Global left ventricular load in asymptomatic aortic stenosis: covariates and prognostic implication (the SEAS trial)
© Rieck et al.; licensee BioMed Central Ltd. 2012
Received: 29 June 2012
Accepted: 22 October 2012
Published: 5 November 2012
Valvuloarterial impedance (Zva) is a measure of global (combined valvular and arterial) load opposing left ventricular (LV) ejection in aortic stenosis (AS). The present study identified covariates and tested the prognostic significance of global LV load in patients with asymptomatic AS.
1418 patients with mild-moderate, asymptomatic AS in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study were followed for a mean of 43±14 months during randomized, placebo-controlled treatment with combined simvastatin 40 mg and ezetimibe 10 mg daily. High global LV load was defined as Zva >5 mm Hg/ml/m2. The impact of baseline global LV load on rate of major cardiovascular (CV) events, aortic valve events and total mortality was assessed in Cox regression models reporting hazard ratio (HR) and 95% Confidence Intervals (CI).
High global LV load was found in 18% (n=252) of patients and associated with female gender, higher age, hypertension, more severe AS and lower ejection fraction (all p<0.05). A total of 476 major CV events, 444 aortic valve events and 132 deaths occurred during follow-up. In multivariate Cox regression analyses, high global LV load predicted higher rate of major CV events (HR 1.35 [95% CI 1.08-1.71], P=0.010) and aortic valve events (HR 1.41 [95% CI 1.12-1.79], P=0.004) independent of hypertension, LV ejection fraction, female gender, age, abnormal LV geometry and AS severity, but failed to predict mortality.
In asymptomatic AS, assessment of global LV load adds complementary information on prognosis to that provided by hypertension or established prognosticators like AS severity and LV ejection fraction.
KeywordsAortic valve stenosis Hypertension Valvuloarterial impedance Prognosis Echocardiography
Patients with aortic stenosis (AS) often have hypertension,[1–5] which is associated with stiffening of the arterial tree, vascular atherosclerosis and increased incidence of ischemic cardiovascular (CV) events in AS[6, 7]. The combined valvular and arterial load imposed on the left ventricle (LV) in AS can be noninvasively quantified by calculation of the valvulo-arterial impedance (Zva). High global LV load was associated with increased mortality in a previous retrospective study of patients with asymptomatic, moderate-to-severe AS. These findings were confirmed in a prospective study by Lancellotti et al. in 163 patients with asymptomatic AS, demonstrating that higher global LV load predicted increased risk of developing symptoms, cardiac death and need for aortic valve replacement, independent of peak aortic jet velocity, left ventricular systolic longitudinal deformation and left atrial area index.
The aim of the present study was to further characterize the phenotype associated with high global LV load and prospectively evaluate if high global LV load predicted increased rate of CV events also in patients with milder AS beyond the increased risk associated with concomitant hypertension and other known prognosticators in AS like AS severity and LV ejection fraction[7, 10].
Study echocardiograms were recorded at 173 SEAS study sites following a standardized protocol and sent for expert interpretation at the SEAS echocardiography core laboratory at Haukeland University Hospital. The echocardiographic protocol has been previously published[1, 15, 16]. All reading was performed using off-line digital workstations with Image Arena® (TomTec Imaging Systems GmbH, Unterschleissheim, Germany) software and proof-read by a single experienced reader (EG).
Assessment of LV geometry and function
LV structure and systolic function were measured following the joined European Association of Echocardiography and American Society of Echocardiography guidelines. LV mass was calculated using an autopsy validated formula. LV hypertrophy was considered present when LV mass/height2.7 exceeded 46.7 g/m2.7 in females and 49.2 g/m2.7 in men, respectively[19, 20]. Relative wall thickness was calculated as the LV posterior wall thickness/LV internal radius ratio at end-diastole, and concentric geometry was defined as relative wall thickness > 0.43. Left ventricular ejection fraction was assessed by biplane Simpson’s method and considered low if <50%.
Assessment of valvular and arterial disease
Severity of AS was assessed following current guidelines. Energy loss index was calculated by a validated equation[23, 24]. Global LV load was assessed as valvulo-arterial impedance (Zva) calculated by the method published in the paper by Briand et al. taking into account the net mean aortic gradient and thus the phenomenon of pressure recovery: Zva = (Systolic arterial pressure + Mean net aortic gradient) / (Stroke volume/body surface area). The net mean gradient was calculated as the mean aortic gradient corrected for actual pressure recovery in the individual patient[25, 26]. Pressure recovery (mm Hg) was calculated at the sinotubular junction level of the aorta as 4v2 × 2AVA/Aa[1 – (AVA/Aa)], where v is the mean aortic jet velocity, AVA is calculated by the continuity equation and Aa is the aortic area. Stroke volume was calculated by the Doppler method and indexed for body surface area.
SEAS study endpoints
The primary endpoint of the prospective SEAS study was major CV events, including hospitalization for heart failure due to progression of AS, death from CV causes, aortic valve replacement, non-fatal myocardial infarction, hospitalization for unstable angina, coronary revascularization and non-hemorrhagic stroke. Secondary endpoints were aortic valve related events (combined congestive heart failure attributed to progression of AS, aortic valve replacement, and death from CV causes) and ischemic CV events (combined death from CV causes, non-fatal myocardial infarction, hospitalization for unstable angina, coronary revascularization, and non-hemorrhagic stroke) analysed separately. Total mortality was a pre-specified tertiary endpoint. All endpoints were adjudicated by an independent committee blinded to study treatment.
IBM SPSS 20.0 (SPSS, Chicago, IL) software was used for data management and analysis. The study had a statistical power of 95% to detect a 30% difference in incidence of major CV events, the primary study end-point, with a significance level of 0.01. Data are expressed as mean ± standard deviation for continuous variables and as percentages for categorical variables. High global left ventricular load was defined as Zva > 5.00 mm Hg/ml/m2[3, 9]. Groups were compared by Students t-test or chi square test as appropriate. Covariates of higher global LV load were identified in univariate correlations and in multivariate linear regression analysis.
Kaplan-Meier curves were used to compare cumulative hazard of CV events in groups of patients who had lower vs. higher global LV load at baseline. Uni- and multivariate Cox regression analyses were used to assess the relation of baseline global LV load to major CV events, aortic valve events, ischemic CV events and total mortality. In the primary multivariate model, global LV load, randomized study treatment, hypertension, LV ejection fraction, female gender, age and abnormal LV geometry were included as covariates. In further models, conventional indices of AS severity, like aortic valve area, mean transaortic gradient and peak aortic jet velocity, were added as covariates. Results are reported as hazard ratio (HR) and 95% confidence interval (CI). A two-tailed p <0.05 was considered statistically significant both in univariate and multivariate analyses.
Characteristics of patients with high global LV load
Clinical and echocardiographic characteristics of the total study population and groups of patients with high vs. normal global left ventricular load at baseline
Total study population (N=1418)
Normal global LV load (N=1166)
High global LV load (N=252)
Female gender (%)
Systolic blood pressure (mmHg)
Diastolic blood pressure (mmHg)
Body mass index (kg/m2)
Mean blood pressure (mmHg)
Pulse pressure (mmHg)
Heart rate (bmp)
Antihypertensive treatment (%)
Angiotensin Converting Enzyme Inhibitor (%)
Angiotensin Receptor Blocker (%)
Calcium Antagonist (%)
Beta Blocker (%)
LV mass index (g/m2.7)
LV hypertrophy (%)
Relative wall thickness (%)
Normal LV geometry (%)
Ejection fraction (%)
Low ejection fraction (%)
Grade 1 (%)
Grade 3 (%)
Grade 1 (%)
Grade 3 (%)
Aortic annulus (cm)
Sinotubular aortic diameter (cm)
Ascending aorta diameter (cm)
Peak aortic jet velocity (m/s)
Aortic valve area (cm2)
Energy loss index
Mean transaortic gradient (mmHg)
Systemic arterial compliance
Zva (mm Hg/ml · m2)
Total cholesterol (mmol/L)
Serum creatinine (mmol/L)
Doppler Stroke volume (ml)
LV end-diastolic volume, by biplane Simpson (ml)
LV end-systolic volume, by biplane Simpson (ml)
Cardiac output by Doppler(L/min)
Cardiac index (L/min/m2)
Covariates of global left ventricular load at study baseline in multivariate linear regression analysis (multiple R 2 = 0.48, p<0.001)
Ejection fraction (%)
Aortic valve area (m2)
Global LV load and prognosis
Incidences of cardiovascular events in groups of patients with normal vs. high global left ventricular load
Type of events
Patients with normal global LV load (N=1166)
Patients with high global LV load (N=252)
Major CV events
Aortic valve events
Ischemic CV events
Impact of high global left ventricular load on patient outcome in multivariate Cox regression analyses
Secondary model §
HR (95% CI) ‡
HR (95% CI) §
Major CV events
Aortic valve events
Ischemic CV events
Concomitant hypertension is common among patients with AS, being found in up to 86% of patients in previous studies[1–5]. As recently demonstrated, hypertension in asymptomatic mild-to-moderate AS is associated with reduced arterial compliance, more subclinical atherosclerosis and increased incidence of ischemic CV events as well as a 2-fold higher mortality from all causes. Our study is the first large prospective analysis of the importance of evaluating combined LV load from valvular and arterial disease by use of non-invasive valvulo-arterial impedance in mild to moderate asymptomatic AS. In particular, the current results contribute to phenotypic characterization of patients with high global LV load in milder degrees of AS, as well as demonstrating the impact of global LV load in prediction of major CV events beyond that provided by presence of hypertension and other well established prognosticators in asymptomatic AS like AS severity and LV ejection fraction[7, 10].
Predictors of high global LV load
The present results add to previous knowledge by demonstrating that also in milder, asymptomatic AS, high global LV load is associated with a high risk phenotype including female gender, older age, concomitant hypertension and reduced LV systolic function, independent of an association with more severe AS by conventional measures like peak aortic jet velocity, mean aortic gradient or aortic valve area. Our finding that older age was associated with higher global LV load is consistent with the consequences of vascular aging. Physiological aging is indeed associated with both increased vascular and ventricular stiffness[29, 30]. The pathophysiological foundation for this finding is uncertain, but multiple mechanisms have been proposed, including reduced endothelial function, modulation of collagen, neurohumoral signaling and vascular remodeling.
Consistent with previous reports, hypertension was a frequent finding among SEAS patients, and associated with reduced arterial compliance and higher global LV load. The association between higher global LV load and female gender is in agreement with previous findings by Gatzka et al. showing that the observed increased arterial stiffening in women is independent of posture.
The negative association between global LV load and LV ejection fraction is in line with previous studies reporting increased global LV load to be associated with reduced LV systolic function assessed by midwall shortening or longitudinal strain[33–35]. In treated hypertensive patients, lower LV systolic function has been associated with presence of subclinical coronary artery disease. Of note, 57% of hypertensive patients in the present study population were treated. Our findings suggest that among patients with milder, asymptomatic AS, the phenotype associated with increased global LV load is typically that of an elderly, hypertensive woman with reduced LV systolic function.
Global LV load and prognosis in AS
Confirming our hypothesis, global LV load predicted an increased rate of major CV events, in particular aortic valve events, independent of hypertension. As previously reported from the SEAS study, concomitant hypertension primarily predicted increased risk of ischemic CV events and mortality. Of note, high global LV load predicted a statistically significant 49% increased rate of major CV events and a 55% increased rate of aortic valve events independent of other features of the high global LV load phenotype, including higher age, female gender, concomitant hypertension, and LV ejection fraction as well as abnormal LV geometry[10, 12]. While the association with these well-known prognostic factors explained the increased mortality attributed to high global LV load in univariate analysis, also after further adjustment for different measures of AS severity, higher global LV load independently predicted a 35% higher rate of major CV events and a 41% increased rate of aortic valve events. These findings suggest that global LV load brings complementary prognostic information in patients with mild to moderate asymptomatic AS without otherwise known CV disease or diabetes.
Our findings expand observations from a retrospective study by Hachicha et al. in 544 patients with asymptomatic moderate AS. In their study, a valvuloarterial impedance > 3.5 mmHg/ml/m2 predicted increased 4-year mortality, while the present study defined high global LV load as valvuloarterial impedance >5.00 mmHg/ml/m2. Of note, the present results add to the finding by Lancellotti et al. from a prospective study in 163 patients with asymptomatic, moderate to severe AS, that higher global LV load predict rate of major CV events independent of peak aortic jet velocity, while longitudinal deformation and left atrial area index were not assessed in the present study. Furthermore, our findings expand the results from a small study by Zito et al. in 52 patients with severe asymptomatic AS and normal LV ejection fraction reporting that combined increased global LV load and reduced global longitudinal speckle strain were the best predictors of combined development of symptoms, aortic valve replacement and death. In contrast, no improvement in risk prediction by global LV load was demonstrated in a multicentre study by Levy et al. in patients with low ejection fraction, low gradient severe, symptomatic AS[36, 37].
It has been suggested that calculating global LV load using central systolic blood pressure might yield better prediction of adverse outcome. Central blood pressure was not recorded in the SEAS trial. However, the use of central instead of brachial aortic blood pressure did not increment the predictive ability of global LV load in a recent publication.
The present study was not designed to assess the effect of different types of medication on the progression of global LV load. 68% of hypertensive SEAS patients were on blood pressure-lowering medication. However, at baseline, no difference in use of different classes of antihypertensive agents was found between patients with lower vs. higher global LV load. Although the study had high power to detect a difference in incidence of major CV events, including total mortality, the study did not have statistical power to detect the observed 20% difference in ischemic CV event incidence between the groups. Thus, a type 2 error cannot be excluded for the lack of association between high global LV load and rate of ischemic CV events in the present study.
Aortic valve stenosis
Simvastatin and Ezetimibe in Aortic Stenosis
- Rieck AE, Cramariuc D, Staal EM, Rossebo AB, Wachtell K, Gerdts E: Impact of hypertension on left ventricular structure in patients with asymptomatic aortic valve stenosis (a SEAS substudy). J Hypertens. 2010, 28: 377-383. 10.1097/HJH.0b013e328332fa44View ArticlePubMedGoogle Scholar
- Masuda C, Dohi K, Sakurai Y, Bessho Y, Fukuda H, Fujii S, Sugimoto T, Tanabe M, Onishi K, Shiraki K, et al.: Impact of chronic kidney disease on the presence and severity of aortic stenosis in patients at high risk for coronary artery disease. Cardiovasc Ultrasound. 2011, 9: 31- 10.1186/1476-7120-9-31View ArticlePubMedPubMed CentralGoogle Scholar
- Briand M, Dumesnil JG, Kadem L, Tongue AG, Rieu R, Garcia D, Pibarot P: Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: implications for diagnosis and treatment. J Am Coll Cardiol. 2005, 46: 291-298. 10.1016/j.jacc.2004.10.081View ArticlePubMedGoogle Scholar
- Herrmann S, Stork S, Niemann M, Lange V, Strotmann JM, Frantz S, Beer M, Gattenlohner S, Voelker W, Ertl G, Weidemann F: Low-gradient aortic valve stenosis myocardial fibrosis and its influence on function and outcome. J Am Coll Cardiol. 2011, 58: 402-412. 10.1016/j.jacc.2011.02.059View ArticlePubMedGoogle Scholar
- Linhartova K, Filipovsky J, Cerbak R, Sterbakova G, Hanisova I, Beranek V: Severe aortic stenosis and its association with hypertension: analysis of clinical and echocardiographic parameters. Blood Press. 2007, 16: 122-128. 10.1080/08037050701343241View ArticlePubMedGoogle Scholar
- Agmon Y, Khandheria BK, Meissner I, Schwartz GL, Petterson TM, O’Fallon WM, Gentile F, Whisnant JP, Wiebers DO, Seward JB: Independent association of high blood pressure and aortic atherosclerosis: A population-based study. Circulation. 2000, 102: 2087-2093. 10.1161/01.CIR.102.17.2087View ArticlePubMedGoogle Scholar
- Rieck AE, Cramariuc D, Boman K, Gohlke-Barwolf C, Staal EM, Lonnebakken MT, Rossebo AB, Gerdts E: Hypertension in aortic stenosis: implications for left ventricular structure and cardiovascular events. Hypertension. 2012, 60: 90-97. 10.1161/HYPERTENSIONAHA.112.194878View ArticlePubMedGoogle Scholar
- Hachicha Z, Dumesnil JG, Pibarot P: Usefulness of the valvuloarterial impedance to predict adverse outcome in asymptomatic aortic stenosis. J Am Coll Cardiol. 2009, 54: 1003-1011. 10.1016/j.jacc.2009.04.079View ArticlePubMedGoogle Scholar
- Lancellotti P, Donal E, Magne J, Moonen M, O’Connor K, Daubert JC, Pierard LA: Risk stratification in asymptomatic moderate to severe aortic stenosis: the importance of the valvular, arterial and ventricular interplay. Heart. 2010, 96: 1364-1371. 10.1136/hrt.2009.190942View ArticlePubMedGoogle Scholar
- Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP, Iung B, Otto CM, Pellikka PA, Quinones M: Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. JAmSocEchocardiogr. 2009, 22: 1-23.Google Scholar
- Rossebo AB, Pedersen TR, Allen C, Boman K, Chambers J, Egstrup K, Gerdts E, Gohlke-Barwolf C, Holme I, Kesaniemi VA, et al.: Design and baseline characteristics of the simvastatin and ezetimibe in aortic stenosis (SEAS) study. Am J Cardiol. 2007, 99: 970-973. 10.1016/j.amjcard.2006.10.064View ArticlePubMedGoogle Scholar
- Gerdts E, Rossebo AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K, Gohlke-Barwolf C, Holme I, Kesaniemi YA, et al.: Impact of baseline severity of aortic valve stenosis on effect of intensive lipid lowering therapy (from the SEAS study). Am J Cardiol. 2010, 106: 1634-1639. 10.1016/j.amjcard.2010.07.042View ArticlePubMedGoogle Scholar
- Rossebo AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K, Gerdts E, Gohlke-Barwolf C, Holme I, Kesaniemi YA, et al.: Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. NEnglJMed. 2008, 359: 1343-1356. 10.1056/NEJMoa0804602.View ArticleGoogle Scholar
- Mancia G, Laurent S, Agabiti-Rosei E, Ambrosioni E, Burnier M, Caulfield MJ, Cifkova R, Clement D, Coca A, Dominiczak A, et al.: Reappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document. J Hypertens. 2009, 27: 2121-2158. 10.1097/HJH.0b013e328333146dView ArticlePubMedGoogle Scholar
- Cramariuc D, Rieck AE, Staal EM, Wachtell K, Eriksen E, Rossebo AB, Gerdts E: Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy). Am J Cardiol. 2008, 101: 510-515. 10.1016/j.amjcard.2007.09.100View ArticlePubMedGoogle Scholar
- Lund BP, Gohlke-Barwolf C, Cramariuc D, Rossebo AB, Rieck AE, Gerdts E: Effect of obesity on left ventricular mass and systolic function in patients with asymptomatic aortic stenosis (a Simvastatin Ezetimibe in Aortic Stenosis [SEAS] substudy). Am J Cardiol. 2010, 105: 1456-1460. 10.1016/j.amjcard.2009.12.069View ArticlePubMedGoogle Scholar
- Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise J, et al.: Recommendations for chamber quantification. Eur J Echocardiogr. 2006, 7: 79-108. 10.1016/j.euje.2005.12.014View ArticlePubMedGoogle Scholar
- Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N: Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986, 57: 450-458. 10.1016/0002-9149(86)90771-XView ArticlePubMedGoogle Scholar
- De Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, De DO, Alderman MH: Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol. 1992, 20: 1251-1260. 10.1016/0735-1097(92)90385-ZView ArticlePubMedGoogle Scholar
- de Simone G, Devereux RB, Daniels SR, Koren MJ, Meyer RA, Laragh JH: Effect of growth on variability of left ventricular mass: assessment of allometric signals in adults and children and their capacity to predict cardiovascular risk. J Am Coll Cardiol. 1995, 25: 1056-1062. 10.1016/0735-1097(94)00540-7View ArticlePubMedGoogle Scholar
- Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB: Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol. 1996, 28: 751-756.View ArticlePubMedGoogle Scholar
- Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise JS, et al.: Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. JAmSocEchocardiogr. 2005, 18: 1440-1463.Google Scholar
- Garcia DPP, Dumesnil J, Sakr F, Durand LG: Assessment of aortic valve stenosis severity: a new Index based on the Energy Loss Concept. Circulation. 2000, 101: 765-771. 10.1161/01.CIR.101.7.765View ArticlePubMedGoogle Scholar
- Baumgartner HST, Niederberger J, Schima H, Maurer G: Overestimation“ of catheter gradients by Doppler ultrasound in patients with aortic stenosis: a predictable manifestation of pressure recovery. J Am Coll Cardiol. 999, 33: 1655-1661.View ArticleGoogle Scholar
- Bahlmann E, Cramariuc D, Gerdts E, Gohlke-Baerwolf C, Nienaber CA, Eriksen E, Wachtell K, Chambers J, Kuck KH, Ray S: Impact of pressure recovery on echocardiographic assessment of asymptomatic aortic stenosis: a SEAS substudy. JACC Cardiovasc Imaging. 2010, 3: 555-562. 10.1016/j.jcmg.2009.11.019View ArticlePubMedGoogle Scholar
- Bahlmann E, Nienaber CA, Cramariuc D, Gohlke-Baerwolf C, Ray S, Devereux RB, Wachtell K, Kuck KH, Davidsen E, Gerdts E: Aortic root geometry in aortic stenosis patients (a SEAS substudy). Eur J Echocardiogr. 2011, 12: 585-590. 10.1093/ejechocard/jer037View ArticlePubMedGoogle Scholar
- Ihlen H, Endresen K, Myreng Y, Myhre E: Reproducibility of cardiac stroke volume estimated by Doppler echocardiography. Am J Cardiol. 1987, 59: 975-978. 10.1016/0002-9149(87)91137-4View ArticlePubMedGoogle Scholar
- Gerdts E, Franklin S, Rieck A, Papademetriou V, Wachtell K, Nieminen M, Dahlof B, Devereux RB: Pulse pressure, left ventricular function and cardiovascular events during antihypertensive treatment (the LIFE study). Blood Press. 2009, 18: 180-186. 10.1080/08037050903047202View ArticlePubMedGoogle Scholar
- Mitchell GF, Parise H, Benjamin EJ, Larson MG, Keyes MJ, Vita JA, Vasan RS, Levy D: Changes in arterial stiffness and wave reflection with advancing age in healthy men and women: the Framingham Heart Study. Hypertension. 2004, 43: 1239-1245. 10.1161/01.HYP.0000128420.01881.aaView ArticlePubMedGoogle Scholar
- Redfield MM, Jacobsen SJ, Borlaug BA, Rodeheffer RJ, Kass DA: Age- and gender-related ventricular-vascular stiffening: a community-based study. Circulation. 2005, 112: 2254-2262. 10.1161/CIRCULATIONAHA.105.541078View ArticlePubMedGoogle Scholar
- Safar ME, Levy BI, Struijker-Boudier H: Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Circulation. 2003, 107: 2864-2869. 10.1161/01.CIR.0000069826.36125.B4View ArticlePubMedGoogle Scholar
- Gatzka CD, Kingwell BA, Cameron JD, Berry KL, Liang YL, Dewar EM, Reid CM, Jennings GL, Dart AM: Gender differences in the timing of arterial wave reflection beyond differences in body height. J Hypertens. 2001, 19: 2197-2203. 10.1097/00004872-200112000-00013View ArticlePubMedGoogle Scholar
- Marechaux S, Carpentier E, Six-Carpentier M, Asseman P, LeJemtel TH, Jude B, Pibarot P, Ennezat PV: Impact of valvuloarterial impedance on left ventricular longitudinal deformation in patients with aortic valve stenosis and preserved ejection fraction. Arch Cardiovasc Dis. 2010, 103: 227-235. 10.1016/j.acvd.2010.03.003View ArticlePubMedGoogle Scholar
- Cramariuc D, Cioffi G, Rieck AE, Devereux RB, Staal EM, Ray S, Wachtell K, Gerdts E: Low-flow aortic stenosis in asymptomatic patients: valvular-arterial impedance and systolic function from the SEAS Substudy. JACC Cardiovasc Imaging. 2009, 2: 390-399. 10.1016/j.jcmg.2008.12.021View ArticlePubMedGoogle Scholar
- Zito C, Salvia J, Cusma-Piccione M, Antonini-Canterin F, Lentini S, Oreto G, Di Bella G, Montericcio V, Carerj S: Prognostic significance of valvuloarterial impedance and left ventricular longitudinal function in asymptomatic severe aortic stenosis involving three-cuspid valves. Am J Cardiol. 2011, 108: 1463-1469. 10.1016/j.amjcard.2011.06.070View ArticlePubMedGoogle Scholar
- Levy F, Luc Monin J, Rusinaru D, Petit-Eisenmann H, Lelguen C, Chauvel C, Adams C, Metz D, Leleu F, Gueret P, Tribouilloy C: Valvuloarterial impedance does not improve risk stratification in low-ejection fraction, low-gradient aortic stenosis: results from a multicentre study. Eur J Echocardiogr. 2011, 12: 358-363. 10.1093/ejechocard/jer022View ArticlePubMedGoogle Scholar
- Lancellotti P, Magne J: Valvuloarterial impedance in aortic stenosis: look at the load, but do not forget the flow. Eur J Echocardiogr. 2011, 12: 354-357. 10.1093/ejechocard/jer044View ArticlePubMedGoogle Scholar
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