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Archives of cardiovascular diseases
Volume 110, n° 8-9
pages 466-474 (août 2017)
Doi : 10.1016/j.acvd.2016.12.009
Received : 12 May 2016 ;  accepted : 15 December 2016
Relationship between exercise pressure gradient and haemodynamic progression of aortic stenosis
Relation entre l’évolution du gradient à l’exercice et la progression hémodynamique de la sténose aortique
 

Anne Ringle a, Franck Levy b, Pierre-Vladimir Ennezat c, Caroline Le Goffic a, Anne-Laure Castel a, François Delelis a, Aymeric Menet a, Dorothée Malaquin b, Pierre Graux a, André Vincentelli d, Christophe Tribouilloy b, e, Sylvestre Maréchaux a, e,
a Service de cardiologie, GCS-groupement des hôpitaux de l’institut catholique de Lille, faculté libre de médecine, université catholique de Lille, 59000 Lille, France 
b Service de cardiologie B, CHU d’Amiens, 80054 Amiens, France 
c Service de cardiologie, CHU de Grenoble, 38000 Grenoble, France 
d Service de chirurgie cardiaque, CHRU de Lille, 59000 Lille, France 
e Inserm U 1088, université de Picardie, 80054 Amiens, France 

Corresponding author at: Cardiology department, GCS-groupement des hôpitaux de l’institut catholique de Lille, faculté libre de médecine, université catholique de Lille, rue du Grand-But, 59160 Lomme, France.
Summary
Background and aims

We hypothesized that large exercise-induced increases in aortic mean pressure gradient can predict haemodynamic progression during follow-up in asymptomatic patients with aortic stenosis.

Methods

We retrospectively identified patients with asymptomatic moderate or severe aortic stenosis (aortic valve area<1.5cm2 or<1cm2) and normal ejection fraction, who underwent an exercise stress echocardiography at baseline with a normal exercise test and a resting echocardiography during follow-up. The relationship between exercise-induced increase in aortic mean pressure gradient and annualised changes in resting mean pressure gradient during follow-up was investigated.

Results

Fifty-five patients (mean age 66±15 years; 45% severe aortic stenosis) were included. Aortic mean pressure gradient significantly increased from rest to peak exercise (P <0.001). During a median follow-up of 1.6 [1.1–3.2] years, resting mean pressure gradient increased from 35±13mmHg to 48±16mmHg, P <0.0001. Median annualised change in resting mean pressure gradient during follow-up was 5 [2–11] mmHg. Exercise-induced increase in aortic mean pressure gradient did correlate with annualised changes in mean pressure gradient during follow-up (r =0.35, P =0.01). Hemodynamic progression of aortic stenosis was faster in patients with large exercise-induced increase in aortic mean pressure gradient (≥20mmHg) as compared to those with exercise-induced increase in aortic mean pressure gradient<20mmHg (median annualised increase in mean pressure gradient 19 [6–28] vs. 4 [2–10] mmHg/y respectively, P =0.002). Similar results were found in the subgroup of 30 patients with moderate aortic stenosis.

Conclusion

Large exercise-induced increases in aortic mean pressure gradient correlate with haemodynamic progression of stenosis during follow-up in patients with asymptomatic aortic stenosis. Further studies are needed to fully establish the role of ESE in the decision-making process in comparison to other prognostic markers in asymptomatic patients with aortic stenosis.

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Résumé
Objectifs

L’objectif principal de l’étude était de déterminer si une élévation importante du gradient moyen trans-aortique à l’échocardiographie d’effort permet de prédire une progression hémodynamique rapide au cours du suivi chez les patients porteurs d’un rétrécissement aortique asymptomatique.

Méthodes

Nous avons identifié rétrospectivement les patients asymptomatiques porteurs d’un rétrécissement aortique modéré ou sévère (surface fonctionnelle aortique<1,5cm2 ou<1cm2) sans dysfonction ventriculaire gauche, ayant bénéficié d’une échographie d’effort initiale avec test d’effort normal puis d’une échographie de repos au cours du suivi. La relation entre l’élévation du gradient moyen à l’effort et la progression du gradient moyen de repos au cours du suivi a été étudiée.

Résultats

Cinquante-cinq patients ont été inclus (âge moyen 66±15 ans), 45 % (n =25) étaient porteurs d’un rétrécissement aortique sévère. Une augmentation significative du gradient moyen était retrouvée entre le repos et le pic de l’effort (p <0,001). Après un suivi médian de 1,6 [1,1–3,2] ans, le gradient moyen de repos augmentait de 35±13mmHg à 48±16mmHg (p <0,0001) avec une augmentation médiane de 5 [1,8–11,1] mmHg/an. L’élévation du gradient moyen à l’effort était corrélée à la progression annuelle du gradient moyen au cours du suivi (r =0,35, p =0,01). La progression de la sténose aortique était plus rapide chez les patients ayant une élévation importante du gradient moyen à l’effort (≥20mmHg) en comparaison aux patients ayant une faible élévation du gradient moyen à l’effort (<20mmHg), avec une progression annuelle médiane du gradient moyen de 19 [6–28] vs. 4 [2–10] mmHg/an respectivement (p =0,002). Des résultats similaires étaient retrouvés dans le sous-groupe des 30 patients présentant un rétrécissement aortique modéré.

Conclusion

Cette étude établit un lien entre l’élévation importante du gradient moyen à l’effort et la progression hémodynamique rapide de la sténose au cours du suivi, chez les patients porteurs d’un rétrécissement aortique asymptomatique. D’autres études seront nécessaires pour établir de façon définitive la place de l’échocardiographie d’effort en comparaison avec les autres marqueurs pronostiques chez les patients porteurs d’un rétrécissement aortique asymptomatique.

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Keywords : Aortic valve, Aortic stenosis, Exercise, Echocardiography, Progression

Mots clés : Valve aortique, Rétrécissement aortique, Test d’effort, Échocardiographie d’effort, Progression

Abbreviations : AS, Exercise Δ MPG, MPG, ESE, Vmax


Background

Determining the optimum time for valve surgery remains a major challenge in asymptomatic aortic stenosis (AS). Stenosis severity is a major predictor of outcome, and previous reports have demonstrated that peak aortic jet velocity is a strong predictor of outcome in asymptomatic patients with AS [1, 2, 3, 4]. Besides baseline stenosis severity, large exercise-induced increases in MPG (exercise Δ MPG) have been associated with an increased risk of death or need for aortic valve replacement motivated by the occurrence of spontaneous symptoms, in both patients with moderate or severe AS [5, 6]. It has been suggested that large exercise Δ MPG may reflect a stiffer non-compliant stenotic valve and hence a more advanced stage of the valve disease [5, 6]. Rapid haemodynamic progression during follow-up portends a poor outcome in asymptomatic patients with severe AS [2, 7, 8]. In addition, a substantial proportion of patients with moderate AS progresses rapidly to the severe stage and these patients display excess mortality [2, 3, 4]. Given the prognostic importance of large exercise Δ MPG during exercise not only in patients with severe but also with moderate asymptomatic AS [5], we hypothesized that patients with large exercise Δ MPG can predict a faster haemodynamic progression of aortic stenosis during follow-up compared with those with lower exercise Δ MPG.

Methods
Patients

We retrospectively reviewed all exercise stress echocardiography (ESE) examinations that were performed to assess asymptomatic AS from 2010 to 2015. We selected patients who met the following criteria:

at least moderate AS as defined by an aortic valve area1.5cm2 [9];
ESE performed at baseline;
availability of a second follow-up Doppler echocardiographic examination without aortic valve replacement.

Severe AS was considered if an aortic valve area was<1 cm2 [9]. Exclusion criteria were:

abnormal exercise test;
coexisting moderate/severe valvular disease;
atrial fibrillation or flutter;
LV ejection fraction<0.50;
maximal MPG recorded from right parasternal window;
inability to perform physical exercise.

Abnormal exercise test was defined as occurrence of limiting breathlessness or fatigue at low workload, angina, dizziness or syncope, fall in systolic blood pressure below baseline and/or complex ventricular arrhythmia during exercise test.

Clinical evaluation included assessment of cardiac and extracardiac comorbidities and current medication at baseline. A comorbidity index summating the patient's individual comorbidities (Charlson score) was calculated [10]. Echocardiographic follow-up was performed when planned in the patient's management or when requested by the patient's referring cardiologist.

Echocardiography

Resting echocardiograms were performed at baseline and follow-up on commercially available ultrasound machines (Philips IE 33, and General Electrics Vivid E9). Left ventricular outflow tract diameter was measured in mid systole on magnified outflow from the parasternal long-axis view. Transvalvular aortic velocity time integral, MPG and peak aortic velocity (Vmax) were obtained using continuous-wave Doppler. Aortic valve area was determined by the continuity equation method using the ratio of the velocity time integral in the left ventricular outflow tract obtained using pulsed-wave Doppler and the velocity time integral across the valve obtained by continuous-wave Doppler, and was indexed to body surface area. In addition, standard echocardiographic parameters were collected according to current EACVI/ASE guidelines on the practice of transthoracic echocardiography [11, 12]. Haemodynamic progression of AS was evaluated by the median annualised rate of increase in MPG and Vmax during follow-up.

Exercise stress echocardiography

Exercise stress echocardiographic data were obtained at baseline using a symptom-limited graded maximum bicycle exercise test. Patients laid in semi-supine position on a dedicated ergometer table tilted to 20°. After an initial workload of 20 Watts maintained for 3min, the workload was increased every 3min by 20 Watts. A 12-lead ECG was monitored continuously and blood pressure was measured at rest and every 2min during exercise. The maximum workload (Watts) was recorded. Changes in left ventricular ejection fraction, LV end-diastolic and end-systolic volumes and MPG from rest to peak exercise were obtained.

Statistical analyses

Quantitative variables are expressed as mean±standard deviation if normally distributed (as assessed by Shapiro–Wilk test), or median [interquartile range] otherwise and were compared with the Student t -test or the Mann–Whitney U test as appropriate. Qualitative variables are expressed as frequencies and percentages and compared using the Pearson's Chi2 or Fisher exact test as appropriate.

To study the evolution between echocardiographic data at baseline and follow-up and the evolution of echocardiographic data from rest to peak exercise, Student paired t -test, Wilcoxon signed-rank test or Mac Nemar test were used as appropriate. Linear correlations were studied using the Spearman rank test. A two-tailed P -value<0.05 was considered statistically significant. Statistical analyses were performed using SPSS version 21.0 (SPSS Inc., Chicago, IL).

Results
Baseline clinical and resting echocardiography data

Fifty-five patients were studied. The clinical characteristics of the population at baseline are depicted in Table 1. Mean age was 66±15 years. Forty-five percent of the study population had severe AS (Table 2). Overall, most patients had concentric LV geometry, type 1 diastolic dysfunction, normal left ventricular filling pressure and mild left atrial dilatation. Seven patients of the study population were in a low flow state as defined by a stroke volume index35mL/m2. Among the 25 patients with severe asymptomatic aortic stenosis, 3 were in a low flow state (13%), with 2 having low flow/low gradient AS (8%) and 1 having low flow/high gradient AS (4%). In the subgroup of patients with moderate AS (AVA between 1.0 and 1.5cm2), mean aortic valve area was 1.15±0.12cm2 (range 1.0–1.4), mean MPG was 28±8mmHg (range 16–41), and mean Vmax was 3.4±0.5m/s (range 2.6–4.3). In the subgroup of patients with severe aortic stenosis (AVA<1.0cm2), mean aortic valve area was 0.82±0.12cm2 (range 0.50–0.99), mean MPG was 44±12mmHg (range 24–72), and mean Vmax was 4.2±0.6m/s (range 3.1–5.5). Among these patients with an aortic valve area<1cm2, 19 (76%) had a Vmax of 4m/s or more and 6 patients (24%) had a Vmax of less than 4m/s. Similarly, 17 patients (68%) with an aortic valve area<1cm2 had a MPG of 40mmHg or more and 8 patients (32%) had an MPG of less than 40mmHg. Among patients with an aortic valve area between 1 and 1.5cm2, 24 (80%) had a MPG of 20mmHg or more and 6 patients (20%) had a MPG<20mmHg. Twenty patients with an aortic valve area between 1 and 1.5cm2 (67%) had a Vmax of 3m/s or more and 10 (33%) had a Vmax<3m/s.

Exercise stress echocardiography data

Mean workload achieved was 86±31 Watts, and mean exercise duration 10±4min. ST segment depression occurred in 8 patients (14%). Heart rate, blood pressure and left ventricular ejection fraction increased significantly during exercise while left ventricular end-systolic volume decreased during exercise (Table 3).

Aortic MPG and peak aortic jet velocity significantly increased from rest to peak exercise: from 35±13mmHg to 46±15mmHg, and from 3.7±0.7m/s to 4.3±0.6m/s respectively (both P <0.001). Seven patients (13%) had an exercise Δ MPG20mmHg. Resting MPG was unrelated to exercise Δ MPG (r =0.05, P =0.70, Figure 1).



Figure 1


Figure 1. 

Scatterplot showing the absence of relationship between resting mean pressure gradient (MPG) and exercise-induced changes in MPG.

Zoom

Follow-up evaluation

Follow-up resting echocardiography was performed at a median duration of 1.6 [1.1–3.2] years. Significant AS progression was observed as MPG increased from 35±13mmHg to 48±16mmHg (P <0.0001, Figure 2A), and Vmax increased from 3.8±0.6m/s to 4.4±0.8m/s. (P <0.001, Figure 2B). The evolution of resting echocardiographic data during follow-up is depicted in Table 2. Median annualised changes during follow-up in MPG and Vmax were 5 [2–11] mmHg and 0.24 [0.14–0.57] m/s, respectively.



Figure 2


Figure 2. 

Individual values of resting mean pressure gradient (MPG – A) and aortic jet velocity (Vmax – B) at baseline and follow-up.

Zoom

AS progression

Exercise Δ MPG modestly correlated with annualised changes in resting MPG and Vmax during follow-up (r =0.35, P =0.01 and r =0.38, P =0.005). Median annualised changes in resting MPG and Vmax were significantly higher in patients with an exercise Δ MPG20mmHg as compared with those with an exercise Δ MPG<20mmHg (19 [6–28] vs. 4 [2–10] mmHg/y, P =0.002 and 0.89 [0.27–1.27] vs. 0.20 [0.12–0.41] m/s/y, P =0.002, respectively, Figure 3). Importantly, all patients with an exercise Δ MPG20mmHg had an annualised progression of aortic stenosis faster than the median value in this study population, i.e. an increase in MPG5mmHg/y and an increase in Vmax0.24m/s/y.



Figure 3


Figure 3. 

Median annualised changes in resting mean pressure gradient (MPG – A) and aortic jet velocity (Vmax – B) in patients with an exercise Δ MPG20mmHg as compared with those with an exercise Δ MPG<20mmHg in the overall study population.

Zoom

Among the subgroup of 30 patients with moderate AS, median annualised changes in resting MPG and Vmax were significantly higher in patients with an exercise Δ MPG20mmHg as compared with those a Δ MPG<20mmHg (19 [8–26] vs. 4 [2–10] mmHg/y, P =0.009 and 0.89 [0.44–1.10] vs. 0.21 [0.14–0.41] m/s/y, P =0.006, Figure 4). Sixteen out of 30 patients with moderate AS experienced an increase in resting MPG5mmHg/year. Consistently, all patients with moderate AS and an exercise Δ MPG20mmHg had an annualised increase in resting MPG5mmHg/year and in Vmax0.24m/s/year. Figure 5 reports the case of a study patient with moderate AS, showing a large exercise Δ MPG at baseline and subsequent rapid progression of AS during follow-up.



Figure 4


Figure 4. 

Median annualised changes in resting mean pressure gradient (MPG – A) and aortic jet velocity (Vmax – B) in patients with an exercise Δ MPG20mmHg as compared with those with an exercise Δ MPG<20mmHg in the subgroup of patients with moderate aortic stenosis.

Zoom



Figure 5


Figure 5. 

Showing the case of a study patient with moderate AS, with a large exercise Δ MPG at baseline and subsequent rapid progression of AS during follow-up.

Zoom

Discussion

The present study reports for the first time the relationship between increase in MPG during exercise and subsequent haemodynamic progression of stenosis during follow-up in asymptomatic patients with AS.

Haemodynamic progression of AS and relation to outcome

Prospective studies have provided various average rates of hemodynamic progression of AS [2, 3, 4, 7, 13]. Older age, coronary artery disease, severe stenosis at baseline and degree of calcifications assessed by echocardiography or cardiac computed tomography have been previously identified as predictors of rapid haemodynamic progression of AS [2, 3, 13, 14, 15]. However, some patients with even mild to moderate AS at baseline may experience a rapid progression of the stenosis [4]. Importantly, rapid haemodynamic progression of AS was identified as a predictor of adverse prognosis independently of baseline severity. Otto et al. [2] showed that the rate of change in jet velocity was an independent predictor of outcome in patients with mild to severe AS. Rosenhek et al. reported a significantly faster haemodynamic progression in patients with an event during follow-up (death or aortic valve replacement necessitated by the development of symptoms) compared with those without event, in both patients with mild to moderate AS [3] and severe AS [8]. Consistently, Nistri et al. [4] also identified the rate of progression as an independent powerful predictor of overall mortality and aortic valve replacement in asymptomatic AS patients.

Exercise stress echocardiography as a predictor of progression

Exercise testing in asymptomatic AS has been found safe and useful to unmask apparently asymptomatic patients [16, 17, 18, 19]. The potential additional value of ESE, as compared to a conventional treadmill test, has been previously reported [5, 6, 20, 21]. Current guidelines [9] recommend performing an ESE in severe asymptomatic AS to unmask false asymptomatic patients and assess the increase in MPG with exercise, in order to further stratify disease severity and plan patients’ follow-up, with a class IIb recommendation for valve intervention. A significant increase in MPG during ESE (>18 to 20mmHg) has been previously related to a worse prognosis with an increased risk of death or aortic valve replacement during follow-up [5, 6]. However, mechanisms underlying MPG changes during exercise in AS are not fully elucidated. Given two stenoses with the same severity at rest, why would one have a larger increase in MPG on exertion? Early works from Otto et al. [22] on changes with exercise in asymptomatic AS, studied by post-treadmill echocardiography, identified different responses to exercise. Some patients showed an increase in orifice area due to increased valve opening during exercise. Conversely, others showed a fixed orifice area, presumably due to stiffer leaflets, corresponding to a more advanced stage of the disease. Exercise changes may well reflect the intrinsic stiffness and pliability of the valve. Das et al. [23] compared resting haemodynamics and valve compliance measured by dobutamine stress echocardiography, and confirmed an association between aortic valve compliance and exercise-limiting symptoms. Valve compliance was not related to resting effective orifice area, and predicted exertional symptoms better than resting parameters [23]. Thus, for a same valve stenosis at rest, a valve with limited compliance produces a larger exercise Δ MPG during ESE and may thereby progress rapidly towards severe and symptomatic AS during follow-up.

Moderate aortic stenosis

Moderate AS is not a benign and uniform process. Outcome widely varies from rapid development of symptomatic severe AS to stable event-free survival for many years [3, 24, 25, 26, 27]. Otto [26] reported a 17% annual rate of symptom onset, leading to 85% of cardiac events (death or valve replacement) over a five-year follow-up.

Exercise testing and ESE are recommended for risk stratification of asymptomatic patients with severe AS [9]. However, we previously demonstrated that ESE may improve clinical management not only in patients with severe AS but also in those with moderate AS [5]. We reported a 2.08-fold increase in the risk of events in patients with moderate AS having a Δ MPG20mmHg. In the present study, the relationship between large exercise Δ MPG and haemodynamic progression of AS was also demonstrated in the subgroup of patients with moderate AS. These data reinforce the usefulness of ESE for risk stratification of asymptomatic patients with moderate and severe aortic stenosis.

Limitations

Whereas echocardiographic data were prospectively collected, clinical data were obtained by review of medical records. Our study therefore presents the limitations inherent to retrospective analyses. However, diagnosis and follow-up were performed by cardiologists experienced in valvular heart disease. The present study included a small number of patients. Indeed, a substantial number of elderly patients with asymptomatic aortic stenosis cannot exercise and were not included in this study. Accordingly, the study population built with patients able to exercise was relatively young as indicated by a mean age of 66 years. In addition, availability of a second echocardiogram in the participating centres was mandatory for inclusion in the present study. However, among all patients who underwent ESE in the 2 participating centres for asymptomatic aortic stenosis, those with severe aortic stenosis and an abnormal exercise test at baseline underwent consequently AVR according to current guidelines and did not undergo a second echocardiogram. Moreover, among patients with a normal exercise test, some patients became symptomatic and underwent AVR or died before a second echocardiogram was performed in the participating centers. Only patients with a maximal MPG recorded from the apical view have been included in the present report, as the MPG recorded from right parasternal window cannot be monitored in most cases during exercise. Multislice computed tomography calcium score may help to refine the prediction of aortic stenosis progression but was not available in the present report.

Conclusions

The present study establishes for the first time the link between exercise Δ MPG obtained during ESE and subsequent haemodynamic progression of stenosis during follow-up in patients with moderate or severe asymptomatic AS. Further studies are needed to fully establish the role of ESE in the decision-making process in comparison to other prognostic markers in asymptomatic patients with AS.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Disclosure of interest

The authors declare that they have no competing interest.

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