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Aortic disease
Assessment of ascending aorta wall stiffness in hypertensive patients by tissue Doppler imaging and strain Doppler echocardiography
  1. Antonio Vitarelli,
  2. Marcello Giordano,
  3. Giuseppe Germanò,
  4. Mario Pergolini,
  5. Paolo Cicconetti,
  6. Francesco Tomei,
  7. Angela Sancini,
  8. Daniela Battaglia,
  9. Olga Dettori,
  10. Lidia Capotosto,
  11. Valentina De Cicco,
  12. Melissa De Maio,
  13. Massimo Vitarelli,
  14. Pasqualina Bruno
  1. Cardiac and Medical Departments, Sapienza Sapienza University, Rome, Italy
  1. Correspondence to Dr Antonio Vitarelli, Via Lima 35, 00198 Rome, Italy; vitar{at}tiscali.it

Abstract

Background Aortic stiffness may be associated with an increased incidence of cardiovascular events and has been reported to be related to arterial wall motion velocities as measured by tissue Doppler imaging.

Objective To investigate the potential clinical application of tissue Doppler imaging (TDI) for assessment of aortic function parameters in healthy and hypertensive adults.

Methods 110 hypertensive and 80 healthy adults were examined. Pulse wave velocity (PWV) and augmentation index (Aix) were measured as standard parameters of arterial stiffness by an oscillometric system. Aortic M-mode and TDI parameters were measured. Aortic distensibility (D) and aortic stiffness index (SI) were calculated using accepted formulae. Anterior wall aortic expansion velocity (SAo), acceleration time (ATAo), early (EAo) and late (AAo) diastolic retraction velocity and peak systolic radial strain (εAo) were determined. Comprehensive echocardiography was performed for the assessment of left ventricular (LV) systolic/diastolic function.

Results SAo, EAo and eAo were significantly lower in hypertensive subjects (p<.001, p<.001, and p<.0001, respectively). Reduced D (p<.05 vs controls) and increased PWV (p<.05 vs controls) and SI (p<.01 vs controls) were consistent with evidence of increased aortic stiffness in both male and female hypertensive patients. PWV and Aix increased and D decreased with increasing age or systolic blood pressure. Multivariate analysis showed εAo to be independently related (R2 = 0.63) to pulse pressure, LV mass index and diastolic function.

Conclusion Ascending aorta TDI provides wall velocity and strain data differentiating hypertensive from healthy adults and reflecting aortic compliance changes related to age and sex and LV diastolic function.

  • Systemic arterial hypertension
  • echocardiography
  • tissue Doppler imaging
  • aortic wall strain
  • aortic wall stiffness
  • arterial pulse wave velocity
  • left ventricular diastolic function
  • diastolic dysfunction
  • tissue Doppler
  • hypertension
  • left ventricular hypertrophy

https://doi.org/10.1136/hrt.2010.198358

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    Introduction

    Aortic stiffness may be associated with an increased incidence of cardiovascular events.1 Several techniques have been used to determine aortic stiffness, including MRI,2 angiography,3 applanation tonometry4 and M-mode echocardiography.5 Some of these methods are invasive or require complex equipment. Arterial wall motion velocities as measured by tissue Doppler imaging (TDI) have been reported to be useful measures of arterial stiffness.6 Moreover, reduced aortic distensibility may contribute to the development of left ventricular (LV) diastolic dysfunction through increased pulse pressure and LV after load, which promote LV hypertrophy and subendocardial ischaemia.7 The aim of this study was to investigate the potential clinical application of TDI for assessment of aortic wall velocities and strain in hypertensive adults as well as their relation to LV diastolic function.

    Methods

    Population

    We examined 110 hypertensive patients without a history of coronary artery disease. Eighty age- and sex-matched healthy subjects free of any diseases were selected as controls. All patients were clinically stable and had normal resting LV systolic function (left ventricular ejection fraction >50%). Eighty-three were taking antihypertensive drugs, 27 had never-treated essential arterial hypertension (systolic blood pressure (SBP) ≥140 mm Hg and/or diastolic blood pressure (DBP) ≥90 mm Hg, as measured with a sphygmomanometer in the supine position). The mean duration of hypertension in the patients enrolled was 9.3±3.5 years. The mean duration of hypertensive treatment was 5.7±1.2 years. Patients with coronary artery disease, significant (more than mild) valvular disease, cardiomyopathy and arrhythmias and diabetes were excluded from this study. Sixty-eight patients underwent coronary angiography and had no signs of coronary artery disease. The remaining 42 had a negative echo-stress test.

    Echocardiography

    All patients underwent transthoracic echocardiography (Vivid E9 ultrasound system, GE, Milwaukee, Wisconsin, USA). All echocardiographic findings were analysed by one of the authors who was blinded to subjects' past histories. The ascending aorta was imaged in an optimised circular plane. Aortic diameters were measured at the level of pulmonary artery bifurcation (2–3 cm above the aortic valve). M-mode diameter measurements (figure 1A) were made in systole (point of maximal anterior motion of aorta) and at end-diastole (q wave on electrocardiogram). The means of five diameter measurements in sequential cardiac cycles were used for data analysis. Systemic arterial blood pressure (BP) was measured at the right brachial artery by manual sphygmomanometry with the patient supine using an adequately sized cuff. BP was measured three times on each occasion at 2 min intervals and averaged. Pulse pressure (PP) was obtained by subtracting the DBP from the SBP. Antihypertensive drugs were not discontinued on the day of the examination.

    Figure 1
    Figure 1

    Two-dimensional, M-mode and tissue Doppler images from aortic short-axis views. (A) M-mode 2D-guided aortic tracing. (B) Velocity profile from the anterior aortic wall site. The systolic and early diastolic induced velocities are shown. (C) Strain profile from the same sample site. Ao, aorta; AT, acceleration time; AAo, wall late diastolic velocity; EAo, wall early diastolic velocity; εAo, wall peak systolic strain; SAo, wall systolic velocity.

    The elastic properties of the aorta were indexed by calculation5 8 9 of aortic distensibility (D), stiffness index (SI) and pressure–strain elastic modulus (Ep) as D=2(As−Ad)/[Ad (Ps−Pd)], SI=ln(Ps/Pd)/(As−Ad)/Ad and Ep=(Ps−Pd)/[(As−Ad)/Ad], respectively, where As=aortic diameter at end-systole, Ad=aortic diameter at end-diastole, Ps=systolic blood pressure, Pd=diastolic blood pressure and ln=natural logarithm.

    Measurements of cardiac chambers were made by transthoracic echocardiography according to established criteria.10–12 Fractional shortening and ejection fraction by modified Simpson method were calculated.10 Left ventricular mass index was estimated.11 Peak early (E) and late (A) diastolic velocities, deceleration time, left ventricular isovolumic relaxation time and pulmonary venous Doppler recording were obtained from apical four-chamber view using standard Doppler practices.13 14 Diastolic function was classified as normal (E/A 0.75–1.5, deceleration time 160–250 ms) or abnormal (impaired relaxation, pseudonormal, or restrictive) according to standard diagnostic criteria.15

    Tissue Doppler imaging

    The general principles that underlie the TDI modalities have been described previously.16 The thoracic aortic wall motion velocities were assessed during the cardiac cycle. Two-dimensional (2D) tissue velocity images of the aortic wall were obtained at 130±15 frames/s, which implies a temporal resolution of approximately 16 ms. The velocity scale was modified to avoid aliasing. To minimise noise, the pulse repetition frequency was set to 0.5–1.0 kHz. A sample volume was placed within the region of interest so that there was no migration beyond the limits of the selected wall. Samples varied from 2 to 4 mm, depending on the size of the region of interest and looking for a compromise between maximising signal-to-noise ratio (large samples) or spatial resolution (small samples). By marking a region of interest on the 2D image in the anterior aspect of the ascending aorta (figure 1B) at the same point as in M-mode measurements, velocities throughout the cardiac cycle for this area can be determined. Offline analysis of the velocity datasets was performed using dedicated software (EchoPAC, version 9.0, GE Ultrasound). TDI tracing displayed accelerated expansion of the aortic wall followed by a slow deceleration, a plateau and then a rapid deceleration into diastole. This trace represents the mean of the instantaneous velocity spectrum. Acceleration time (AT, ms, time to peak systolic velocity), systolic maximum wall expansion velocity (SAo, cm/s), wall contraction early (EAo) and late (AAo) diastolic velocities (cm/s) and wall peak systolic radial strain (εAo, %) were derived.

    Velocity and strain traces were processed from the same wall site in transverse aortic views (figure 1B, C). Strain (change in length per unit length) in each segment was defined17 and represented as peak strain. From tissue Doppler data, incremental strain rate can be estimated by calculating the velocity gradient. The time integral of incremental strain rate yields logarithmic strain: ε=log(L/L0). In this study, the logarithmic strain was converted to Lagrangian strain: ε=(L−L0)/L0. The velocity gradient was estimated between two points with an offset distance (strain length) of 3 mm. This spatial offset was lower than the optimal intersite distance required for ventricular strain measurements and selected as a compromise between acceptable signal-to-noise ratio and longitudinal spatial resolution. The motion of the aortic wall was automatically tracked throughout the cardiac cycle in order to be sure we were measuring changes within the vessel wall and avoiding the partial volume effect of endoluminal blood pool.

    Mitral annulus velocities (Sa, Ea, Aa) were also measured on the transthoracic four-chamber views. E/Ea ratio was used to estimate LV filling pressures and diastolic function.18 19

    Oscillometry

    Pulse wave velocity (PWV) and augmentation index (Aix) were measured as standard parameters of arterial stiffness by oscillometric pulse wave analysis system (TensioMed Arteriograph, Hungary), a recently validated technique.20 21 This technique is based on the fact that the contraction of the myocardium initiates pulse waves in the aorta. The first wave becomes reflected from the aortic wall at the bifurcation, whereas a second reflected wave appears as a late systolic peak. The morphology of this second reflected wave depends on the stiffness of the large artery, the reflection time at 35 mm Hg suprasystolic pressure of the brachial artery (RT S35) and the peripheral resistance-dependent amplitude. Aix (%) is calculated from the amplitudes of the first and second waves as the pressure difference between the late systolic peak pressure and the early systolic peak pressure divided by the late systolic peak pressure.20 21 PWV (m/s) is the quotient of the jugular fossa–symphysis distance and RT S35. The jugular fossa–symphysis distance is anatomically identical with the distance between the aortic trunk and the bifurcation.

    Statistics

    Data are presented as mean value±SD. A Student t test was used for comparison of variables between sex-matched healthy subjects and hypertensive patients. Stepwise multiple regression analysis was performed to assess linear associations between aortic wall parameters as the dependent variables and determinants of clinical and cardiovascular parameters, including age, sex, body mass index (BMI), SBP, DBP, PP and heart rate. Differences were considered statistically significant when the p value was <0.05. To test intraobserver variability, measurements of systolic and diastolic TDI were made at different sites in different people on two different occasions. For interobserver variability, a second investigator randomly made measurements at the above different sites without knowledge of other echocardiographic parameters. The intraobserver and interobserver variabilities were determined (as the difference between the two sets of observations divided by the mean of the observations, and expressed as a percentage).

    Results

    One hundred ten of 118 initially evaluated hypertensive patients were included in the study. Though great care was taken to ensure the quality of the data collected, some aortic segments had to be excluded from analysis as the velocity/strain traces were non-interpretable. Intraobserver variation of velocity/strain parameters ranged from 3% to 6% and interobserver variation ranged from 4% to 9%. The patients demographic data are given in table 1. The main echocardiographic features in the controls and hypertensive groups are compared in table 2.

    View this table:
    Table 1

    Clinical features of study population

    View this table:
    Table 2

    Left ventricular and aortic findings in hypertensive patients and controls

    Correlation between TDI- and standard M-mode-derived indexes of Ao function

    The relationship between TDI measurements and aortic stiffness and distensibility was tested. Univariate correlations in the hypertensive group showed significant inverse relationships of SI and SAo velocities (r=−0.66, p<0.01), EAo velocities (r=−0.61, p<0.01) and SI and εAo (r=−0.75, p<0.001). Aortic distensibility was positively related to SAo velocities (r=0.61, p<0.01) and εAo (r=0.65, p<0.01). Elastic modulus was negatively related to SAo velocities (r=−0.59, p<0.05) and εAo (r=−0.67, p<0.01).

    Compared with controls, in hypertensive patients there was a significant increase of elastic modulus and SI and significant decrease of distensibility (table 2, figure 2). SAo, EAo and εAo were significantly decreased (table 2) compared with controls. A significant increase of AT was also shown.

    Figure 2
    Figure 2

    M-mode-derived (A) and tissue Doppler imaging-derived values (B) in hypertensive (HTN) patients and in controls (CTR). PWV, pulse wave velocity.

    The exclusion of the 42 patients who did not perform coronary angiography did not significantly affect the results.

    Correlation between TDI-derived indexes of Ao function and parameters derived by oscillometric pulse wave analysis system

    Reduced D and RT S35 and increased PWV, Aix and SI were consistent with evidence of increased aortic stiffness in both male and female hypertensive subjects (table 2). PWV was negatively related to SAo velocities (r=−0.52, p<0.05) and εAo (r=−0.56, p<0.01). Age, diastolic blood pressure and sex were significant independent factors modulating SAo and PWV, while DBP and age were significant independent factors modulating EAo. PWV increased and D decreased with increasing age or systolic blood pressure.

    Duration of hypertension correlated with SI (r=0.59, p<0.005), D (r=−0.55, p<0.005), PWV (r=0.61, p<0.005), SAo (r=−0.62, p<0.005), EAo (r=−0.65, p<0.001) and εAo (r=−0.68, p<0.001).

    Correlation between TDI-derived indexes of Ao function, LV mass and LV diastolic function

    Thirty-nine patients had echocardiographic evidence of LV diastolic dysfunction as assessed by standard Doppler; 15 of these patients had E/Ea >12, suggesting high filling pressures. LV mass index (LVMI) was related to peak SBP (r=0.49; p<0.05) and SI (r=0.51; p<0.05) and inversely related to SAo (r=−0.54; p<0.01), EAo (r=−0.51; p<0.01) and εAo (r=−0.61; p<0.005). A significant negative correlation existed between LVMI and LV Ea (r=−0.71, p<0.001). LV Ea was significantly reduced compared with controls (table 2) and related to EAo (r=0.59; p<0.005) and εAo (r=0.64; p<0.005).

    Aortic wall peak systolic radial strain (εAo) was also directly related (table 3) to sex and height and inversely related to age, blood pressure, LVMI, relative wall thickness and E/Ea. Arterial εAo was significantly lower in women, even if indexed to height. Multivariate analysis of all these variables showed εAo to be independently related (R2=0.63) to LVMI, PP and LV diastolic function (Ea). Figure 3 compares εAo between controls and different groups of hypertensive patients (treatment vs no treatment, normal LV function vs LV diastolic dysfunction). Aortic εAo was highest in controls and progressively reduced in different groups (p=0.026 by analysis of variance), being lowest in patients with never-treated hypertension and LV diastolic dysfunction.

    View this table:
    Table 3

    Analysis of aortic wall strain (εAo) in hypertensive patients

    Figure 3
    Figure 3

    Aortic wall strain in hypertensive groups. Ao, aorta; CTR, controls; NT-DD, never-treated hypertension diastolic dysfunction; NT-NF, never-treated hypertension normal left ventricular function; T-DD, treated hypertension diastolic dysfunction; T-NF, treated hypertension normal left ventricular function.

    Discussion

    Our study shows that adult hypertensive patients have increased aortic stiffness and reduced wall velocities and wall strain as measured by TDI and strain Doppler echocardiography.

    Strain represents the fractional or percentages change from the original or unstressed dimension and equals the relative change of segmental length occurring between the reference state and the state of deformation expressed in percentage of end-systolic aortic wall length. Radial, circumferential and axial components of arterial strain have been reported.9 22 23 A pressure–strain elastic modulus for the arterial wall has been described as well as a relationship between elastic modulus and PWV.9

    Tissue Doppler echocardiography has enabled the measurement of ventricular and arterial strain on the basis of velocity wall gradients. It has been shown17 that the strain Doppler technique is a sensitive method for detecting regional ischaemic myocardial wall motion abnormalities and adds significant new data on abnormalities of regional myocardial deformation in an important number of disease entities. Our previous reports16 24 and this study indicate that the decreased vessel wall radial strain measured by Doppler imaging may be an important supplement to the assessment of the elastic properties of thoracic aorta and even more accurate than wall velocities, presumably because the systolic deformation is more uniformly distributed in all aortic segments.

    The aortic wall systolic velocity and strain showed a negative correlation with the rise in stiffness index and a positive correlation with distensibility. Compared with stiffness index and distensibility assessed by M-mode echocardiography, TDI values in the ascending aorta had a greater discriminating power in differentiating hypertensive patients from controls (as seen in table 2). We have previously shown that the assessment of these parameters is particularly relevant in the follow-up of patients with Marfan syndrome16 because aortic dissection may occur in the absence of marked aortic root dilatation, and in patients with aortic coarctation24 because ascending aorta distensibility may be reduced even after surgical repair. Positive results validating TDI assessment of arterial wall properties have also been obtained in the evaluation of abdominal aorta disease25 26 and characterisation of common carotid artery and aortic stiffness6 27 28 in normal adults.

    Decreased wall strain and increased stiffness may be one of the contributors to arterial hypertension and subsequent cardiovascular complications. Blood pressure could function both as cause and effect: increased arterial stiffness and decreased distensibility increase systolic blood pressure, whereas increased blood pressure contributes to decreased arterial elastic properties. In other words, reduced arterial strain and elevated blood pressure may be mutually causally related. However, the potential of aortic strain as a reliable predictor of the risk of progression to hypertension in normotensive subjects still needs further investigation.

    We also demonstrated the value of strain/TDI echocardiography in assessing both aortic wall mechanics and LV diastolic function in hypertensive patients. We have shown that peak systolic radial strain in the anterior wall segment of the ascending aorta is independently related to LV mass index and diastolic function. LV mass is another important predictor of cardiovascular events in the general population, independent of blood pressure. Increase might be an adaptation of haemodynamic changes in arterial pressure wave and/or decrease in aortic wall strain. It might also be determined by hormonal differences such as resetting of the sympathetic nervous and/or renin–angiotensin system.29 It has also been hypothesised that a genetically determined hypertrophic response may occur.30 Increased LV mass and a parallel decrease in LV annular early diastolic velocity suggest LV diastolic dysfunction. This finding is consistent with previous studies31 showing that elevation of LV filling pressures is an early abnormality in the progression of hypertensive heart disease. Measurement of TDI-derived Ea velocities appeared31 to be a robust technique for the assessment of LV relaxation and relatively load-independent compared with pulsed Doppler-derived E/A ratio and deceleration time intervals. Alterations of diastolic function may precede a significant increase in LV mass in subjects at risk of essential hypertension.32 Other studies have shown that in hypertensive heart disease arterial compliance is an independent predictor of LV diastolic dysfunction as assessed by TDI,7 33 suggesting a possible interaction between arterial compliance and diastolic heart failure.

    The increase in LV mass is likely to evolve with age but its potential to progress to high-risk levels requires a serial longitudinal assessment. No attempt was made in our study to connect these pathophysiological changes to clinical outcome. Age-related changes in arterial stiffness have been reported in pre-hypertensive subjects and linked to progression to hypertension.34

    This study has some limitations. First, the technical limitations of strain Doppler echocardiography should be considered. Strain measurements are angle-dependent deformation, therefore interpretations of strains should be made with caution if tissue direction deviates more than 30 degrees from the beam direction. Second, only one vessel bed (ascending aorta) was examined, whereas at different points the arterial wall distensibility may be different. Third, we included patients who did not have coronary angiography. However, our patients had no clinical or echo-stress results that might suggest coronary artery disease. Moreover, in our study the exclusion of these patients did not significantly affect the results. Lastly, no causal relation was investigated between the association of decreased arterial strain and TDI parameters of diastolic dysfunction in these patients.

    Conclusion

    Adult hypertensive patients have reduced TDI-derived ascending aorta wall strain and increased stiffness. Aortic wall strain has a higher discriminating power in differentiating patients from controls than standard M-mode indexes and is independently related to LV mass index and diastolic function. Long-term tracking data would be helpful to confirm the relationship between reduced aortic strain and the occurrence of cardiovascular diseases in these patients.

    Acknowledgments

    We thank GE Healthcare for helpful support and Bruno Montella for technical assistance.

    References

    1. ↵
      1. Mattace-Raso FU,
      2. van der Cammen TJ,
      3. Hofman A,
      4. et al
      . Arterial stiffness and risk of coronary heart disease and stroke: The Rotterdam study. Circulation 2006;113:657–63.
      OpenUrlAbstract/FREE Full Text
    2. ↵
      1. Mohiaddin RH,
      2. Underwood SR,
      3. Bogren HG,
      4. et al
      . Regional aortic compliance studied by magnetic resonance imaging: the effects of age, training and coronary heart disease. Br Heart J 1989;62:90–6.
      OpenUrlAbstract/FREE Full Text
    3. ↵
      1. Stefanadis C,
      2. Stratos C,
      3. Vlachopoulos C,
      4. et al
      . Pressure–diameter relation of the human aorta. A new method of determination by the application of a special ultrasonic dimension catheter. Circulation 1995;92:2210–19.
      OpenUrlAbstract/FREE Full Text
    4. ↵
      1. Chen CH,
      2. Ting CT,
      3. Nussbacher A,
      4. et al
      . Validation of carotid artery tonometry as a means of estimating augmentation index of ascending aortic pressure. Hypertension 1996;27:168–75.
      OpenUrlAbstract/FREE Full Text
    5. ↵
      1. Stefanadis C,
      2. Stratos C,
      3. Boudoulas H,
      4. et al
      . Distensibility of the ascending aorta: comparison of invasive and non-invasive techniques in healthy men and in men with coronary artery disease. Eur Heart J 1990;11:990–6.
      OpenUrlAbstract/FREE Full Text
    6. ↵
      1. Schmidt-Trucksass A,
      2. Grathwohl D,
      3. Schmid A,
      4. et al
      . Assessment of carotid wall motion and stiffness with tissue Doppler imaging. Ultrasound Med Biol 1998;24:639–46.
      OpenUrlCrossRefPubMedWeb of Science
    7. ↵
      1. Mottram PM,
      2. Haluska BA,
      3. Leano R,
      4. et al
      . Relation of arterial stiffness to diastolic dysfunction in hypertensive heart disease. Heart 2005;91:1551–6.
      OpenUrlAbstract/FREE Full Text
    8. ↵
      1. Dernellis J,
      2. Panaretou M
      . Aortic stiffness is an independent predictor of progression to hypertension in nonhypertensive subjects. Hypertension 2005;45:426–31.
      OpenUrlAbstract/FREE Full Text
    9. ↵
      1. Nemes A,
      2. Geleijnse ML,
      3. Forster T,
      4. et al
      . Echocardiographic evaluation and clinical implications of aortic stiffness and coronary flow reserve and their relation. Clin Cardiol 2008;31:304–9.
      OpenUrlCrossRefPubMedWeb of Science
    10. ↵
      1. Schiller NB,
      2. Shah PM,
      3. Crawford M,
      4. et al
      . Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358–67.
      OpenUrlCrossRefPubMed
    11. ↵
      1. Devereux RB,
      2. Alonso DR,
      3. Lutas EM,
      4. et al
      . Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450–8.
      OpenUrlCrossRefPubMedWeb of Science
    12. ↵
      1. Mirsky I,
      2. Corin WJ,
      3. Murakami T,
      4. et al
      . Correction for preload in assessment of myocardial contractility in aortic and mitral valve disease. Application of the concept of systolic myocardial stiffness. Circulation 1988;78:68–80.
      OpenUrlAbstract/FREE Full Text
    13. ↵
      1. Tenenbaum A,
      2. Motro M,
      3. Hod H,
      4. et al
      . Shortened Doppler-derived mitral A wave deceleration time: an important predictor of elevated left ventricular filling pressure. J Am Coll Cardiol 1996;27:700–5.
      OpenUrlCrossRefPubMedWeb of Science
    14. ↵
      1. Appleton CP,
      2. Galloway JM,
      3. Gonzalez MS,
      4. et al
      . Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult cardiac patients. Additional value of analysing left atrial size, left atrial ejection fraction and the difference in the duration of pulmonary venous and mitral flow velocities at atrial contraction. J Am Coll Cardiol 1993;22:1972–82.
      OpenUrlCrossRefPubMedWeb of Science
    15. ↵
      1. Gabriel RS,
      2. Klein AL
      . Modern evaluation of left ventricular diastolic function using Doppler echocardiography. Curr Cardiol Rep 2009;11:231–8.
      OpenUrlCrossRefPubMed
    16. ↵
      1. Vitarelli A,
      2. Conde Y,
      3. Cimino E,
      4. et al
      . Assessment of aortic wall mechanics in Marfan syndrome by transesophageal tissue Doppler echocardiography. Am J Cardiol 2006;97:571–7.
      OpenUrlCrossRefPubMedWeb of Science
    17. ↵
      1. Sutherland GR,
      2. Di Salvo G,
      3. Claus P,
      4. et al
      . Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr 2004;17:788–802.
      OpenUrlCrossRefPubMedWeb of Science
    18. ↵
      1. Ommen SR,
      2. Nishimura RA,
      3. Appleton CP,
      4. et al
      . Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation 2000;102:1788–94.
      OpenUrlAbstract/FREE Full Text
    19. ↵
      1. Takamura T,
      2. Onishi K,
      3. Sugimoto T,
      4. et al
      . Patients with a hypertensive response to exercise have impaired left ventricular diastolic function. Hypertens Res 2008;31:257–63.
      OpenUrlCrossRefPubMed
    20. ↵
      1. Baulmann J,
      2. Schillings U,
      3. Rickert S,
      4. et al
      . A new oscillometric method for assessment of arterial stiffness: comparison with tonometric and piezo-electronic methods. J Hypertens 2008;26:523–8.
      OpenUrlCrossRefPubMedWeb of Science
    21. ↵
      1. Soltész P,
      2. Dér H,
      3. Kerekes G,
      4. et al
      . A comparative study of arterial stiffness, flow-mediated vasodilation of the brachial artery and the thickness of the carotid artery intima-media in patients with systemic autoimmune diseases. Clin Rheumatol 2009;28:655–62.
      OpenUrlCrossRefPubMedWeb of Science
    22. ↵
      1. Reneman RS,
      2. Meinders JM,
      3. Hoeks AP
      . Non-invasive ultrasound in arterial wall dynamics in humans: what have we learned and what remains to be solved. Eur Heart J 2005;26:960–6.
      OpenUrlAbstract/FREE Full Text
    23. ↵
      1. Laurent S,
      2. Cockcroft J,
      3. Van Bortel L,
      4. et al
      . European network for non-invasive investigation of large arteries. Expert consensus document on arterial stiffness: methodological issues and clinical applications. Eur Heart J 2006;27:2588–2605.
      OpenUrlAbstract/FREE Full Text
    24. ↵
      1. Vitarelli A,
      2. Conde Y,
      3. Cimino E,
      4. et al
      . Assessment of ascending aorta distensibility after successful coarctation repair by strain Doppler echocardiography. J Am Soc Echocardiogr 2008;21:729–36.
      OpenUrlCrossRefPubMedWeb of Science
    25. ↵
      1. Harada K,
      2. Yasuoka K,
      3. Shimada Y
      . Usefulness of tissue Doppler imaging for assessing aortic wall stiffness in children with the Marfan syndrome. Am J Cardiol 2004;93:1072–5.
      OpenUrlCrossRefPubMedWeb of Science
    26. ↵
      1. Long A,
      2. Rouet L,
      3. Vitry F,
      4. et al
      . Compliance of abdominal aortic aneurysms before and after stenting with tissue Doppler imaging: evolution during follow-up and correlation with aneurysm diameter. Ann Vasc Surg 2009;23:49–59.
      OpenUrlCrossRefPubMed
    27. ↵
      1. Haiden M,
      2. Kimura Y,
      3. Miyasaka Y,
      4. et al
      . New index of regional arterial stiffness assessed by tissue Doppler imaging. Acta Cardiol 2008;63:603–8.
      OpenUrlCrossRefPubMed
    28. ↵
      1. Suh SY,
      2. Kim EJ,
      3. Choi CU,
      4. et al
      . Aortic upper wall tissue Doppler image velocity: relation to aortic elasticity and left ventricular diastolic function. Echocardiography 2009;26:1069–74.
      OpenUrlCrossRefPubMed
    29. ↵
      1. Redon J,
      2. Cifkova R,
      3. Laurent S,
      4. et al
      . Mechanisms of hypertension in the cardiometabolic syndrome. J Hypertens 2009;27:441–51.
      OpenUrlCrossRefPubMedWeb of Science
    30. ↵
      1. de Divitiis M,
      2. Pilla C,
      3. Kattenhorn M,
      4. et al
      . Ambulatory blood pressure, left ventricular mass and conduit artery function late after successful repair of coarctation of the aorta. J Am Coll Cardiol 2003;41:2259–65.
      OpenUrlCrossRefPubMedWeb of Science
    31. ↵
      1. Rovner A,
      2. de las Fuentes L,
      3. Waggoner AD,
      4. et al
      . Characterization of left ventricular diastolic function in hypertension by use of Doppler tissue imaging and color M-mode techniques. J Am Soc Echocardiogr 2006;19:872–9.
      OpenUrlCrossRefPubMedWeb of Science
    32. ↵
      1. Aeschbacher BC,
      2. Hutter D,
      3. Fuhrer J,
      4. et al
      . Diastolic dysfunction precedes myocardial hypertrophy in the development of hypertension. Am J Hypertens 2001;14:106–13.
      OpenUrlAbstract/FREE Full Text
    33. ↵
      1. Toprak A,
      2. Reddy J,
      3. Chen W,
      4. et al
      . Relation of pulse pressure and arterial stiffness to concentric left ventricular hypertrophy in young men (from the Bogalusa Heart Study). Am J Cardiol 2009;103:978–84.
      OpenUrlCrossRefPubMedWeb of Science
    34. ↵
      1. Yambe M,
      2. Tomiyama H,
      3. Yamada J,
      4. et al
      . Arterial stiffness and progression to hypertension in Japanese male subjects with high normal blood pressure. J Hypertens 2007;25:87–93.
      OpenUrlCrossRefPubMedWeb of Science
    View Abstract

    Footnotes

    • Presented in part at the 63rd High Blood Pressure Research (HBPR) Conference, 23–26 September 2009, Chicago, Illinois, USA

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval This study was conducted with the approval of the Sapienza University, Rome, Italy.

    • Provenance and peer review Not commissioned; externally peer reviewed.