Left ventricular systolic performance in asymptomatic aortic stenosis
Department of Medicine B2142, The Heart Center, Rigshospitalet, 9 Blegdamsvej DK-2100, Copenhagen, Denmark
* Corresponding author. Tel: +45 3545 0888; fax: +45 3545 2513. E-mail address: kristian{at}wachtell.net
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Abstract |
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 Top Abstract IntroductionImpact of low left-ventricular...Factors associated with clinical...Subgroups of patients with...SummaryClinical implicationsConclusionFundingAcknowledgementsReferences |
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Some asymptomatic patients with aortic stenosis (AS) are at higher risk of impending symptom onset or adverse clinical outcome than others. This article explores whether parameters of left ventricular (LV) systolic performance may identify asymptomatic patients with AS who are most likely to benefit from aggressive treatment interventions. Studies evaluating the influence of LV systolic function on outcomes in asymptomatic patients with AS were reviewed. Several factors are associated with poor outcomes in AS, including low chamber function (assessed by LV ejection fraction; LVEF) and depressed myocardial contractility (assessed by low midwall fractional shortening; MFS). In most patients, LV wall stress is inversely correlated with LVEF; LV hypertrophy and LV systolic dysfunction develop from the high wall-stress and afterload mismatch. Depressed myocardial contractility may as well identify patients with poor prognoses before clinical symptoms. High global afterload (reflected by a valvulo-arterial impedance Zva
5.5 mmHg/mL/m2) seen in patients with paradoxically low-flow/low-gradient AS can identify patients at high risk of adverse outcomes, and finally high LV stroke work loss (25%) can also identify patients at risk. Parameters of LV systolic performance can identify patients with asymptomatic AS who are at high risk of impending symptoms of heart failure and adverse clinical outcomes. Such patients may benefit from more aggressive treatment interventions, including aortic valve replacement.
Key Words: Aortic stenosis • Left ventricular wall stress • Midwall fractional shortening • Global afterload • Left ventricular stroke work loss
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Introduction |
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TopAbstractIntroductionImpact of low left-ventricular...Factors associated with clinical...Subgroups of patients with...SummaryClinical implicationsConclusionFundingAcknowledgementsReferences |
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Therapeutic decisions in patients with aortic stenosis (AS) are based on symptomatic status and, to a lesser extent, haemodynamic severity.1 AS reflects a disease continuum but is often graded in terms of disease severity on the basis of aortic jet velocity, mean transvalvular pressure gradient, and aortic valve area (AVA). Mild disease is characterised by a jet velocity <3 m/s, pressure gradient <25 mmHg, and AVA > 1.5 cm2, and severe disease by a jet velocity >4 m/s, pressure gradient >40 mmHg, and AVA < 1.0 cm2.1 Moderate AS falls within these partition values. Aortic valve replacement is indicated for most symptomatic patients with severe AS; because it improves symptoms and survival.1 However, expert opinion differs about the role of aortic valve replacement in asymptomatic patients with severe AS. Although clinical features may identify patients at greater risk of impending symptom onset or adverse clinical outcome,1 there is general agreement that heart failure in AS is a definite criterion for aortic valve replacement. This article discusses parameters of left ventricular (LV) systolic performance that may help to identify asymptomatic patients with AS, who are most likely to benefit from more aggressive intervention.
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Impact of low left-ventricular ejection fraction and left-ventricular hypertrophy on outcome |
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Although aortic valve replacement is indicated for symptomatic severe AS, many patients, especially older individuals and those with low LV ejection fraction (LVEF), are not offered surgery. The Euro-Heart Survey, which evaluated management of valvular heart disease at 92 European centres between April and July 2001, included 216 patients with isolated severe AS who were
75 years of age.2 A decision not to operate was made by the clinician in 33% of cases, increasing in frequency with increasing age (from 27% in patients aged 75–80 years to 100% in those aged >90 years) and decreasing LVEF (from 21% in patients with LVEF > 60% to 73% in those with LVEF < 30%). By multivariate analysis, older age (P = 0.008), lower LVEF (P = 0.003), but not the Charlson comorbidity index, were independently associated with the decision not to surgically replace the aortic valve. However, when specific comorbid conditions were considered in the multivariate model, only neurological dysfunction was independently linked with the decision not to operate (P = 0.02). A decision not to perform surgery in patients with low LVEF is important, given that LVEF < 45% is a powerful predictor of cardiovascular outcomes in patients with symptomatic heart failure. The Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM) Program enrolled 7599 patients with symptomatic heart failure.3 All-cause mortality, cardiovascular mortality, and its individual components (sudden death, heart failure death, and fatal myocardial infarction) increased with decreasing LVEF, after a median follow-up of 38 months. On multivariate analysis, all-cause mortality increased by 39% for each 10% decrease in LVEF below 45% [hazard ratio (HR) = 1.39, 95% confidence interval (CI) = 1.32–1.46], with even greater increases in risk seen for cardiovascular mortality and the components. Conversely, each of these outcomes remained relatively stable once LVEF exceeded 45%.
The presence of LV hypertrophy is associated with an even greater attributable risk of all-cause mortality than low LVEF or other measures of coronary disease severity. Liao et al.4 evaluated the relative impacts of LV hypertrophy, coronary artery disease, and low LVEF on survival in a cohort of 1089 consecutive adults of African descent who underwent evaluation by coronary angiography and echocardiography. After a mean follow-up of 5 years, LV hypertrophy independently accounted for 37 of every 100 deaths, a proportion that was higher than the attributable risk associated with multivessel coronary artery disease (22 of 100), one-vessel coronary artery disease (1 of 100), or LVEF < 45% (9 of 100).
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Factors associated with clinical outcomes in patients with asymptomatic aortic stenosis |
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Patients with asymptomatic mild-to-moderate AS have significantly poorer survival than age- and gender-matched controls. Rosenhek et al.5 followed 176 consecutive asymptomatic patients with an aortic jet velocity of 2.5–3.9 m/s and normal LV systolic function as defined by an LVEF > 50%. During a median follow-up of 55 months, overall mortality in this cohort was 80% higher than that in the general population (P = 0.004), with both cardiac and non-cardiac mortality significantly increased (both P = 0.001). On multivariate analysis, aortic valve calcification was the most powerful predictor of event-free survival (without death or aortic valve replacement). Five-year event-free survival was 42% in patients with moderate-to-severe calcification (score 3 or 4) compared with 82% for those with mild or no calcification (P = 0.0001). Other independent predictors of poorer longevity included the presence of coronary artery disease (P = 0.006) and aortic valve jet velocity
3 m/s (i.e. moderate AS, P = 0.034). Haemodynamic progression of AS, defined by an increase in aortic jet velocity over time, occurred more rapidly among patients with cardiovascular events (+0.45 m/s/year) than those without events (0.14 m/s/year, P = 0.0001) during the follow-up period. Haemodynamic progression was also significantly more rapid in patients with moderate-to-severe aortic calcification than in those with mild or no calcification (0.35 vs. 0.16 m/s/year, P = 0.0004) and in patients with coronary artery disease than in those without (0.34 vs. 0.18 m/s/year, P = 0.004). In contrast, conventional cardiovascular risk factors, including hypercholesterolaemia, hypertension, and diabetes mellitus were not independently associated with cardiovascular outcomes or haemodynamic progression in this cohort. These findings show that the outcome of mild-to-moderate AS may be worse than commonly assumed, with significant valve calcification, coronary artery disease, and rapid haemodynamic progression portending a poor outcome.
Myocardial function
LV systolic function evaluated by echocardiography may also influence outcome.6 The ventricular wall, from outside to inside, is composed of the subepicardial longitudinal layer, midwall circumferential layer, and subendocardial longitudinal layer. Chamber function is measured by endocardial fractional shortening (EFS), which is in turn calculated from the change in LV internal diameter in diastole to LV internal diameter at end-systole divided by LV internal diameter in diastole both measured at the subendocardial layer. Similarly, LVEF is calculated from systolic and diastolic volumes derived from measurements at the subendocardial layer. However, as the myocardial contractile element is situated in the LV midwall, the assumption for use of EFS or LVEF is that the distance to the midwall is very small. This is a reasonable assumption in eccentric geometry, in which normal wall thickness is seen with eccentric LV hypertrophy. However, in concentric geometry (i.e. concentric remodelling and concentric LV hypertrophy) which is most often the case in AS, when relative wall thickness exceeds 0.43, the use of EFS leads to an overestimation of the LV systolic performance.
Myocardial function takes the distance to the midwall longitudinal layer into account in a two-chamber model. The location in the LV wall at end-systole of the surface between the inner and outer halves of the myocardium at end-diastole was identified by assuming that the ratio of inner/outer myocardial shell volumes remains constant through the cardiac cycle.7 Midwall shortening is calculated as
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Midwall shortening <14%, the 2.5th percentile of values in normal subjects,8–10 identifies depressed LV midwall shortening. End-systolic stress, as the primary measure of myocardial afterload, can be estimated at the midwall using a cylindrical model described by Gaasch et al.11,12 An end-systolic stress13 of 174 kdynes/cm2 corresponds to the 97.5th percentile in normals;8,10 accordingly, higher values identify increased myocardial afterload. Stress-corrected EFS and midwall shortening can be derived from observed/predicted shortening. Stress-corrected fractional shortening <94% and stress-corrected midwall shortening <83% correspond to the 2.5th percentiles of normal values,8,10 and can be considered indicative of low LV chamber and myocardial function, respectively.
In a cohort of 294 patients with initially uncomplicated hypertension, de Simone et al.14 found that depressed MFS, but not reduced EFS, had prognostic significance for adverse cardiovascular outcomes over a mean 10-year follow-up period. In this cohort, 56 patients (19%) had depressed MFS at study enrolment. Patients with lower MFS at baseline, whether evaluated as an absolute value or as a percentage of the predicted value, were significantly more likely to experience major cardiovascular events (P < 0.004) and cardiovascular mortality (P < 0.01) than those with normal MFS values. In contrast, EFS did not predict outcomes in this cohort.
When analysed over time using Kaplan–Meier methods, low MFS was associated with significantly lower event-free survival (P < 0.003) and cardiovascular survival (P < 0.001) independently of patient age (Figure 1).14 Notably, MFS (but not EFS) was inversely related to LV mass index (r = –0.53, P < 0.0001). Patients with low MFS and high LV mass index were at particularly high risk of adverse cardiovascular outcomes. Patients in the two lowest quartiles of MFS who were also in the two highest quartiles of LV mass index had significantly higher rates of cardiovascular events (29 vs. 11%, P < 0.0001) and cardiovascular mortality (10 vs. 2%, P < 0.006) compared with the remaining patients. This study showed that depressed MFS predicts adverse outcomes in patients with hypertension, particularly when accompanied by LV hypertrophy.
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Ventricular wall stress
LV hypertrophy is generally considered a compensatory response designed to maintain normal wall stress and systolic function in the face of chronic pressure overload states, such as hypertension and AS. The normal human AVA is
3–4 cm2. According to the Gorlin formula,15 the pressure gradient across the aortic valve orifice is defined by CO2/AVA2, where CO is the cardiac output. Accordingly, when CO is constant, a two-fold decrease in AVA leads to a four-fold increase in the pressure gradient across the valve. For example, at a constant CO of 5.0 L/min, a reduction in AVA from 1.3 to 0.65 cm2, reflecting progression from moderate AS to severe AS, leads to an increase in the pressure gradient from 15 to 60 mmHg. In this case, when systolic blood pressure is 120 mmHg, LV pressure is 180 mmHg. According to the law of LaPlace, LV wall stress is defined by the LV pressure multiplied by the radius of the ventricular chamber divided by twice the LV weight. Therefore, LV wall stress increases with increases in LV pressure and decreases in LV weight. In concentric LV hypertrophy, LVEF may be above normal, but, if the thickening of the ventricular wall fails to reduce wall stress, then LVEF will be reduced, although a decrease in LVEF does not necessarily indicate reduced myocardial performance.
Wall stress correlates with LVEF in patients with isolated AS. Gunther and Grossman16 evaluated haemodynamic and geometric factors in a cohort of 14 patients with isolated AS and varying degrees of LV dysfunction. LVEF was strongly and inversely correlated with midwall circumferential wall stress (r = –0.96). In this small group of patients, midwall circumferential wall stress was a more reliable predictor of ventricular function than systolic blood pressure or AVA.
More recently, Kupari et al.17 evaluated LV systolic function in 137 patients with isolated AS. LVEF correlated directly with relative wall thickness (r = 0.36, P < 0.001) and inversely with LV mass index (r = –0.30, P < 0.001) (Figure 2).17 AVA indexed by body surface area (AVAI) was also independently associated with LVEF in the multivariate analysis (P = 0.004). Higher LV mass index (P = 0.0004) and smaller AVAI (P = 0.003) were also found to be independently predictive of the presence of heart failure. In a subset of 85 patients with critical AS defined by an AVAI < 0.4 cm2/m2, those without LV hypertrophy had a significantly higher mean LVEF (64 vs. 57%, P = 0.045) and a lower incidence of heart failure (16 vs. 48%, P = 0.025) than those with LV hypertrophy. No patient who had critical AS without LV hypertrophy also had systolic dysfunction. Therefore, LV mass index predicts the presence of systolic dysfunction and heart failure independently of AS severity, implying that LV hypertrophy constitutes a maladaptive, rather than a true homeostatic, response in patients with AS.
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Aortic valve area index
The impact of AS on systolic LV function was also assessed in 1762 patients with mild-to-moderate asymptomatic AS who participated in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study.18 Patients were grouped according to quartile of baseline AVAI: < 0.34; 0.34 to <0.42; 0.42 to <0.51; and
0.51 cm2/m2. AVAI was significantly related to both EFS (r = 0.111, P < 0.001) and MFS (r = 0.122, P < 0.001). However, low AVAI predicted low midwall shortening (defined as MFS < 14%; P < 0.001) but not low EFS (defined by EFS < 27%, P = 0.457) (Figure 3). Low AVAI was also associated with higher LV mass index, as mean LV mass index increased from 70.8 to 74.9 g/m2 from the highest to lowest AVAI quartile (P < 0.05). In the multivariate analysis, low AVAI predicted low MFS (β = 0.90, P < 0.001) independently of higher LV mass index (β = –0.457, P < 0.001), with neither gender nor systolic blood pressure entering into the model. Low AVAI was also significantly associated with stress-corrected MFS (r = 0.115, P < 0.001). Thus, in these patients with mild-to-moderate AS, low AVAI was related to lower systolic LV function independently of LV hypertrophy, with patients in the lowest AVAI quartile having the highest prevalence of impaired systolic LV function. These findings indicate that AS impairs systolic LV function even in asymptomatic patients.
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Subgroups of patients with aortic stenosis |
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Afterload mismatch vs. depressed myocardial contractility
Patients with critical AS and advanced systolic dysfunction fall into two subgroups.19 One subgroup has LV failure due to excessively high wall stress and afterload mismatch. Carabello et al.19 found a close inverse linear relationship between wall stress and LVEF in this subgroup (r = –0.93). Most patients in this subgroup showed major clinical improvement with normalisation of systolic function following aortic valve replacement.
The second subgroup has more severe LV dysfunction than the first subgroup despite less severe AS. In this second subgroup, LVEF is lower than expected on the basis of wall stress, suggesting that the systolic dysfunction is caused by depressed myocardial contractility rather than an afterload mismatch. This subgroup has a poor prognosis, with no recovery of systolic function following aortic valve replacement. These findings indicate that patients with AS may develop LV dysfunction because of either an afterload mismatch or depressed myocardial contractility and that these patients' prognoses depend partly on the underlying cause of dysfunction.
Gender differences
Women tend to have higher mean transvalvular pressure gradients, LVEF, and relative wall thickness, lower circumferential stress, and smaller end-systolic and end-diastolic chamber size compared with men, despite similar degrees of AS. Milavetz et al.20 examined differences in LV geometry in 92 women and 82 men who underwent echocardiography before valve replacement for AS. Despite a similar AVAI, women had a higher mean LVEF (59 vs. 54%, P = 0.02) and smaller chamber size (LV end-diastolic diameter: 48.2 vs. 53.6 mm, P = 0.0001) than men. In a cohort of 65 patients with AS who underwent cardiac catheterisation and echocardiography, Aurigemma et al.21 also found that the women had higher peak LV pressure (205 vs. 188 mmHg, P < 0.01), higher LVEF (66 vs. 57%, P < 0.05), smaller LV end-diastolic diameter (43 vs. 51 mm, P < 0.01), and higher relative wall thickness (0.66 vs. 0.50, P < 0.01) than men, although both had a similar degree of AS.
After aortic valve replacement, women are more likely than men to develop an intracavitary gradient because of dynamic obstruction at the mid-ventricular level. Women with pre-operative LV dysfunction are also more likely to experience improved LVEF after aortic valve replacement compared with their male counterparts.
Low-flow/low-gradient aortic stenosis
The term low-flow/low-gradient is usually used to describe the condition in which AS coexists with severely impaired LVEF, usually related to coronary artery disease. Although a consensus is lacking, many authors require a mean gradient <30 mmHg and a valve area <1 cm2.22–24
Hachicha et al.25 conducted a retrospective analysis of 512 consecutive patents with severe AS (AVAI 
0.6 cm2/m2) and preserved LVEF 50%. Sixty-five percent of patients had normal LV flow output, with a stroke volume index >35 mL/m2, whereas the other 35% had a paradoxically low-flow output with stroke volume index 35 mL/m2. Patients with low flow were more likely to be women than those with normal flow (51 vs. 39%, P < 0.05) and to have a significantly lower transvalvular gradient (32 vs. 40 mmHg, P < 0.001), lower LV end-diastolic volume index (52 vs. 59 mL/m2, P < 0.001), lower LVEF (62 vs. 68%, P < 0.001), and higher LV global afterload as reflected by the valvulo-arterial impedance (Zva; 5.3 vs. 4.1 mmHg/mL/m2, P < 0.001). Three-year survival was significantly lower among patients with paradoxically low flow than those with normal flow (76 vs. 86%, P = 0.006) and among patients with higher valvulo-arterial impedance (Zva 5.5 vs. <5.5 mmHg/mL/m2: 62 vs. 85%, P = 0.003) (Figure 4).25 Low-flow patients who received medical treatment also had significantly lower 3-year survival than those undergoing aortic valve replacement (58 vs. 93%, P = 0.001). Overall, a multivariate model found that three factors independently predicted mortality in the entire cohort: older age (P = 0.025), Zva 5.5 mmHg/mL/m2 (P = 0.017), and medical treatment (compared with aortic valve replacement, P = 0.0003).
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These findings indicate that patients with low transvalvular flow and low gradients despite normal LVEF may have a more advanced stage of AS and a poorer prognosis.25
Left ventricular stroke work loss
LV stroke work, calculated from the ratio of the mean systolic transvalvular gradient to the mean systolic LV pressure, reflects the portion of the LV pressure–volume work per stroke that is lost because of outflow tract obstruction.26 The predictive capacity of LV stroke work loss was compared with other measures, including peak jet velocity, mean pressure gradient, AVA, and aortic valve resistance in a consecutive cohort of 307 patients with AS, with a mean age of 71 years and mean peak jet velocity of 3.7 m/s.27 Receiver-operator-characteristic (ROC) curve analysis was used for the comparisons. Non-flow-corrected indices performed better than AVA and aortic valve resistance, and, of these, LV stroke work loss had the highest predictive capacity for AS symptoms, critical AS, risk of late AS events, and all-cause mortality (Figure 5).27 Patients with LV stroke work loss 25% tended to have poor outcomes. Of more than 95% of symptomatic patients with LV stroke work loss 25% died from cardiac causes or underwent valve replacement within 3 years. Moreover, all patients with LV stroke work loss 25% who had LVEF < 45% experienced an AS event within 1 year, irrespective of their symptomatic status. This study indicated that an LV stroke work loss cutpoint 25% is effective in discriminating patients at high risk of adverse clinical outcomes.27 As a result, measurement of LV stroke work loss could be considered to aid in patient management in otherwise unclear clinical situations.
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Summary |
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TopAbstractIntroductionImpact of low left-ventricular...Factors associated with clinical...Subgroups of patients with...SummaryClinical implicationsConclusionFundingAcknowledgementsReferences |
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Patients with asymptomatic AS have poorer survival than age- and gender-matched individuals.5 Several factors have been associated with poorer outcomes in this population, including moderate-to-severe aortic valve calcification, the presence of coronary artery disease, rapid haemodynamic progression, and depressed myocardial function (low MFS), particularly when combined with high LV mass index or the presence of LV hypertrophy.5,7 Low AVAI is associated with low MFS in asymptomatic patients with mild-to-moderate AS and predicts lower systolic LV function independently of LV hypertrophy.18 Increased LV wall stress, which is inversely correlated with LVEF in patients with isolated AS, also predicts lower systolic LV function.16,17
Patients with AS may have systolic dysfunction because of either high wall stress and afterload mismatch or depressed myocardial contractility.19 Patients with high wall stress and afterload mismatch will usually have systolic function restored by aortic valve replacement, whereas those with depressed myocardial contractility tend to have a poor prognosis even after surgical intervention. Patients with low-flow/low-gradient AS have high LV global afterload (high Zva) even though LVEF may be preserved.25 These patients have a poorer prognosis than those with normal flow and achieve better outcomes with aortic valve replacement than medical treatment. Finally, LV stroke work loss 25% has higher predictive value than flow-related parameters for identifying patients at risk of adverse outcomes and may help to identify which asymptomatic patients would benefit from surgical intervention.27
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Clinical implications |
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TopAbstractIntroductionImpact of low left-ventricular...Factors associated with clinical...Subgroups of patients with...SummaryClinical implicationsConclusionFundingAcknowledgementsReferences |
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The role of aortic valve replacement in asymptomatic patients with severe AS is controversial.1 Several parameters of LV systolic function may help to identify (1) which asymptomatic patients are at the highest risk of impending symptom onset or adverse clinical outcome and (2) individuals who might benefit from surgical intervention. These parameters include low LVEF, low midwall shortening, high LV wall stress, high global afterload (reflected by Zva
5.5 mmHg/mL/m2), and LV stroke work loss 25%.17,19,25,27 Patients with paradoxically low-flow/low-gradient AS are also at higher risk of adverse outcomes than expected on the basis of their preserved LVEF and tend to derive greater benefit from surgical compared with medical intervention.25 |
Conclusion |
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TopAbstractIntroductionImpact of low left-ventricular...Factors associated with clinical...Subgroups of patients with...SummaryClinical implicationsConclusionFundingAcknowledgementsReferences |
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Current guidelines recommend echocardiography for the diagnosis and assessment of AS severity, as well as for the assessment of LV wall thickness, chamber size, and function.1 Such evaluations allow calculation of traditional parameters, such as LVEF, midwall shortening, LV mass index, and AVA, and consequently provide a measure of both cardiovascular risk and AS severity. For asymptomatic patients with severe AS, aortic valve replacement is recommended when LVEF is <50% or when LVEF is normal but severe aortic valve calcification or rapid haemodynamic progression occurs.1 Additional parameters of LV function aside from LVEF can be derived from echocardiographic evaluations to provide additional prognostic information that may be useful in making treatment decisions, especially in otherwise unclear cases. Specifically, the presence of high LV wall stress, high global afterload, or high LV stroke work loss identifies patients at high risk of adverse clinical outcomes. In addition, patients showing a paradoxically low-flow/low-gradient profile are at higher risk of adverse outcomes than expected on the basis of their preserved LVEF. In summary, information about systolic LV performance may be useful in identifying asymptomatic patients with AS who would benefit from more aggressive treatment interventions.
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Funding |
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K.W. has received research grants from the Merck/Schering-Plough Joint Venture.
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Acknowledgements |
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The manuscript preparation was assisted by Rete Biomedical Communications Corp. (Ridgewood, NJ, USA).
Conflict of interest: K.W. is on the steering committee of the Simvastatin and Ezetimibe for Aortic Stenosis study.
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