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Archives of cardiovascular diseases
Volume 103, n° 4
pages 227-235 (avril 2010)
Doi : 10.1016/j.acvd.2010.03.003
Received : 30 December 2009 ;  accepted : 4 Mars 2010
Impact of valvuloarterial impedance on left ventricular longitudinal deformation in patients with aortic valve stenosis and preserved ejection fraction
Impact de l’impédance valvulo-artérielle sur la déformation longitudinale du ventricule gauche de patients porteurs d’une sténose valvulaire aortique avec une fraction d’éjection préservée

Sylvestre Maréchaux a, b, 1, Émilie Carpentier a, b, 1, Marie Six-Carpentier a, b, Philippe Asseman a, b, Thierry H. LeJemtel c, Brigitte Jude a, b, Philippe Pibarot d, Pierre Vladimir Ennezat a, b,
a Division of Cardiology, Centre hospitalier régional et universitaire de Lille, Lille 59037, France 
b EA 2693, université de Lille 2, Lille 59045, France 
c Division of Cardiology, Tulane University School of Medicine, New Orleans, Louisiana, United States 
d Institut universitaire de cardiologie et de pneumologie de Québec (Québec Heart & Lung Institute), Laval University Quebec, Quebec, G1V-4G5 Canada 

Corresponding author. Intensive Care Unit, Cardiology Hospital, boulevard Pr-J.-Leclercq, 59037 Lille cedex, France. Fax: +33 3 20 44 65 04.

Left ventricular (LV) longitudinal deformation is a good marker of intrinsic myocardial dysfunction in pressure overload cardiomyopathies.


To assess the effect of valvuloarterial haemodynamic load on LV longitudinal deformation in patients with aortic valve stenosis (AVS) and preserved LV ejection fraction (LVEF).


Global LV longitudinal strain (GLS) was measured using speckle tracking imaging in a series of 82 consecutive patients with AVS (mean age 75±10years; 50% men). The global (valvular+arterial) haemodynamic load imposed on the LV was estimated by the valvuloarterial impedance (Zva ), and was calculated using either arm-cuff systolic peripheral blood pressure or systolic central aortic blood pressure estimated by SphygmoCor®.


Among this series of 82 patients with preserved LVEF, 79% had reduced LV GLS (<−18%). LV GLS correlated weakly with AVS severity, systemic vascular resistance and systemic arterial compliance. However, there was a good inverse correlation between increase in Zva and impairment of LV GLS (r =0.41 p <0.0001). On multivariable analysis, impaired GLS was associated with increased Zva (p <0.0001), increased E/Ea ratio (p =0.001) and increased LV end-diastolic volume index (p =0.021), while indices of valvular load were not. Utilization of estimated central aortic blood pressure in place of brachial pressure did not improve the performance of Zva to predict GLS.


The magnitude of the global haemodynamic load as reflected by Zva is a powerful determinant of altered LV longitudinal deformation in AVS patients with preserved LVEF. The calculation of Zva may be useful to identify the patients who are potentially at higher risk for the development of myocardial dysfunction. Use of estimated central aortic pressure in the calculation of Zva does not appear to provide any incremental predictive value over that calculated with the simple measurement of brachial pressure.

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La déformation longitudinale du ventricule gauche (VG) est un bon marqueur de dysfonction myocardique intrinsèque dans les cardiomyopathies avec surcharge de pression.


Évaluer l’effet de la charge hémodynamique valvulo-artérielle sur la déformation longitudinale du VG de patients porteurs d’une sténose valvulaire aortique et d’une fraction d’éjection préservée.


La déformation globale longitudinale du VG a été mesurée à l’aide de l’imagerie speckle tracking dans une série de 82 patients consécutifs porteurs d’une sténose valvulaire aortique (âge moyen 75±10ans, 50 % d’hommes). La charge hémodynamique globale (valvulaire+artérielle) imposée au VG a été estimée par l’impédance valvulo-artérielle (Zva ) et a été calculée en utilisant soit la pression périphérique systolique brachiale au brassard, soit la pression systolique centrale aortique estimée par le SphygmoCor®.


Parmi cette série de 82 patients avec une fraction d’éjection préservée, 79 % avaient une déformation globale longitudinale du VG réduite (<−18 %). La déformation globale longitudinale du VG été faiblement corrélée avec la sévérité de la sténose aortique, les résistances vasculaires systémiques et la compliance artérielle systémique. Toutefois, une bonne corrélation était observée entre l’augmentation du Zva et l’altération de la déformation globale longitudinale du VG (r =0,41 p <0,0001). En analyse multivariée, l’altération de la déformation longitudinale du VG était associée avec un Zva (p <0,0001), un rapport E/Ea (p =0,001) et un volume télédiastolique du VG indexé (p =0,021) plus élevés. L’utilisation de l’estimation de la pression aortique centrale en remplacement de la pression brachiale n’améliorait pas la performance du Zva comme déterminant de la déformation longitudinale du VG.


L’importance de la charge hémodynamique globale représentée par le Zva est un déterminant puissant de l’altération de la déformation longitudinale du VG des patients porteurs d’une sténose aortique avec une fraction d’éjection préservée. Le calcul du Zva pourrait être utile pour identifier les patients potentiellement à risque de développement de dysfonction myocardique. L’utilisation de la pression aortique centrale dans le calcul du Zva ne semble pas apporter de valeur prédictive supplémentaire par rapport au calcul incluant la simple mesure de pression brachiale.

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Keywords : Aortic stenosis, Valvuloarterial impedance, Speckle tracking, Left ventricular function

Mots clés : Sténose aortique, Impédance valvuloartérielle, Speckle tracking , Fonction ventriculaire gauche


Aortic valve replacement is indicated in patients with severe aortic valve stenosis (AVS) when symptoms and/or left ventricular (LV) systolic dysfunction (defined as LV ejection fraction [LVEF] less than 50%) develops. However, LVEF may remain unaltered during the course of the disease despite latent and potentially irreversible alterations in myocardial function. Using M-mode tracings, Dumesnil et al. reported in the 1970s that LV longitudinal systolic shortening is depressed despite normal LVEF in patients with AVS compared with controls [1]. Very recently, Cramariuc et al. demonstrated that a higher degree of LV hypertrophy and concentric remodelling is associated with decreased LV longitudinal deformation assessed by two-dimensional speckle tracking in patients with AVS [2, 3]. In addition, impairment of LV longitudinal shortening or strain correlates with the presence of symptoms in patients with AVS and predicts elicited symptoms during exercise testing in the subset of asymptomatic patients [4, 5]. However, the relatively weak relationship between the LV longitudinal strain and the severity of the valve stenosis suggests that, beyond the narrowed valvular orifice, other factors may impact on LV longitudinal contraction in the setting of AVS [6]. Recently, Briand et al. have demonstrated that systemic arterial compliance (SAC) is frequently reduced in AVS patients [7]. Hence these patients often have a double haemodynamic load: a valvular load caused by the stenosis and an arterial load caused by reduced arterial compliance and/or increased vascular resistance. It is logical to believe that the development of LV dysfunction as well as the occurrence of symptoms and adverse events is related to the global haemodynamic load that results from the additive effects of AVS and hypertension. Briand et al. proposed a new index measurable by Doppler echocardiography – valvuloarterial impedance (Zva ) – to estimate the global haemodynamic load imposed on the left ventricle [7]. This index integrates the mean transvalvular gradient, the brachial systolic blood pressure and the stroke volume index. Recent studies have reported that elevated Zva is an independent predictor of reduced stress-corrected LV midwall fractional shortening [8] and mortality [9] in AVS patients.

Use of central aortic blood pressure instead of peripheral brachial pressure in the calculation of Zva potentially allows a more precise assessment of the global LV haemodynamic load. To this effect, several devices have been developed to estimate non-invasively central aortic pressure. The aim of the present study was to examine the relationship between Zva and LV longitudinal deformation using either arm-cuff systolic blood pressure or estimated aortic systolic blood pressure in a prospective cohort of patients with AVS and preserved LV ejection fraction.

Clinical data

During a 6-month period, consecutive patients with AVS (peak aortic velocity>2.5m/s) and LVEF greater or equal to 50% referred to our echocardiography laboratory were enrolled prospectively into the present study. Exclusion criteria were atrial fibrillation, LV systolic dysfunction (LVEF<50%), greater than mild aortic or mitral regurgitation and history of myocardial infarction.

Significant coronary artery disease was defined as the presence of a luminal narrowing greater than 50% on coronary angiography. Body mass index was calculated as weight in kilogram divided by height in metre square. Clinical data included age, sex, history of smoking, documented history of hypertension (including antihypertensive medications), hypercholesterolaemia (patients on cholesterol-lowering medication or with a low-density lipoprotein cholesterol concentration greater than 160mg/dL in the absence of treatment), diabetes mellitus (fasting blood glucose greater than 126mg/dL on two occasions or patients currently receiving an oral hypoglycaemic medication or insulin). Plasma levels of BNP were measured using the ACS 180 BNP dosage (Bayer®).

Vascular function analysis

Patients were studied in the supine position over a 1-hour period following an overnight fast. The radial wave-form was obtained using a high-fidelity micromanometer (Millar Instrument, Houston, Texas) and 20 wave-forms were averaged. A series of radial pressure waves over an 8-second period was together averaged and calibrated for the peak and nadir of the wave, with the best estimate of upper limb systolic and diastolic pressures using a cuff sphygmomanometer and phase I and V, respectively, of Korotkoff sounds. The ascending aorta waveform was obtained by applying a generalized mathematical transfer function to the radial artery waveform using a SphygmoCor® system device (AtCor Medical System, Australia). This device allowed the determination of the aortic systolic, diastolic, pulse (difference between systolic and diastolic pressure) and mean (diastolic pressure plus one third of pulse pressure) pressures. Measurements were performed by two experienced operators (E.C., M.M.-S.C.) until the operator index, an index of signal quality and reproducibility among the 20 cycles, was greater than 70%.

Pulse wave velocity (PWV) (i.e., the speed at which the pressure waveform travels along the aorta and large arteries during each cardiac cycle) is the gold standard for the assessment of aortic stiffness and is measured using the SphygmoCor® system. PWV is measured using the foot-to-foot velocity method from femoral and carotid waveforms. The time between the R wave of the electrocardiogram and the foot of each waveform is calculated and the difference between times is the delay (Δt). The distance (D) covered by the waves was calculated as the difference between the sternum femoral distance and carotid sternum distance. PWV is calculated as

Doppler echocardiographic analysis

Echocardiograms were performed by two experienced echocardiographers (S.M., P.V.E.) using a Vivid 7 ultrasound system (GE Medical Systems, Horten, Norway). Three cardiac cycles were stored for each measurement, for subsequent offline analysis. Measurements were made over at least three cardiac cycles and the average value calculated.

Severity of aortic valve stenosis

Left ventricular outflow tract (LVOT) diameter was measured in mid systole from the parasternal long-axis view after the outflow tract had been magnified. Transvalvular aortic velocity time integral (VTI), mean pressure gradient (MPG) and peak aortic velocity were obtained using non-imaging continuous wave Doppler and the right parasternal view, whenever possible. Aortic valve effective orifice area (EOA) was determined by the continuity equation method using the ratio of the VTI across the valve and in the LVOT obtained using pulsed-wave Doppler and was indexed to body surface area (BSA). The energy loss index (ELI) (i.e., the EOA corrected for pressure recovery) was calculated using the following formula:
ELI=(EOA*(Aa/Aa−EOA)/BSA),where Aa is the aortic cross-sectional area calculated from the diameter of the aorta measured at the sinotubular junction [7, 10, 11].

Systemic arterial haemodynamics

Assuming a two-element Windkessel model, systemic arterial compliance (SAC) was calculated as the ratio of stroke volume index (SVi) to pulse pressure (PP) using either aortic PP (SACAo ) or brachial PP (SACb ). The systemic vascular resistance (SVR) was calculated as follows:
([80×meanbloodpressure]/cardiacoutput),using either aortic (SVRAo ) or brachial (SVRb ) mean blood pressure.

Global LV haemodynamic load

As a measure of global LV haemodynamic load, valvuloarterial impedance was calculated as follows:
Zva=(MPG+SBP)/SVi,using either aortic (Zva Ao ) or brachial (Zva b ) systolic blood pressure (SBP), where ZVa represents the valvular and arterial factors that oppose ventricular ejection by absorption of the mechanical energy developed by the left ventricle.

LV diastolic function

Diastolic function was assessed by measuring peak velocities of the E wave (early diastole), the A wave (late diastole), the deceleration time of the E wave, and the Ea wave (average of early diastolic lateral and septal mitral annulus velocity). The ratio of peak early mitral inflow velocity (E) to peak early diastolic myocardial velocity (Ea) was calculated.

LV geometry

Septal wall, posterior wall thickness (PWth) and left ventricular internal diameter (LVID) were measured at end diastole (d) and end systole (s). The LV mass was calculated using M-mode with the corrected formula of the American Society of Echocardiography and indexed for BSA. Relative wall thickness (RWth) was calculated as follows:

LV systolic function

Volumes and ejection fraction (EF) were calculated using the Simpson biplane method. Velocity time integrals (VTIs) were measured in the apical five-chamber view at the level of the LV outflow tract using pulsed-wave Doppler to obtain LV stroke volume (SV) and cardiac output.

The midwall fractional shortening (MWFS) was calculated using this formula:

LV longitudinal strain measurement was performed blindly offline by a single investigator (E.C.) using the EchoPAC PC software BT 08 release (GE Medical Systems, Horten, Norway). Three cycle loops obtained from the apical four, two chamber and long axis views and recorded at a frame rate between 50 and 70frames per second were used for this analysis. The left ventricle was divided into 18segments and longitudinal strain was computed on six basal, six mid-left ventricle and six apical segments after having determined aortic valve opening and closure using Doppler recordings. The automatic tracking of the endocardial contour on an end-systolic frame was verified carefully and the region of interest was corrected manually to ensure optimal tracking. Global longitudinal strain was obtained as the average of regional strains.

Statistical analysis

Continuous variables are expressed as mean±standard deviation. Categorical variables are summarized as percentages. The relationships between strain values and continuous parameters were analysed by Pearson’s correlation coefficients. To identify independent predictors of continuous variables, all variables with a p -value less than 0.05 in univariate analysis were submitted to a stepwise backward multiple-regression analysis. Multivariable models were considered relevant if the variables entered in the model were significant (p <0.05) and had a tolerance measure (equal to the inverse of the variance inflation factor) greater than 0.7. The relationship between estimated aortic systolic blood pressure and brachial systolic blood pressure was analysed with the use of linear regression, paired t tests and Bland-Altman analyses [12]. The reproducibility in the measurement of GLS was assessed offline, calculating the mean difference±standard deviation among 10 studies (average of three cardiac cycles) on two occasions within a 2-month period by the same investigator. Ten subjects were used for reliability analysis between two observers (average of three cardiac cycles). A two-tailed p -value less than 0.05 was required for statistical significance. Analyses were conducted using SPSS 11.0 software (SPSS Inc., Chicago, IL, USA) and GraphPad Prism InStat™ version 5.0.

Patient characteristics

Eighty-two consecutive patients were enrolled prospectively into the study. Clinical and echocardiographic characteristics of the study population are presented in Table 1. Fifty-seven (70%) patients had severe AVS (ELI0.55cm2/m2 BSA) and 25 had mild or moderate AVS. Of the 57 patients with severe AVS, 45 reported significant breathlessness, 19 exertional chest pain and five syncope. Sixteen patients had a history of acute pulmonary oedema.

Determinants of global longitudinal strain
Measurement variability

The reproducibility in the GLS measurement was 0.57±0.77% (Figure 1); the intraobserver regression coefficient was 0.98 (p <0.0001). The mean difference±standard deviation for GLS was 0.31±0.88 (Figure 1) and interobserver regression was 0.96 (p <0.0001).

Figure 1

Figure 1. 

Scatter plots of the difference between two measurements of global longitudinal strain (GLS) and the mean values obtained by two measurements performed by the same observer (upper panel) and by two observers (lower panel).


Clinical and demographic data

Among the 1476 myocardial segments studied, longitudinal strain analysis was feasible in 1386 (94%). The average GLS values in the whole cohort was –15.2±3.2% (median –15.6%; 25th–75th percentiles –17.5, –12.8%). GLS was abnormally low (<–18%) in 65 (79%) of the patients [6, 13]. GLS was reduced significantly in patients with exertional breathlessness or with a history of acute pulmonary edema compared with patients without (–14.7±3.2 vs –17.1±–2.6%, p =0.004 and –13.3±3.2 vs –15.8±3.0%, p =0.002, respectively). GLS was similar in men and women, and in patients with versus without hypertension, diabetes, hypercholesterolaemia and a history of coronary artery disease. Similarly, there was no significant association between GLS and age, BMI and BSA. However, reduced GLS correlated with increased plasma B-type natriuretic peptide concentration (r =0.294, p =0.012).

Aortic valve function

Reduced GLS correlated with decreased ELI (r =–0.363, p =0.001, Figure 2, Table 2) but not with MPG or peak aortic velocity (Table 2).

Figure 2

Figure 2. 

Relationship between global longitudinal strain (%) and (A) systemic arterial compliance; (B) systemic vascular resistance; (C) energy loss index; (D) valvuloarterial impedance; (E) E/Ea ratio; and (F) left ventricular end-diastolic volume (LVEDV) index. Systemic arterial compliance, systemic vascular resistance and valvuloarterial impedance were calculated using arm-cuff brachial blood pressure.


Systemic arterial haemodynamics

There was no correlation between GLS and systolic or diastolic aortic blood pressures. Reduced GLS correlated with increased SVRb (r =0.236, p =0.033) and SVRAo (r =0.251, p =0.023), and correlated with decreased SACb (r =–0.220, p =0.047). There was a trend for SACAo (r =–0.183, p =0.10) (Table 2). No relationship was observed between GLS and PWV (r =–0.134, p =0.24). Both increased Zva Ao and Zva b were related to reduced GLS (r =0.398, p <0.0001 and r =0.407, p <0.0001) (Figure 2, Table 2).

LV systolic and diastolic function

Reduced GLS correlated with other indices of impaired LV systolic function such as lower LVEF, MWFS, SVi and cardiac output. Increased LV mass index, PWthd, LV end-diastolic volume index and LV filling pressure (as estimated by E/Ea ratio) were associated with reduced GLS (Table 3 and Figure 2).

Multivariable analysis

On multivariable regression analysis including variables of vascular and LV diastolic function, the independent determinants of reduced GLS were increased Zva b (p <0.0001), increased E/Ea ratio (p =0.001) and increased LV end-diastolic volume index (p =0.021) (multiple R2 of the model=0.35). Replacing Zva b with Zva Ao did not change the variables that were selected into the model: increased Zva Ao (p <0.0001), E/Ea ratio (p =0.001) and LV end-diastolic volume index (p =0.023) (multiple R2=0.34).

After including the variables of LV systolic function and geometry into the model (i.e., LVEF, LV midwall fractional shortening and LV mass index), higher E/Ea ratio (p <0.0001), lower LV ejection fraction (p =0.001) and higher Zva b (p =0.001) were associated independently with reduced GLS (multiple R2=0.40). Similar findings were obtained using Zva Ao in the multivariable model (p <0.0001 for E/Ea, p =0.001 for LVEF and p =0.002 for Zva Ao ; multiple R2=0.39). Exclusion of patients with moderate AVS (ELI>0.55cm2/m2) did not alter the results. Independent predictors of impaired GLS in the 57 patients with severe AVS were higher Zva b (p =0.013), higher E/Ea ratio (p =0.001) and lower LV ejection fraction (p <0.0001) (multiple R2=0.49). Similar findings were observed using Zva Ao in this multivariable model (multiple R2=0.48).


The main findings of the study are that the global (i.e., combined valvular and arterial) load estimated by the valvuloarterial impedance is superior to indices of stenosis severity to predict impairment of longitudinal shortening in patients with AVS and preserved LVEF; second, LV longitudinal contraction is, in large part, determined by indices of LV preload and afterload; third, the assessment of central arterial pressure does not appear to improve the predictive value of the valvuloarterial impedance.

During the natural course of AVS disease, the progressive rise in LV pressure and wall stress impairs LV systolic function and subsequently outcome. Identifying preclinical or subtle myocardial dysfunction is of interest to prevent overt LV systolic dysfunction and has been shown using myocardial deformation in various settings such as hypertensive or hypertrophic cardiomyopathy [14]. Lafitte et al. reported that asymptomatic AVS patients with normal LVEF have significantly lower global longitudinal deformation compared with healthy controls [6]. In addition, the reduction in longitudinal function correlated with symptoms and abnormal pressure response revealed by exercise testing [4, 6]. Of note, the average GLS observed in our series was lower than that of Lafitte et al., and is likely due to the enrolment of patients with exertional symptoms or a history of heart failure in our study.

The onset of symptoms or LV systolic dysfunction does not always correlate with the classical markers of haemodynamic AVS severity (effective AVA, transvalvular gradient or velocity, etc.). Several papers have demonstrated that calcific AVS cannot be viewed as an isolated disease of the valve but needs to integrate also the arterial haemodynamic [15]. In a model that accounts for the cyclic phenomenon of blood pressure, the aortic input impedance is the main arterial factor that opposes LV ejection. The aortic input impedance mainly depends on peripheral vascular resistance and arterial compliance. Owing to the high prevalence of ageing and systemic hypertension (30–40%) in the population of patients with AVS, the LV afterload not only depends on the reduction in AVA but also on the arterial load. To this effect, Briand et al. proposed a new and easy measureable index of global LV load, i.e., the valvuloarterial impedance Zva [7]. This index was found to correlate with the presence of LV diastolic and systolic dysfunction and with patient outcome [7, 8]. As expected, we also observed a significant relationship both in univariate and multivariable analysis between the LV longitudinal deformation and Zva , while indices of valvular severity were found to be weak univariate predictors of GLS. It is worthy to note that the use of brachial or estimated aortic systolic blood pressure did not alter the predictive value of Zva . In fact, in this elderly population, there was a strong correlation and agreement between central aortic and brachial pressures (r =0.99, p <0.0001; mean difference of 8.7mmHg, p <0.0001) (Figure 3). In addition, Rajani et al. recently demonstrated that in patients with AVS, arm-cuff brachial pressure correlates better with directly measured invasive aortic pressure than with radial-derived aortic systolic pressure [16].

Figure 3

Figure 3. 

Correlation between arm-cuff brachial systolic blood pressure (SBPb) and central aortic systolic blood pressure (SBPAo), derived by the application of a transfer function applied to radial pressure waveform recorded by the SphygmoCor® system (upper panel), and scatter plot of the difference between the two methods and the mean values obtained by the two methods (lower panel).


In the present study, the PWV measured by SphygmoCor® did not correlate with LV longitudinal deformation. The measurement of PWV estimates only the large artery stiffness. These data are also in agreement with previous work demonstrating that PWV did not differ between patients with AVS and age- and sex-matched controls [17].

Interestingly, we found that increased LV preload, as reflected by increased E/Ea ratio, correlated with impaired LV longitudinal deformation. Whether increased LV preload is a cause or a consequence of decreased LV longitudinal deformation cannot be ascertained from the present data and deserves further study. On the one hand, one may consider that the increased LV diastolic pressure affects LV wall stress and subendocardial function. On the other, one may speculate that myocyte hypertrophy and myocardial fibrosis primary alters LV filling capacity and thereby the Franck–Starling relationship.

Impairment of GLS did also correlate with increasing LV end-diastolic volume. According to the Laplace Law, patients with high global haemodynamic (i.e., pressure) overload as reflected by elevated Zva combined to large LV end-diastolic volume are likely to have markedly increased wall stress and thus afterload, which may, in turn, translate into depressed myocardial contractility.


The main limitation of this study is the relatively small sample size and its cross-sectional nature that precludes determining whether the changes in valvuloarterial impedance after aortic valve replacement correlate with those in longitudinal contraction [18]. Further longitudinal studies are needed to assess the reversibility of impaired GLS and the respective contribution of the valvular load and that of the vascular load that is generally unchanged after aortic valve replacement. In addition, the high proportion of patients with symptomatic AVS in our series limits the interpretation of the present results. Whether the impact of valvuloarterial impedance on longitudinal contraction remains significant in the subset of asymptomatic AVS patients deserves further studies. Last, the percentage of variance (R2) of GLS explicated by the echocardiographic variables of the present study ranged from 0.34–0.49, thereby suggesting that other unidentified factors such as myocardial fibrosis detected at best by cardiac magnetic resonance imaging may have contributed to lower GLS.


Both preload and afterload conditions and especially the combination of valvular and arterial haemodynamic load determine LV longitudinal deformation in patients with AVS and preserved LVEF. Identifying subclinical myocardial dysfunction at an early stage of the disease may be useful to optimize therapeutic management and thereby potentially prevent irreversible LV systolic dysfunction. The integration of measurements of LV longitudinal deformation in the decision-making process in a patient with AVS should be interpreted in light of the level of the valvuloarterial impedance that can be routinely appreciated using arm-cuff brachial blood pressure. In addition to aortic valve replacement, treatment aimed at reducing the arterial load should be considered in AVS patients in order to improve ventriculoarterial coupling and cardiac performance and thereby to prevent symptoms and adverse events.

Conflict of interest statement



Dr Pibarot holds the Canada Research Chair in Valvular Heart Diseases, Canadian Institutes of Health Research (Ottawa, Canada). This study was funded, in part, by a grant from Laboratoires Servier, France.


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1  S.M. and É.C. contributed equally to this manuscript.

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