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European Journal of Echocardiography 2005 6(6):419-428; doi:10.1016/j.euje.2005.01.005
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Copyright © 2005, The European Society of Cardiology

The E/e filling index and right ventricular pressure in relation to applied international Doppler recommendations of left ventricular filling assessment

Cecilia Wallentin Gurona,*, Odd Bech-Hanssenb, Ronny Wikhb, Annika Rosengrenc, Marianne Hartfordd and Kenneth Caidahlb,e

aDepartment of Clinical Physiology, Sahlgrenska University Hospital, SE 416 85 Göteborg, Sweden
bDepartment of Clinical Physiology, Sahlgrenska University Hospital, SE 413 45 Göteborg, Sweden
cDepartment of Internal Medicine, Sahlgrenska University Hospital, SE 416 85 Göteborg, Sweden
dDepartment of Cardiology, Sahlgrenska University Hospital, SE 413 45 Göteborg, Sweden
eDepartment of Clinical Physiology, Karolinska Institute, SE 171 76 Stockholm, Sweden

Received 15 September 2004; received in revised form 3 January 2005; accepted after revision 15 January 2005.

c.wallentin{at}home.se

* Corresponding author. Tel.: +46 703 127772; fax: +46 31 7780551.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Study limitations/concerns
 Conclusions
 References
 
Aim

A ratio >15 between the early diastolic pulsed Doppler velocities of the mitral inflow (E) and the basal left ventricular (LV) tissue (e) has been demonstrated to predict an elevated LV filling pressure (FP). An elevated LVFP implies an elevated right ventricular pressure (RVp). In order to investigate the sensitivity of the E/e filling index, we compared E/e and RVp, in their ability to identify a Doppler-assumed elevation of LVFP.

Methods and results

Application of pulsed Doppler international recommendations grouped 134 patients with acute coronary syndromes (ACS) and 50 age- and sex-matched controls, according to LV filling: normal; delayed relaxation; an isolated pathological mitral–pulmonary venous-A-wave-duration difference; pseudo normal; or a restrictive filling pattern. An E/e >15 and an RVp >30mmHg showed the following (%) sensitivity (32/94), specificity (95/76), positive (68/59), and negative (80/97) predictive values of a Doppler-assumed elevation of LVFP, in terms of either a pseudo normal or a restrictive filling pattern.

Conclusion

The low sensitivity of E/e to detect a Doppler-assumed elevation of LVFP could limit its clinical usefulness as a single variable, in ACS. The high sensitivity and negative predictive value of RVp support its use as an additional LV filling variable in these patients.

Keywords: Left ventricular filling; Diastolic function; Left ventricular filling pressure; Doppler; Tissue Doppler; Right ventricular pressure


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Study limitations/concerns
 Conclusions
 References
 
Tissue Doppler has opened new possibilities to study left ventricular (LV) diastolic both function and filling. The ratio between the early diastolic pulsed Doppler velocities of the mitral inflow (E) and the basal left ventricular (LV) tissue (e) is a suggested new tool in the identification of an elevated LV filling pressure (FP).1–3 Among non-invasive filling variables, the E/e index >15 was shown, by Ommen et al., to be the single best predictor of an invasively confirmed elevation of LVFP, to have a high specificity,3 and also to point to an adverse outcome.4 Its clinical value over traditional pulsed Doppler in LV filling assessment, however, is not established.

Even though pulsed Doppler echocardiography cannot measure LVFP, it can describe the degree of LV filling dysfunction,5,6 of which the most severe forms, i.e. the pseudo normal and the restrictive filling pattern, include an assumed elevated LVFP.6 Since Doppler variables pseudo normalize, combining them enhances diagnostic accuracy. To our knowledge, E/e has not been viewed in relation to a semi-quantitative LV filling assessment, based on internationally recommended7–9 combinations of Doppler variables.

When LVFP is elevated, the pressure difference, physiologically required for blood flow, is maintained by increased pressure generated from the right ventricle. Pulmonary capillary wedge pressure and pulsed Doppler determinants both correlate to an invasively measured pulmonary artery pressure,10 clinically exemplified by secondary pulmonary artery hypertension in LV heart failure.11 Still, right ventricular pressure (RVp) is not routinely considered when estimating LV filling.8,9,12,13

The clinical usefulness of the E/e filling index would depend also on its sensitivity – in relation to currently recommended non-invasive technique – to detect an elevation of LVFP. We hypothesized that the sensitivity of E/e might be lower than previously evident (from E/e set against Doppler variables one by one). As an elevated RVp is a prerequisite for an elevated LVFP, we aimed to compare the sensitivity of the E/e filling index to that of RVp, in predicting an assumed elevation of LVFP, as semi-quantitatively determined from an internationally recommended combined Doppler assessment, in patients with acute coronary syndromes (ACS).


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Study limitations/concerns
 Conclusions
 References
 
Study population
We studied 160 consecutive patients with ACS14 admitted to the coronary care unit at Sahlgrenska University Hospital, Göteborg, Sweden, who were echocardiographically examined, with tissue Doppler recordings, in sinus rhythm and without any hemodynamically significant valvular disease. The echocardiogram was performed in the early stable phase (approximately three days from admission) using an ultrasonic machine (Acuson XP, Acuson/Siemens Mountain View, California) with a 2.5–4MHz transducer.

We defined ACS as an ST-elevation or a non-ST-elevation acute myocardial infarction (AMI) or unstable angina pectoris, the latter with typical chest pain and either ECG signs of myocardial ischemia (ST depression of ≥0.1mV or T-wave inversion in at least two adjacent leads), a minor increase in biochemical markers (CK-MB 5–10µg/l or troponin T 0.05–0.19µg/l) or previously diagnosed ischemic heart disease. Spirometry-verified chronic obstructive pulmonary disease in association with an RVp exceeding 30mmHg (n=4) resulted in exclusion, as did poor image quality or inadequate recordings of the pulsed Doppler (n=6) or the tricuspid regurgitation velocity gradient (n=16), leaving a total of 134 patients.

The patients were clinically categorized as having an ST-elevation AMI in 41% (n=55), a non-ST-elevation AMI in 46% (n=61) or unstable angina pectoris in 13% (n=18). Prior to admission, 19% of the patients had a previous myocardial infarction, 45% had angina pectoris, 46% had systemic hypertension, 8% had symptomatic LV heart failure, 20% had diabetes mellitus and 10% had undergone coronary artery by-pass surgery and/or percutaneous coronary intervention therapy.

Fifty healthy individuals, age- and sex-matched to the cases (Table 1) and selected from a randomly sampled population within the County Census base, served as controls. They were all free of cardiovascular, pulmonary, other systemic disease or chest pain, had no medication and a normal ECG. Their measured cardiovascular risk related variables were; serum-cholesterol 5.3±0.7mmol/l, serum-triglycerides 1.0±0.4mmol/l, blood pressure after 1h rest; 129±16/73±6mmHg, body mass index 23.6±3.8 and 60% had never smoked.


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  		Table 1 Descriptive data, including pulsed Doppler absolute values and ratios

 
Patients and controls underwent an identical echocardiographic examination. All enrolled participants gave their informed consent and the regional scientific ethics committee (Göteborg University) approved the protocol.

Echocardiography and Doppler
The examination was carried out in accordance with the recommendations of the American Society of Echocardiography.15 In addition, in order to optimize image quality, the subjects were, from the left recumbent position, facing the examiner, who had an extra monitor opposite and two hands free for the transducer, as an assisting technician mastered the ultrasonic machine. Registrations were made, whenever possible, in relaxed end expiratory apnoea at a sweep rate of 100mm/s. A cut-out in the mattress facilitated a proper access to the apical LV views. We applied pulsed tissue Doppler to the septal, lateral, inferior and anterior LV basal walls. Pulsed blood pool Doppler from between the mitral tips, the upper right pulmonary vein and the LV outflow tract were recorded. Care was taken to register any tricuspid regurgitation with a small single continuous wave transducer, and in case of a non-definable pressure gradient in a patient, the signal was enhanced by transvenous contrast (agitated Haemaccel®). Central venous pressure was semi-quantitatively assessed, as is routine in our laboratory, as normal, presumably 0–5mmHg; suspected or mildly elevated, 5–10mmHg; moderately elevated, 10–15mmHg; or, severely elevated, 15–20mmHg, from the dimension and breathing variation of the inferior vena cava.16 Central venous pressure (for calculation purposes set to 2.5, 7.5, 12.5 and 17.5mmHg, respectively) was added to the right ventricular–right atrial pressure gradient for an estimation of systolic RVp.16–18 A normal RVp was defined as ≤30mmHg.19 Ejection fraction was measured on-line using the biplanar disc sum method (Simpson's rule), or (in 11%) visually estimated.

Analyses
Each measurement and evaluation was performed blinded to all other information. All Doppler curves were digitized for off-line analyses in a computer program,20 developed by our group. The pulsed aortic, mitral and pulmonary venous Doppler signals were manually outlined around their outer envelope and vertical lines were set to further define events. The blood pool peak mitral early diastolic velocity, E, and velocity at atrial contraction, A, were measured to calculate the E/A ratio. The isovolumic relaxation time (IVRT) and the deceleration time (DT) were defined. The systolic, S, and diastolic, D, pulmonary venous peak flow velocities were likewise measured to render the S/D ratio. The temporal difference between the mitral and pulmonary venous A-waves at their point of cessation, with the nearest ECG R-wave as a reference, was established, diagnostically equivalent to the difference in mitral–pulmonary venous-A-wave duration.8

In accordance with international recommendations,7–9 we used all pulsed Doppler variables to semi-quantitatively classify each individual, with increasing degree of impaired LV filling:

Group 0, normal, a normal S/D ratio, a normal mitral–pulmonary venous-A-wave-duration difference, a normal E/A ratio, a normal DT and IVRT,
Group 1, delayed relaxation, a normal/increased S/D ratio, a normal mitral–pulmonary venous-A-wave-duration difference, a decreased E/A ratio, an increased DT and IVRT,
Group 2, an isolated pathological A-wave-duration difference, a pathological mitral–pulmonary venous-A-wave-duration difference, a normal/increased S/D ratio, a normal/decreased E/A ratio, a normal/increased DT and IVRT,
Group 3, pseudo normal, a decreased S/D ratio, a pathological mitral–pulmonary venous-A-wave-duration difference, a normal E/A and a normal DT and IVRT,
Group 4, a restrictive filling pattern, a decreased S/D ratio, a pathological mitral–pulmonary venous-A-wave-duration difference, an increased E/A ratio, a decreased DT and IVRT.

A mitral–pulmonary venous-A-wave-duration difference of >20ms was regarded as abnormal.21 Reference values of E/A, DT, IVRT and S/D were defined from the control group, considering age and heart rate in regression models (see Results). Hence, prior to the LV filling classification, control correlations were used to adjust the patient variables in order to identify them as normal (within 2 SDs), increased or decreased. The most compatible diastolic filling group was then chosen, but with three of five fulfilled criteria as a minimum. Mandatory, however, for group 3, was either a 2 SD decrease in S/D ratio, or a pathological mitral–pulmonary venous-A-wave-duration difference in combination with at least 1 SD decrease in either the S/D or E/A ratio or the DT. The consensus of two doctors with long echocardiographical experience was entered.

We further merged the study population into four classes: (I) controls, and (II) patients with a presumed normal LVFP (groups 0 and 1), (III) patients with presumed normal mean LVFP but signs of an elevated end-diastolic pressure (group 2), and (IV) patients with a presumed elevated mean LVFP (groups 3 and 4).

The E/e filling index was calculated as the ratio between the peak early mitral inflow (E) and the maximal basal septal velocity (e).

Reproducibility
Two doctors initially independently performed a semi-quantitative LV filling assessment in all patients before their consensus decision on LV filling group. Intra observer Doppler measurement variability was investigated in 10% (14/134) of the patients.

Statistics
Values are presented as mean and SD, when not stated otherwise. Mann–Whitney U test investigated differences between patients and controls. Relations to diastolic groups of LV filling were evaluated by Spearman's rank correlation. We applied logistic regression to compare the relation of E/e and RVp to Doppler-estimated LV filling.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Study limitations/concerns
 Conclusions
 References
 
Descriptive data
Among the controls there was an age correlation for the pulsed mitral Doppler E/A ratio (r=–0.46, p=0.0009), and the pulmonary venous S/D ratio correlated both with age (r=0.36, p=0.012) and heart rate (r=0.35, p=0.014). These relationships, which were used to define the adjusted Doppler reference limits, could be expressed as ‘E/A=2.464–(0.018xage)’ and ‘S/D=–0.219+(0.011xage)+(0.015xheart rate)’. Absolute values and ratios of pulsed Doppler are presented in Table 1, and values of RVp and E/e in Table 2. Three controls (6%) were diagnosed as group 1 and the remaining as group 0. Examples of pulsed Doppler combinations for the five LV filling groups, as well as of the E/e measurement, are shown in Fig. 1.


Figure 1
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  		Figure 1 Top image: examples of mitral (left) and pulmonary venous Doppler (right) constellations for the five left ventricular filling groups; 0, normal; 1, delayed relaxation; 2, an isolated pathological A-wave-duration difference; 3, pseudo normal; and 4, a restrictive filling pattern. Bottom image: example of E and e (e from the basal septal LV wall), which constitute the E/e filling index.

 


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  		Table 2 Variables related to the assessment of RVp and the E/e filling index

 
Reproducibility
The inter observer concordance in semi-quantitative LV filling grading was 97% (as 130/134 patients were identically graded). Repeated measurements in 10% of the patients revealed a coefficient of variation of: 4% for the E/A ratio, IVRT 4%, DT 5%, S/D ratio 2%, delta A-wave duration 4%, E velocity 2%, septal e velocity 5%, the E/e filling index 5% and the tricuspid velocity gradient 3%.

Analyses of E/e and RVp
The proportion with an RVp exceeding 30mmHg of controls (class I) and patients with a Doppler-assumed: normal LVFP (class II), elevated pressure at end-diastole only (class III) and elevated mean LVFP (class IV), are shown in Fig. 2A. Correspondingly, the proportion of subjects with an E/e >15, 8–15, and <8 are presented in Fig. 2B. Conversely, the patient class distribution for an RVp >30mmHg (n=75) versus that of ≤30mmHg (n=59) is shown in Fig. 3A and likewise for an E/e >15 (n=22), 8–15 (n=77) and <8 (n=35) in Fig. 3B.


Figure 2
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  		Figure 2 The percentage individuals of class I, controls; class II, patients with an assumed normal LVFP; class III, patients with signs of an elevated end-diastolic pressure; and class IV, patients with an assumed elevated mean LVFP, who display (A) an estimated RVp >30mmHg (black bars), (B) E/e >15, 8–15 and <8 (black, grey and white bars).

 


Figure 3
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  		Figure 3 The distribution of class II, patients with assumed normal LVFP (white bar area); class III, patients with signs of an elevated end-diastolic pressure (grey bar area); and class IV, patients with an assumed elevated LVFP (black bar area), in percentages of all patients with (A) an estimated RVp >30mmHg (left bar) and ≤30mm Hg (right bar), (B) E/e >15 (left bar), 8–15 (middle bar) and <8 (right bar).

 
An E/e >15 and an RVp >30mmHg had the following (%) sensitivity (32/94), specificity (95/76), positive (68/59), and negative (80/97) predictive values of a Doppler-assumed elevated LVFP (class IV), Table 3. For E/e<8 to predict an assumed normal LVFP (class I and II) these values were 46, 81, 76 and 53%, Table 4.


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  		Table 3 Class I, II, III versus IV distribution with E/e ≤ or > s15 and RVp ≤ or > 30mmHg

 


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  		Table 4 Class I, II versus III, IV distribution with E/e < or ≥ 8

 
Systolic RVp for patients differed significantly from controls (34±11 versus 21±3mmHg, p<0.0001), as did E/e (11.2±4.4 versus 7.5±1.3mmHg, p<0.0001). Both RVp and E/e related to Doppler-assessed LV filling, for patients (rs=0.63 and rs=0.40, respectively, p<0.0001) as well as for all individuals (rs=0.71 and rs=0.53, respectively, p<0.0001). Both RVp (p<0.0001) and E/e (p<0.05) contributed, in a logistic regression model, to predict a Doppler-assumed elevated LVFP.

When dividing the patients with either a pseudo normal or restrictive filling pattern (=a Doppler-assumed elevated LVFP, n=47) into two categories according to their LV ejection fraction: as either reduced, <50% (n=29) or normal/near-normal, ≥50% (n=18), E/e >15 identified 13/29=45% and 2/18=11% and RVp >30mmHg identified 28/29=97% and 16/18=89%, respectively.

Success rate
After having excluded 4% (6/156) due to inadequate Doppler recordings for the LV filling assessment, the success rates for the finally included 134 patients (and 50 controls) were; for E/A ratio: 100% (98%), IVRT: 99% (100%), DT: 100% (100%), S/D ratio 100% (98%), Delta A-wave duration 78% (96%) and E/e 100% (98%). An RVp was obtained in 89% (134/150) of the patients and 84% (42/50) of the controls.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Study limitations/concerns
 Conclusions
 References
 
We have in this study visualized the E/e filling index in relation to the combined contents of pulsed Doppler, in comparison with RVp. Our approach revealed that E/e >15 may have a limited sensitivity to predict an elevated LVFP. This might not be apparent from comparisons to Doppler variables one by one. Moreover, the previously suggested cut off value for normality, E/e<8,3 may not exclude an elevated pressure. In our study, 20% of these patients showed Doppler signs of an elevated mean LVFP, and an additional 20% at atrial contraction only.

The difficulties of LV filling assessment allow no single Doppler variable to be sufficient in itself. As a consequence, it is internationally recommended that variables are interpreted in combination. LV filling assessment includes the analysis of the biphasic, pseudo normalizable, courses for several variables, which render them different informative weight depending on the situation. A longer pulmonary venous than mitral A-wave duration, for instance, is an informative sign when present, as healthy individuals do not display it. However, the difference in A-wave duration can be difficult to register, and may also disappear as the left atrial contraction weakens, a not uncommon finding in a seriously dysfunctional left ventricle. The mitral DT, on the other hand, possesses great predictive value, for pulmonary capillary artery wedge pressure22 and prognosis,23 when registered short, but the identification of an elevated LVFP should preferably precede that stage. These well-known conditions can explain why E/e was the single best non-invasive predictor of an elevated LVFP.3

A moderate specificity in detecting an elevated LVFP is an expected clinical feature for RVp, as there are alternative reasons for RVp to be elevated (pulmonary disease or embolism etc.). The LV filling history of the patient (i.e., the variations in pressure over time, for instance with physical activity, intermittent ischemia, medications etc.) may also interfere, since longstanding pulmonary hypertension can lead to persistently increased resistance in the pulmonary circulation. Pulmonary artery pressure, as well as its relation to pulmonary capillary wedge pressure, varies considerably between patients.11 RVp can therefore not be used as a direct measurement of LV filling. Nevertheless, it has been shown to decrease if heart failure is treated, with concomitant improvement of the non-invasive LV filling variables.24,25

In the present study, intensified pharmacological treatment – according to the clinical condition on and after admission – could hence have contributed to reduce the specificity of RVp. Even though medications can influence both the Doppler signals and RVp through altered loading conditions, variables may not be equally affected,25 for instance due to the less reversible changes in the pulmonary vasculature. However, in our study, the high sensitivity of RVp strongly supported the accuracy of our combined Doppler assessment. In the clinical setting, a reliably registered low RVp should rule out a currently elevated LVFP. If considered with care, RVp could also add information when estimating LV filling. In heart failure patients with a restrictive LV filling pattern and secondary pulmonary hypertension, one mechanism through which the LV function may be influenced is by ventricular interaction,26 but whether this has played a role for any of our patients can only be speculated upon.

Our study population – patients with ACS – is not identical to that of previous studies exploring the E/e filling index,27–29 even though coronary artery disease has been represented.2,3 Clinically, patients with ACS form an important subset of patients with LV filling dysfunction. Methodologically, differences in study populations might account for differences in results, as ACS/coronary artery disease usually affect the left ventricle asymmetrically. There is not, to our knowledge, a consensus with respect to which LV wall to calculate E/e from. Some investigators have, when using the septum, excluded individuals with septal wall motion abnormalities.2 In our population, that would have excluded the majority of the patients. It should be noted, however, that when using the septum, information is gathered also from the right ventricle. If we had applied the present E/e values to calculations based on the lateral wall,12,27,28 E/e would have recognized even fewer patients, since lateral tissue velocities tend to be higher, unless the lateral wall is exclusively affected. Also a mean value of all the four LV wall velocities would require lower upper limits for the E/e filling index.

Our data do not restrain the E/e filling index from being of possible greater value in sub groups of patients, where ordinary Doppler variables are less easily achieved and/or correlate less well with LVFP, such as in patients with atrial fibrillation29 or hypertrofic cardiomyopathy.27 This, however, goes beyond the scoop of our study, as we can make no conclusion concerning patient groups other than those included here.

All in all, we do not find our results contradictive of those of Ommen et al., who registered scattering for E/e8–15, where traditional Doppler further advanced the diagnosis, as well as for E/e<8, where an elevated LV pressure could be present.3 Still, no quantifications were made in relation to the semi-quantitatively assessed degree of LV filling impairment. With this paper we wish to draw attention to an aspect that has not, to our knowledge, been highlighted before.


   Study limitations/concerns
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations/concerns
Conclusions
 References
 
Without access to invasively measured LV pressures we obviously cannot, for each individual, guarantee our combined Doppler assessment to have predicted or excluded an elevation of LVFP correctly. Some error of assessment is inevitable and possibly also accounts for the failure of RVp to have identified all patients with a presumed elevation of LVFP. One advantage of the E/e index is its applicability, also when acoustic windows are poor. Thus, patients excluded due to lack of a measurable RVp may have had adequate signals for the E/e calculation.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations/concerns
 Conclusions
References
 
The sensitivity of E/e >15 to detect a Doppler-assumed elevated LVFP was only one third of that of RVp >30mmHg. Moreover, E/e<8 could coexist with Doppler signs of affected LV pressures. Our findings indicate a limitation in the clinical usefulness for E/e, as a single variable, to predict or exclude an elevation of LVFP in patients with ACS. Furthermore, our data allow us to suggest that RVp is included in the LV filling assessment of these patients, especially as a negative predictor of an elevated LVFP, if RVp is reliably registered as being normal, ≤30mmHg.


   Acknowledgements
 
The authors are grateful to the staff at the Departments of Clinical Physiology and Cardiology for their valuable assistance with the patient investigations. We also thank Ingemar Wallentin, M.D., Ph.D., for consult work as the second LV filling assessor, and Georgios Lappas for statistical assistance. The Swedish Research Council (14231), the Swedish Heart and Lung Foundation, the Västra Götaland Region, the Vardal Foundation, Göteborg University and the Göteborg Medical Society supported this study.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations/concerns
 Conclusions
 References
 

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P. Lindqvist, G. Wikstrom, and A. Waldenstrom
The use of E/Em and the time interval difference of isovolumic relaxation (TIVRT-IVRTm) in estimating left ventricular filling pressures
Eur J Heart Fail, May 1, 2008; 10(5): 490 - 497.
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