© 2014, Wiley Periodicals, Inc. DOI: 10.1111/echo.12528



Assessment of Aortic Stiffness by Transesophageal Echocardiography Orson D. Go, M.D.,* Michel E. Safar, M.D.,† and Harold Smulyan, M.D.* *Cardiology Division, Department of Medicine, Upstate Medical University, State University of New York, ^ pital Ho ^ tel Dieu, Paris, France Syracuse, New York; and †Centre de Diagnostique et de Therapeutique, Ho

Background: Aortic stiffness, often measured by the carotid/femoral pulse-wave velocity (PWV) method, has become an attractive predictor for cardiovascular (CV) risk. Although noninvasive, PWV requires additional equipment and training. Aortic diameters measured at transesophageal echocardiography (TEE) provide high spatial resolution images as an alternative to PWV, and permit a more routine assessment of aortic stiffness. The purpose of this study was to measure aortic diameters at TEE, calculate aortic stiffness and compare these data to those of the more established PWV as estimates of CV risk and survival. Methods: Systolic and diastolic aortic dimensions were measured retrospectively in 500 consecutive patients who had a clinically indicated TEE. Aortic compliance, distensibility, and stiffness index were calculated using the aortic diameters and corrected brachial cuff blood pressures (BP). Results: Compliance significantly related to age and mean BP (both P < 0.0001) and nearly significantly to chronic renal disease (P = 0.064). The results for distensibility and stiffness index were similar. When analyzed by Kaplan–Meier curves, all stiffness tertiles were significantly predictive of 4.5to 7.5-year survival. These calculated values behaved similar to those of PWV reported in the literature. Conclusions: This study showed that in patients undergoing routine TEE, aortic stiffness can be readily measured and that the derived values offer relationships comparable to those of PWV, including survival prediction. The method may also find use in assessing aortic stiffness in the TEE evaluation of patients with a bicuspid aortic valve or in preparation for transcatheter aortic valve replacement. (Echocardiography 2014;00:1–8) Key words: aorta, transesophageal echocardiography Aortic stiffness is now recognized as a single value that can represent multiple cardiovascular (CV) risk factors cumulatively over time.1 A recent meta-analysis of 15,877 subjects has confirmed its ability to predict CV events and all-cause mortality.2 However, aortic stiffness is not easy to measure. Currently, carotid to femoral pulse-wave velocity (PWV) is the favored technique for assessing aortic stiffness as it is noninvasive, mathematically related to distensibility through the Bramwell–Hill equation and integrates stiffness from one arterial site to another with a single number.1,3 But like other aortic stiffness measurements, PWV has its limitations. It is highly dependent upon the accuracy of the path length of pulse travel, and differences in path lengths vary the PWV by as much as 30%.4–6 Although pulse arrival times are usually accurate, the pressure waves may be difficult to record in the settings of obesity or focal occlusive disease of the Address for Correspondence and reprint requests: Harold Smulyan M.D., Cardiology Division, Department of Medicine, Upstate Medical University, 90 Presidential Plaza, Syracuse NY 13208. Fax: 315-464-1938; E-mail: [email protected]

peripheral arteries.1 Finally, while stiffness increases over the antegrade course of the aortic pulse path, PWV offers a single integrated measure of stiffness over the measured length but does not assess stiffness at a single aortic location.3 Unlike PWV, vascular imaging is a direct method of evaluating arterial stiffness that allows for measurements at specific locations and has been used widely in the sonographic evaluation of carotid artery stiffness.1 Alternatively, magnetic resonance imaging permits direct, accurate measurements of aortic diameters at a single location 7 but is time consuming and expensive compared to simpler sonographic imaging procedures. The calculation of aortic stiffness using measurements of aortic dimensions by transesophageal echocardiography (TEE) is not new8 and was first utilized for the evaluation of aortic stiffness by Lang et al. in 1994.9 In that study, aortic stiffness was calculated in 25 patients from measurements of TEE-derived aortic diameters with simultaneously calibrated pressures pulses from the subclavian artery. These calculated values for aortic stiffness were shown to be related to age. More recently, TEE velocity vector imaging has 1

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been described that utilizes two-dimensional speckle-based imaging to evaluate aortic stiffness.10 This complicated method, however, requires offline analysis using manual border tracking and dedicated software. The value of aortic stiffness measurements using clinically available direct imaging has not been reported in large numbers of patients and its prognostic value has not been verified. The purpose of this study was to determine if measurement of aortic diameters from TEE images and the calculated values of aortic stiffness would be as effective as PWV as a risk predictor. If so, risk prediction could be estimated in any patient undergoing TEE without additional investigation. Therefore, the systolic and diastolic changes in diameter of the descending aorta were measured in 500 patients whose TEE’s were obtained for routine clinical indications. Three indices of aortic stiffness were calculated and patient survival was followed from 4.5 to 7.5 years. The study demonstrated the usefulness of this method for measuring thoracic aortic stiffness in a large group of patients and determined that the method’s capability for predicting longterm survival was comparable to that of PWV.

mild sedation was provided with appropriate doses of intravenous fentanyl and midazolam. The descending aorta and aortic arch were routinely imaged at the end of each study. Transesophageal echocardiography aortic images were reviewed retrospectively. Using an electronic caliper, measurements of systolic and diastolic diameters from the inner border of the aortic media were recorded at a site in the descending aorta just distal to the aortic arch. With the single-lead electrocardiogram as a guide, the systolic dimension was taken as the largest and the diastolic dimension the smallest diameter. Orthogonal dimensions were checked in every case, to avoid the inclusion of oblique images, and atherosclerotic sites were avoided. All measurements were performed by a single investigator (O. G.). Three brachial oscillometric BPs were measured during the TEE, nearest in time to that of aortic imaging. These values were averaged and converted to aortic pressures using the following regression equations from data obtained at cardiac catheterization by Smulyan et al.11

Methods: Patient Selection: Consecutive patients >18 years of age who had undergone TEE at the State University of New York Upstate Medical University from January 1, 2003 to December 31, 2005 were included in the study. The indications for TEE varied widely and included the search for intracardiac thrombi, valvular vegetations, aortic atherosclerosis, images of the LV or RV function, and valvular dysfunction. Those patients who had multiple TEE’s during that time period were registered once— only the initial TEE was considered as the study procedure for that patient. Patients in atrial fibrillation were excluded because a stable beat-tobeat blood pressure (BP) is necessary for stiffness calculation. Patients under general anesthesia were also excluded because of the varying and uncertain effects of different anesthetic agents on BP and aortic stiffness. Also excluded were those patients on intra-aortic balloon pumps. Images, technically unsuitable for accurate aortic measurements in less than 5% of patients, were also excluded. A total of 500 technically adequate TEEs comprised the study. The protocol was approved by the Institutional Review Board of the Upstate Medical University.

where AoSBP = aortic systolic blood pressure; AoDBP = aortic diastolic blood pressure; SBP = brachial artery systolic blood pressure; DBP = brachial artery diastolic blood pressure. The pulse pressure (PP) was the arithmetic difference between the systolic blood pressure (SBP) and the diastolic blood pressure (DBP). Mean blood pressure (MBP) was calculated as the DBP plus 1/3 the PP and assumed to be equal to the aortic MBP. The aortic diameters and pressures were used to calculate three measures of aortic stiffness – compliance, distensibility, and stiffness index.

TEE and Measures of Aortic Stiffness: The posterior pharynx of each patient was topically anesthetized with 2% lidocaine spray and


AoSBP ¼ 0:9  SBP þ 14:6 AoDBP ¼ 0:78  DBP þ 15:2

Aortic Compliance (AoC) ¼ (AoSD-AoDD)=(SBP-DBP) Aortic Distensibility (AoD) ¼ (AoSD-AoDD)=(AoDD)  (SBP-DBP) Aortic stiffness index (SI) ¼ ½ln (SBP/DBP)=½(AoSD-AoDD)/(AoDD) where, ln = natural logarithm; AoSD = aortic systolic diameter; AoDD = aortic diastolic diameter. Medical History: The patients medical records were retrospectively reviewed for demographic data, CV risk factors and comorbidities. These included hypertension, diabetes mellitus, and dyslipidemia or if patients were currently receiving therapy for

Aortic Stiffness by Echocardiography

these conditions. Dyslipidemia was defined as a recorded total cholesterol value of >200 mg%, a LDL of >100 mg% or a history of statin therapy. Coronary artery disease was noted if previously demonstrated by coronary angiography or by a previous clinical event (e.g., non-ST elevation myocardial infarction). A family history of coronary artery heart disease was recorded if a parent or sibling had been affected but the chart was often vague indicating only that the history was either positive or not. Chronic renal disease was defined as a serum creatinine concentration greater than 1.5 mg/dL at that time or during the 6-month period prior to the procedure. The weight and height at the time of procedure were used to calculate body mass index. Medical records were also examined for the use of cardiac medications at the time of the TEE. Complete data were not consistently available in many of the clinical records and the presence of some of these items may have been underestimated. Follow-Up Information: Patients’ survival was tracked until July 15, 2010, providing follow-up from 4.5 to 7.5 years. Mortality was determined by examination of the Social Security Death Index. Attempts were made to determine the cause of death, but the data were not consistently available and not used in the study. Statistical Analysis: Basic measurements are presented as means and standard deviations. Multivariate linear regression was used to predict measures of aortic stiffness with CV risk factors, comorbidities, age, and gender as variables. Cumulative probability curves were constructed using the Kaplan–Meier method, with patients segregated by tertiles (low, intermediate, and high) for each measure of aortic stiffness. Cox regression was used to confirm the association with survival for each measure of aortic stiffness after adjusting for cardiac risk factors, comorbidities, age, and gender. Statistical analysis was performed using the software SPSS ver. 14 (International Business Machines Inc., Armonk, NY, USA). Results: The characteristics of the cohort are summarized in Table I. The sample was primarily Caucasian (83.2%), had a mean age of 58 years (range 18– 92 years), mean body mass index of 29.2 kg/m2, and consisted of 54.6% men. In this heterogeneous group, there were high percentages of patients with hypertension, diabetes mellitus, dyslipidemia, coronary heart disease, valvular heart disease, and left ventricular hypertrophy.

TABLE I Characteristics of the Study Population (N = 500) Mean (Standard Deviation) or Percentage (Number) Demographic characteristic Age (years) 58 (16) Gender Male 54.6 (273) Female 45.4 (227) Ethnicity Caucasian 83.2 (416) African American 10.2 (51) Others (Hispanic, 6.6 (33) Asian, multiracial) 29.28 (8) Body mass index (kg/m2) Mean aortic pressure 70.43 (16) (mmHg) Systolic blood pressure 135 (27) (mmHg) Diastolic blood pressure 70 (16) (mmHg) Pulse pressure (mmHg) 92 (22) Cardiovascular risk factors and conditions Hypertension 62.8 (314) Diabetes mellitus 30.2 (151) Dyslipidemia 37.6 (188) Family history of coronary 48 (240) artery disease Chronic kidney disease 18 (90) Coronary artery disease 30 (150) Tobacco use 32.2 (161) Echocardiogram findings Left ventricular 35.6 (178) hypertrophy Right ventricular 6.4 (32) enlargement Presence of wall motion 27.4 (137) abnormalities Aortic stenosis None 69 (345) Mild 22 (110) Moderate 6 (30) Severe 3 (15) Mitral regurgitation None 29 (147) Mild 50 (249) Moderate 15 (77) Severe 5 (27) Measures of arterial stiffness Aortic compliance 43.97 9 104 (45) 9 104 (cm/mmHg) Aortic distensibility 20.26 9 104 (26) 9 104 (/mmHg) Aortic stiffness index 12.14 (18) Follow-up information Mortality on July 44.4 (222) 15, 2010


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The severity of the illnesses in the group is illustrated by the mortality of 44.4% over the follow-up period. Information from previous studies has shown that aortic stiffness bears a nonlinear relationship with age.12 This was confirmed, as shown in Figure 1A, where aortic compliance is plotted against age. Exploratory plots were then prepared and the exponential transformation of measures of aortic stiffness by 0.1 yielded the most linear relationships and was subsequently used for all analyses. These transformed values are henceforth referred to as aortic compliance, distensibility, and stiffness index throughout the rest of the study. Figure 1B shows this transformation for aortic compliance versus age with the

Aortic Compliance (cm/mmHg x 10-1)


resultant significant linear regression (r = 0.535; P < 0.0001). Almost identical plots for aortic distensibility versus age are available but not shown (r = 0.60; P < 0.0001). Figure 2A and B show the similar relationships between untransformed and transformed stiffness indices versus age (r = 0.595; P < 0.0001). After adjusting by multivariable analysis for the many demographic factors, CV risks and comorbidities listed in Table I, age and MBP were found significantly (P < 0.0001) related to compliance while chronic kidney disease approached statistical significance (P = 0.064) (Table II). Significant relationships for distensibility were also found for age, MBP, and chronic kidney disease

(A) 400


200 300

150 200





0 20







Age (Years) (B)

0.75 0.70


Aortic Compliance (cm/mmHg x 10-4)0.1










0.60 0.55

1.2 0.50 0.45


0.40 20





Age (Years) r = 0.532, P < 0.0001

Figure 1. A. Relationship of aortic compliance and B. its exponential transformation (aortic compliance0.1) with age. The middle line is the fitted regression line and the outer lines are 2 SE of estimate that include 95% of all values.



Age (Years)




Age (Years) r = 0.595, P < 0.000

Figure 2. A. Relationship of aortic stiffness index and B. its exponential transformation (aortic stiffness index0.1) with age. The middle line is the fitted regression line and the outer lines are 2 SE of estimate that include 95% of all values.

Aortic Stiffness by Echocardiography

TABLE II Linear Regression of Demographic Factors, Cardiovascular Risks, and Comorbidities as Predictors of Aortic Compliance Standardized Coefficients b

Unstandardized Coefficients

(Constant) Age Gender Body mass index Hypertension Diabetes mellitus Dyslipidemia Chronic kidney disease Coronary artery disease Smoking Mean aortic pressure Family history



0.708 0.002 0.003 7.72E-005 0.002 0.003 0.001 0.009 0.001 0.002 0.001 0.002

0.016 0.000 0.004 0.000 0.004 0.004 0.004 0.005 0.004 0.004 0.000 0.004

0.561 0.029 0.014 0.017 0.025 0.009 0.074 0.010 0.023 0.185 0.023



43.933 12.625 0.765 0.339 0.410 0.604 0.208 1.853 0.222 0.592 4.780 0.602

0.000 0.000 0.445 0.735 0.682 0.546 0.835 0.064 0.824 0.554 0.000 0.548

Dependent variable: aortic compliance0.1.

Discussion: This study evaluated three measures of aortic stiffness calculated from direct measurements of

TEE generated aortic diameters. The results showed individual associations of compliance and distensibility with age, MBP, and chronic kidney disease. Apart from MBP, stiffness index correlated with these variables as well. The follow-up information of the patients also demonstrated that these measures of aortic stiffness alone were



Cumulative Survival

(P < 0.0001, P < 0.0001, P = 0.048, respectively). Similar to compliance, stiffness index significantly correlated with age (P < 0.0001) and marginally with chronic kidney disease (P = 0.081) but, as expected, was independent of MBP (P = 0.89) (Tables S1 and S2). Reanalysis of the entire dataset using aortic diameters alone and aortic diameters indexed to body surface area showed no improvement over the results with aortic stiffness. On follow-up, 222 patients had died (44.4%). Kaplan–Meier curves showed that cumulative survival was significantly different when the stiffness data were separated by tertiles (P < 0.0001). An example using aortic compliance is shown in Figure 3. The + signs on the plots indicate censored surviving patients at the time of their follow-up. Kaplan–Meier curves for distensibility and stiffness index are also significantly separated and nearly identical (data available but not shown). Cox regression analysis showed that after controlling for demographic factors, comorbidities, and CV risks, age, diabetes mellitus, chronic kidney disease, and MBP all were predictive of mortality with P values less than 0.05. Stiffness index was also predictive of mortality with a P-value of 0.047, but aortic compliance and distensibility only approached statistical significance with p values of 0.082 and 0.066, respectively (Table III). Complete tabular data are available for distensibility and stiffness index in the supporting information Tables S3 and S4.




0.0 0







Days from TEE to Follow-up chi-square



Log Rank (Mantel-Cox) Breslow (Generalized Wilcoxon)

20.505 16.210

2 2

.000 .000





Figure 3. Kaplan–Meier survival curves for patients categorized according to tertiles of aortic compliance and tests of equality of survival distributions for the different tertiles of aortic compliance. Lines represent tertiles of aortic compliance (from above downward – high, intermediate, low). Censored (+) refers to the final time of follow-up for survivors.


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TABLE III Demographic Factors, Cardiovascular Risks, Comorbidities, and Aortic Compliance as Predictors of Mortality by Cox Regression Analysis

Age Gender Body mass index Hypertension Diabetes mellitus Dyslipidemia Family history Chronic kidney disease Coronary artery disease Smoking Mean aortic pressure Aortic compliance






Exp (B)

0.233 0.153 0.014 0.003 0.336 0.096 0.155 0.742 0.249 0.010 0.196 3.158

0.058 0.136 0.010 0.164 0.150 0.149 0.142 0.158 0.157 0.160 0.044 1.729

16.220 1.268 2.005 0.000 4.997 0.421 1.188 22.215 2.502 0.004 19.404 3.337

1 1 1 1 1 1 1 1 1 1 1 1

0.000 0.260 0.157 0.984 0.025 0.517 0.276 0.000 0.114 0.952 0.000 0.068

1.262 1.165 0.986 1.003 1.399 0.908 0.857 2.101 1.282 0.990 0.822 0.042

B = regression coefficient; SE = standard error; Wald = Wald statistic; df = degrees of freedom; Sig = significance (P values); Exp (B) = hazard ratio (age by 10-year increments; mean blood pressure by 10 mmHg increments).

predictors of survival. However, the prognostic values of stiffness were marginal predictors of survival after accounting for other demographic factors, CV risks, and comorbidities. To date, this is the first longitudinal study of the relationship of direct measurements of aortic stiffness with outcomes based on intermediate to long-term follow-up. To determine if these findings are useful, they are compared with results from the better studied and recognized PWV. Relationship with Age, Mean Aortic Pressure, and Chronic Kidney Disease: Our findings are similar to observations made using PWV. A previous systematic review in 2009, observed that age and blood pressure explained the majority of variance in aortic PWV, but had little association with CV risk factors.13 Two major observational studies have since replicated these findings. In the Anglo-Cardiff Collaborative Trial, PWV was assessed in 4421 individuals ranging from 18 to 92 years to evaluate factors associated with aortic stiffness.14 Age and blood pressure were most strongly associated with increased PWV accounting for about 70% of its variance while CV risk factors exerted a much more modest effect. A second study of 11,092 untreated individuals, free from overt CV disease or diabetes, was carried out from 13 different centers across eight European countries. PWV— the increase with age being stronger for the higher blood pressure categories.15 Other than age and blood pressure, increased aortic stiffness has been linked to chronic kidney disease and its progression. In 150 patients with chronic kidney disease who underwent multislice spiral CT for aortic calcification, there was a significant increase in PWV with decreasing renal 6

function.16 Among 133 patients with stages 3 and 4 kidney disease, aortic PWV was independently associated with their reciprocal creatinine plots, the timing of 25% decline in renal function and the start of dialysis treatment.17 Furthermore, an independent relationship was also demonstrated between aortic PWV and plasma creatinine in patients with coronary heart disease.18 In 241 end-stage renal disease patients on dialysis for 11 years and followed up for 6 years, age and PWV were independently associated with all-cause mortality. In this group, despite blood pressure improvement, persistently elevated pulse-wave velocity was shown to be associated with mortality.19 Failure of antihypertensive therapy to lower PWV was an independent predictor of death in 150 end-stage renal disease patients followed up for a mean of 51 months.20 In 512 renal transplant patients with a mean follow-up of 5 years, PWV was an independent predictor of CV events.21 Whether the association of aortic stiffness, as measured by PWV, with chronic kidney disease is direct or simply a parallel observation is subject to debate, as current evidence suggests that glomerular damage may not be the underlying mechanism.22,23 Relationship with Survival: In 1980, a study of hypertensive patients of average age 50 years and mean follow-up of more than 9 years showed that PWV was a predictor of all-cause and CV mortality independent of age, diabetes, or previous CV disease.24 These findings were confirmed in a more recent study.25 In another observational study of 2200 patients with a mean follow-up of more than 1.7 years, PWV was found to be independently correlated with major adverse events.26 In a Framingham

Aortic Stiffness by Echocardiography

cohort of 2232 individuals, mean age of 63 years and followed up for 8.9 years, PWV was also independently related to CV events. When added to the standard CV risk factors, PWV significantly improved risk discrimination and risk classification.27 Our cumulative Kaplan–Meier probability curves demonstrate progressively and significantly separated reduced survival in the tertiles of patients with stiffer aortas. Cox regression analysis, after adjustment for other variables, showed a significant association for stiffness index to overall mortality and approached significance, for compliance and distensibility. Although PWV has been more intensively studied,2,27 our data using direct aortic measurements showed similar support for aortic stiffness as a risk predictor. New Uses: Although a recognized risk predictor, aortic stiffness has thus far found limited clinical application. One for example, by applying aortic diameters from transthoracic echocardiographic images, aortic stiffness has been used to predict perioperative complications from noncardiac surgery.28 However, two new potential applications for our method include the addition of aortic stiffness to the TEE evaluation of patients with bicuspid aortic valves 29 and in the preparation of patients for transcatheter aortic valve replacement. When TEE is required for these purposes, our method represents a readily available alternative to other more complex methods for the evaluation of aortic stiffness. Data of this sort might serve as future risk predictors in these selected populations. Limitations: The study has several important limitations. It is an observational study of both in and outpatient, primarily middle-aged Caucasians who underwent TEE for the investigation of a variety of diseases of varying severity. Many patients were quite ill, as evidenced by the high incidence of death during a follow-up of 4.5–7.5 years. Our data, therefore, may not be readily applicable to other populations. The method is not useable in atrial fibrillation and unfortunately cannot be applied to those undergoing electrical cardioversion. Our data may also not be applicable to those under general anesthesia, but could be used during their preoperative evaluation. The method assumes that the PP is recorded at the same site as the dimensional measurements. In an effort to account for this discrepancy, we measured oscillometric brachial artery pressures and converted them to aortic pressures, using previously developed regressions from directly recorded aortic pressures. Although our data on

aortic stiffness paralleled that of PWV in the literature, measures of aortic stiffness by imaging and PWV are not identical. PWV integrates stiffness over the course of pulse travel while imaging localizes it to a single site. Nonetheless, similarities to the performance of PWV suggest that data from this and other imaging modalities might be used as a more readily available alternative to PWV. Conclusions: The current study provides the first evidence in a large cohort of patients, of the relationship of 3 direct measures of aortic stiffness by TEE to age, MBP, and chronic kidney disease. Alone, stiffness measured by TEE also predicted survival. These values of aortic stiffness derived from TEE images can be readily obtained from a routine clinical study with no additional equipment. Although compliance was easiest to calculate, there was near equivalence of all 3 measures of aortic stiffness, suggesting that any of the 3 could be used for clinical purposes. Credence for the method is supported by noting its comparability to aortic stiffness as measured by PWV, including its estimates of survival. Acknowledgment: The authors acknowledge the statistical and textual advice of James Schmeidler, Ph.D., Mount Sinai School of Medicine, New York, NY.

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Supporting Information Additional Supporting Information may be found in the online version of this article: Table S1. Linear regression of demographic factors, cardiovascular risks, and comorbidities as predictors of aortic distensibility. Table S2. Linear regression of demographic factors, cardiovascular risks, and comorbidities as predictors of aortic stiffness index. Table S3. Demographic factors, cardiovascular risks, comorbidities, and aortic distensibility as predictors of mortality by Cox regression analysis. Table S4. Demographic factors, cardiovascular risks, comorbidities, and stiffness index as predictors of mortality by Cox regression analysis.

Assessment of aortic stiffness by transesophageal echocardiography.

Aortic stiffness, often measured by the carotid/femoral pulse-wave velocity (PWV) method, has become an attractive predictor for cardiovascular (CV) r...
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