Mark , Erik , Stefan , Christer , Manuel , and Per: Left atrial strain rate estimates PCWP.


Raised left atrial (LA) pressure is a common pathway for many different cardiac pathologies and is known for its complications including symptoms, cavity enlargement and arrhythmias 1-3. A number of echocardiographic methods have been proposed to estimate LA pressure or pulmonary capillary wedge pressure (PCWP) in a wide range of patients with different etiologies and during different hemodynamic conditions but with only modest accuracy. 4-8 LA volume has been shown to correlate with LV filling pressure and to have prognostic value. 9 Speckle tracking echocardiography (STE) assessment of myocardial deformation with strain and strain rate measurements is useful in detecting abnormalities in LA systolic function independent of LA size, suggesting a good potential role for objective assessment of its intrinsic function.10

Recently, Cameli et al reported a correlation between simultaneous recordings of LA reservoir function (left ventricular systole) and PCWP. 10 Wakami et al also reported similar results in patients with both reduced and preserved LVEF. 11 In addition, Kurt et al showed that LA reservoir deformation function (ventricular systole) correlates with both LVEDP and NT-pro-BNP. 12 In general, the increase in LA cavity size is only achieved by myocardial stretch and potentially impaired intrinsic function 13-14, two markers which also predict the rate of success of DC cardioversion. With this in mind, we hypothesized that irrespective of the underlying pathology, LA myocardial systolic function correlates with the degree of cavity pressure. Since direct measurements of LA pressure are technically difficult, we sought to compare simultaneous recordings of LA systolic function and pulmonary capillary wedge pressure (PCWP) which reflects LA pressure, in a cohort of patients undergoing right heart catheterization (RHC) as an attempt to determine potential relationships between the two.


We prospectively investigated 47 consecutive patients (mean age 61 ±13 years, 19 males) referred to cardiac catheterization procedure with a simultaneous Doppler echocardiography examination. Due to the study set up patients included had different diagnoses: 18 with pulmonary arterial hypertension (PAH) including idiopathic (n=6) and associated PAH (n=12), 6 with chronic thrombo-embolism, 1 with interstitial lung disease, 16 with left heart failure due to diastolic dysfunction and normal LVEF (n=8) and dilated cardiomyopathy with reduced LVVEF (n=8), 2 with pericardial constriction, 1 with SLE and 3 with clinical signs of heart failure but proved to have normal findings at RHC. All patients were in sinus rhythm and none had more than mild valve regurgitation.

Right heart catheterization (RHC)

Venous access was established by inserting a cannula in a medial cubital vein or in the femoral vein. Cardiac catheterization was then performed using a Swan-Ganz® Standard Thermodilution Catheters (Edwards Life sciences) 15. Mean right atrial pressure (RAP), systolic and end-diastolic right ventricular pressure, mean pulmonary artery systolic and diastolic pressures (PASP, PAMP and PADP, respectively) and PCWP were measured. Blood samples for estimation of oxygen saturation were also drawn from the superior and inferior caval veins, right atrium, and from the pulmonary and femoral arteries for calculation of cardiac output (CO) and for screening for intracardiac shunts. CO was determined by thermodilution. PVR was calculated using the equation PVR = mPAP – PCWP (transpulmonary gradient) divided by CO.

Echocardiographic examination

The echocardiographic examination was performed at the same time in all subjects but 3, in whom it was performed within 24 hours of the RHC. A Vivid 7 system (GE Medical Systems, Horten, Norway) equipped with an adult 1.5-4.3 MHz phased array transducer was used for all examinations. Standard views from the parasternal long and short axis and apical 4 chamber views were used. Flow velocities were obtained using pulsed and continuous wave Doppler techniques as proposed by the American Society of Echocardiography 16-17. All Doppler recordings were made at a sweep speed of 50-100 mm/s with a superimposed ECG (lead II). The study protocol was approved by the Regional Ethics Committee of Umeå (DNR 07-092M), and all subjects gave an informed consent to participate in the study.


Left atrial structure and function

LA volume was measured by manually drawing its maximum volume during ventricular systole from the 4 chamber view. LA myocardial function was assessed using speckle tracking echocardiography (STE) technique, from the apical four chamber view and grey scale images 18-19. Effort was made to exclude LA appendage from the images to avoid affecting the global strain rate (SR) measurements. Analysis of the acquired images was performed using the commercially available semiautomated two dimensional (2D) strain software (Echo PAC version 5.0.1, Waukesha, GE, USA). One cardiac cycle was selected, from which end-diastolic frame was determined from the apical 4-chamber view (mean frame rate 63 ± 11/sec.). LA wall was tracked on a frame-frame basis and the endocardial border was traced to delineate the region of interest (ROI). This was composed of 6 segments in a horseshoe shape at the inner side of the septal wall, the lateral walls and the rear of the LA. Only clearly displayed segments were accepted by the software which provided their detailed analysis throughout the cardiac cycle. When segments were automatically excluded because of difficulty in achieving adequate myocardial tracking, the longitudinal global strain was calculated as the average value of the remaining segments, with a minimum of 5 out of 6 segments 20. LA strain and strain rate plots were produced automatically by the software and peak negative strain (LAS) and strain rate during atrial systole (LASRa) as indexes for LA pump function as well as left arial strain during ventricular systole (PALS) were determined, Figure 1A and B.

LV structure and function

LV dimensions were measured from M-mode recordings of the basal region using conventional methods 21. LV ejection fraction was measured using single plane Simpson technique and cardiac output was calculated using the methods proposed by the European Society of Cardiology and ASE 17 LV mass was measured using the M-mode recording of basal LV dimensions, from which posterior wall thickness and septal thickness were measured using conventional methods 17. LV myocardial velocities of the lateral and septal wall were studied using pulsed wave tissue Doppler imaging technique with the sample volume placed approximately 1 cm proximal to the mitral annulus level. From the tissue Doppler recordings we measured peak annulus systolic velocity (s’), early diastolic velocity (e’) and late atrial diastolic velocity (a’). LV filling pattern was obtained from the transmitral Doppler velocities with the pulsed wave Doppler sample volume placed at the tips of the mitral valve leaflets from the apical 4 chamber view. From LV filling velocities recording we measured peak early (E) diastolic velocity, E wave deceleration time and E/A ratio was calculated. LV isovolumic relaxation time (IVRT) was measured as the time interval between LV end-ejection (from the pulsed Doppler recording of the outflow tract velocity) and the onset of E wave velocity. The E/e’ ratio with the e’ from lateral wall and mean e’ from lateral and septal walls were also calculated and taken as an index of raised LV filling pressures. From pulmonary venous flow (PVF) we measured the systolic and diastolic peak velocities and calculated the systolic filling fraction (sff) as peak systolic velocity divided by the sum of systolic and diastolic peak velocities.

Statistical Analysis

The statistical software package (IBM, SPSS, version 20) was used for all calculations. Normally distributed continuous data were expressed as mean ± standard deviation. Linear relationships between the echocardiographic variables and PCWP were tested using Pearson’s correlation coefficient analysis. Receiver Operator Curve (ROC) analysis was used to assess the accuracy of the variables in identifying PCWP > 15 mmHg. The area-under-the curve (AUC) was used including bootstrapping, to quantify overall power of each variable. An optimal threshold and corresponding predictive accuracy was estimated using bootstrapped accuracy-threshold curves. The bootstrapping procedure was done using 5000 iterations, and is based on resampling the data to obtain an estimate of the true distribution of a variable, without influence of random extreme data points which might be the case in the empirical distribution.

Figure 1A

LASRa in a patient with normal PCWP


Figure 1B

LASRa in a a patient with elevated PCWP



Test of LASRa reproducibility was performed in 7 patients using the calcualation of coefficiant of variation (CV) by calculating the difference of standard deviation divided by the mean of the same operator (intra observer CV) and between two different operators (inter observer CV) as well as the variance of LASRa between two different cardiac beats (test re-test) We also calculated the intra class correlation (ICC) by using one way random model with subjects as random factor where ICC> 0.75 was defined as a good agreement between observers.


Table 1 shows the general charactherstics and hemodynamic invasive measurements obtained from the right heart catheterisation and Table 2 displays patients’ echocardiographic measurments of LA and LV structure and function. Table 3 shows correlation results between pulmonary capillary wedge pressure measurements, LA structure and function and indirect Doppler measures of LV filling pressures. 32% of the patients had PCWP of > 15 mmHg and 70% of patients had LVEF > 50%.

PCWP strongly correlated with global LASRa irrespective of LVEF (r = 0.77, p<0.001, Figure 2) and PALS (0.58, p<0.001) as well as LAS (0.58, p<0.001) but weakly with LA volume (r = 0.42, p<0.01). A correlation was also found between PCWP and indirect measures of LV filling pressures such as E/A (r = 0.69, p<0.001) and to a lesser extent with E wave deceleration time (r = 0.54, p<0.001), E/e’ of the LV lateral wall and as a mean of septal and lateral (r = 0.47 and 0.58, p<0.01), PVFsff (r=0.51, p<0.001) and LV IVRT (r = 0.41, p<0.01).

ROC curve analysis showed that LASRa and PVF sff had the highest AUC (0.86 and 0.91) in predicting PCWP >15 mmHg (Table 4). Using LASRa, a value <0.9 1/s had high accuracy (87%) in predicting a PCWP > 15mmHg, with a sensitivity of 97%, a specificity of 72% and a PPV of 85%, figure 3. A cut off value of < 1 1/s in the same prediction showed an accuracy 85%, a sensitivity of 93%, a specificity of 72 and a PPV of 84%.

Reproducibility of the LASRa measurements

The inter observer CV was 9.3 % with a ICC of 0.984, the intra observer CV was 9.5% with ICC of 0.986 and finally the test-re test showed a CV of 13.5% with ICC of 0.940.


Our findings show that PCWP correlated with different measurements of LA size and function but with the strongest relationship with LA wall deformation rate (strain rate) which had the largest AUC on our ROC analysis. A LASRa cut off value of < 1 1/s accurately discriminated between patients with PCWP of > or < than 15 mmHg with an area under the ROC curve of 0.83. PCWP also correlated to a lesser extent with cavity volume and LV and LA filling velocities. In addition, PCWP correlated modestly with Doppler based indirect measures of raised LV filling pressures as shown by E/A, E deceleration time, E/e’ and pulmonary venous flow systolic filling fraction, but to a lesser extent than the LA strain rate. None of the LV filling measurements achieved a ROC analysis (AUC) nearly equal to that of the LASRa.

Data interpretation: PCWP is the conventional invasive measure of LA pressure, calculated by averaging early systolic and early diastolic pressures in the wedge level of the pulmonary artery, with the former reflecting atrial compliance (LA preload) and the latter the LA driving pressure of LV filling (LA afterload). We have found that PCWP invasive measurements correlate with LV and LA filling velocity measurements with E/A the strongest variable followed by PVF sff, E wave deceleration time, and the poorest correlation with LV a’, LV IVRT-ivrt’ and IVRT. E/e’, irrespective of the e’ site, lateral or mean, only correlated modestly with PCWP which support the previous report that E/e’ is not useful in a wide span of patients with different LVEF. These results are also in line with previously documented findings using non- invasive measurements of LA pressure 22-23. On the other hand, the significantly stronger inverse relationship we found between PCWP and LA strain rate (during atrial systole) deserves further explanation since it is a relation between two events, occurring at different phases of the cardiac cycle. This pattern is not strange since the relationship between different phases of the cardiac cycle is well established in the left ventricle, with systolic and diastolic events often related 24. The likely explanation of our findings is the increased LA pressure causing raised wall stress, increased cavity volume and hence myocardial dysfunction as is the case in the left ventricle 25, a sequence of events suggesting maintained Frank-Starling law in the LA. This explanation is further supported by the relationship we found between systolic PVF velocity and LASRa (r=0.55, p<0.001).

Our findings mirror those shown by Cameli et al 10 and Wakami et al 11 and Kurt 12, although the relationships they found was with LA strain during LV systole, rather than strain rate during atrial systole. In fact, in our cohort PALS correlated with PCWP but to a much lesser extent than LASRa. In addition, the patients studied by Cameli et al were different from ours, having shown significantly raised E/A and E/e’ and much lower LVEF, thus suggesting stiffer LV and more advanced disease. Furthermore, the studies from Kurt et al and Wakami et al were not done in a simultaneous approach.

Our second observation was the cut off value of 1 1/s using LA strain rate which differentiated patients according to the LA pressure, with high sensitivity and specificity. The cohort of patients we studied represents a wide range of breathless patients referred to cardiology clinics rather than those with end-stage LV disease, in whom E/e’ has previously been shown to be predictive of LA pressures 4. E/e’ did not score high enough in its relationship with PCWP in our patients, suggesting its potential limitation in similar patients. It is well known that swinging in LA pressure 8 is very common which makes patients respond to pressure lowering medications e.g. renin-angiotensin blocking agents 26-27. With such variability in pressure measurements, we believe that the cut off value we identified which stratifies patients with such degree of accuracy, an area under the ROC curve of 84%, is quite satisfactory for daily clinical use. We also find pulmonary venous systolic filling fraction flow useful in predicting PCWP, despite its technical limitation, particularly in patients with enlarged LA. However, PVF sff was measurable in only 80% of our patients compared to LASRa that was measureable in 100%.

Clinical implications: A cut off value for LA global strain rate of <1 l/s should be of great help in identifying patients with raised LA pressure, who should benefit from pressure lowering medications. This is applicable in patients with heart failure irrespective of EF in whom previous studies have shown difficulties in identifying accurate measures for estimating PCWP 7. LA strain rate measured by speckle tracking echocardiography represents a practical and reproducible tool for studying all patients with breathlessness admitted to cardiac units and heart failure clinics. It might even be of help in establishing one stop breathlessness clinics, being able to identifying left ventricular dysfunction as the cause of dyspnoea. Among the indirect measurements of raised LA pressures, obtained from LV filling pattern was the E/A and systolic filling fraction from pulmonary venous flow which remains the second best method in identifying patients with elevated PCWP.


Patient’ demographics and hemodynamic data (RHC)

Variables Mean±SD
Age, year 61±13
Heart rate, bpm 74±17
Sex, f/m (%) 28/19 (60/40)
Hemodynamics (RHC)
PASP, mmHg 53±21
PVR, WU 4.6±3.8
RAP, mmHg 9±7
PCWP, mmHg 13 ±7
CO, l/min 5.0±1.5

PASP: pulmonary artery systolic pressure; PVR; pulmonary vascular resistance; RAP: right atrial pressure; PCWP: pulmonary capillary wedge pressures; CO: cardiac output.


LV and LA size and function (Doppler echocardiography)

Variables Mean±SD
Posterior wall, mm 7.1±2.0
Septum, mm 10.1±2.3
LV diastole, mm 51±11
LV systole, mm 33±11
LVEF, % 58±14
LVSRs, 1/s -0.71±0.37
LVSRe, 1/s 0.85±0.46
LVSRa, 1/s 0.83±0.37
CO, l/min 4.7±1.3
Mitral E wave deceleration time, ms 177±98
Mitral IVRT, ms 79±29
Mitral E/A 1.3±0.8
LV lateral wall E/e’ 9.2±4.5
LV mean E/e’ 8.2±4.5
PALS, % 19.5±10
LAS,% 9.6±5.8
LV lateral a’,cm/s 7.4±3.1
LA volume, ml 53±29
LASRa, 1/s 1.2±0.6

LV: left ventricular; EF: ejection fraction; SR: strain rate, s: systole, e: early diastole, a: atrial contraction, CO: cardiac output; IVRT: isovolumic relaxation time; LA: left atrial; E: early diastolic LV filling velocity; A: LV late diastolic filling velocity; e’: LV lateral wall early diastolic velocity; PALS : left atrial strain during ventricular systole, LAS: left atrial strain during atrial contraction, LASRa: left atrial strain rate during atrial contraction.


Relationships between PCWP and LA structure and function

Variables Correlation coefficiant p- value
LA volume, ml 0.42 <0.01
LASRa, 1/s 0.77 <0.001
PALS, % 0.58 <0.001
LAS, % 0.58 <0.001
PVFsff 0.51 <0.001
LV E/A 0.69 <0.001
LV E-DT, ms 0.54 <0.001
E/e’ lateral wall 0.47 <0.01
LV IVRT, ms 0.41 <0.01
E/e’ mean 0.58 <0.001
LV IVRT-ivrt’ -0.44 <0.05
LV lateral a’ -0.38 <0.05
LVSRs, 1/s 0.26 Ns
LVSRe, 1/s 0.16 Ns
LVSRa, 1/s -0.41 <0.01

LA: left atrial; PALS : left atrial strain during ventricular systole, LV: left ventricular, SR=strain rate; S=strain ; PVFssf=pulmonary venous flow systolic filling fraction; E: early diastolic LV filling velocity; A: LV late diastolic filling velocity; e’: LV lateral wall early diastolic velocity, SR: strain rate, s: systole, e: early diastole, a: atrial contraction


Area-under-curve (AUC) statistic of the ROC analysis

Variable AUC Bootstrapped 95% CI Rank (1-10)
LA volume, ml 0.778 0.768 0.787 8
LASRa, 1/s 0.864 0.857 0.870 2
PALS, % 0.789 0.780 0.793 6
LAS, % 0.809 0.802 0.818 5
PVFsff 0.912 0.905 0.919 1
LV E/A 0.830 0.819 0.836 3
LV E-DT, ms 0.764 0.756 0.768 10
E/e’ lateral wall 0.743 0.736 0.755
LV IVRT, ms 0.768 0.760 0.780 9
E/e’ mean 0.746 0.733 0.754
LV IVRT-ivrt’ 0.782 0.770 0.790 7
LV lateral a’ 0.652 0.641 0.660
LVSRs, 1/s 0.695 0.686 0.704
LVSRe, 1/s 0.649 0.642 0.664
LVSRa, 1/s 0.823 0.814 0.830 4

LA strain rate in heart failure and breathlessness clinics for identifying patients with raised LA pressure, irrespective of the etiology of LV dysfunction.

Limitations: The group of patients we studied was heterogeneous with various right and left cardiac pathologies, but they reflect real cohort of patients commonly presenting to cardiology clinics. The apical measurements, we acquired, were obtained with the patient lying flat on the catheter table, which might have affected the accuracy of the LV filling velocities and hence the modest relationship with PCWP. LASRa was only measured from one apical view and should, in optimal approach, be measured also from apical two chamber view. IVRT was measured from Doppler recordings of LV filling which does not literally reflect the accurate definition of the phase, in view of the known time difference between mitral valve opening and onset of LV filling 28. Bi-plane volume measurements of both left atrium and ventricle should have been optimal but was technically difficult to obtain in our cohort.

Figure 2

Scatterplot between LASRa and PCWP.


Figure 3

Accuracy in LASRa identifying elevated PCWP.


Conclusion: Invasively measured PCWP correlates strongly with direct measurements of LA structure and function, with global LA systolic strain rate being the most accurate in identifying abnormally raised pressures. Doppler indices of LV filling pressures also correlate with PCWP but to a much lesser extent. These findings suggest a vital place for routine use of LA strain rate in heart failure and breathlessness clinics for identifying patients with raised LA pressure, irrespective of the etiology of LV dysfunction.


Umeå University Faculty Foundations and Swedish Heart and Lung Foundation



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Copyright (c) 2015 Michael Henein, Erik Tossavainen, Stefan Söderberg, Christer Grönlund, Manuel Gonzalez, Per Lindqvist

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