arthritis, osteoarthritis, or osteoporosis), or other significant comorbidities that would hinder exercise stress testing. The study consisted of echocardiography, applanation tonometry of the radial artery, the measurement of aortic stiffness by PWV, and a treadmill exercise test. All patients gave written informed consent, and the study was approved by the local ethics committee.
A Vingmed System 5 (GE Vingmed Ultrasound AS, Horten, Norway) was used with a 3-2 20-mm duplex probe and a 1.9-MHz continuous-wave stand-alone probe. M-mode or two-dimensional recordings were made at a level immediately apical to the tips of the mitral valve leaflets, and end-diastolic measurements were made using the American Society of Echocardiography convention. The subaortic diameter was measured on parasternal long-axis frames frozen in systole taking an average of three estimates from inner edge to inner edge just below the base of the cusps. Pulsed Doppler recordings were made in the apical five-chamber view just below the aortic valve to obtain the velocity-time integral and mean pressure difference of the subaortic flow. Continuous-wave recordings were made from the apex and right intercostal positions, and the optimal signal was traced to obtain peak velocity, mean pressure difference, and velocity-time integral. The systolic ejection time was also measured from the continuous-wave Doppler recording as the time from the onset of systolic flow to its cessation. EOA in square centimeters was calculated using the classical continuity equation using the ratio of subaortic to transaortic velocity integrals. For all Doppler measurements, the average of three signals was taken. Aortic diameter was measured at the sinotubular junction and was used with the EOA to calculate the energy loss index (ELI):
ELI ( cm 2 / m 2 ) = ( EOA × aortic area ) ( aortic area − EOA ) / body surface area .
As a measure of total LV afterload, Z va was calculated:
Z va ( mm Hg / mL / m 2 ) = systolic blood pressure + mean transvalvular pressure difference stroke volume index .