European Journal of Echocardiography Advance Access originally published online on March 14, 2008
European Journal of Echocardiography 2008 9(4):547-554; doi:10.1093/ejechocard/jen121
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Usefulness of right ventricular isovolumic relaxation time in predicting systolic pulmonary artery pressure
1 Department of Cardiology, University Hospital of Bordeaux-Pessac, Bordeaux-Pessac, France
2 Department of Public Health, University Hospital Pitié-Salpêtrière, Paris, France
Received 8 May 2007; accepted after revision 30 September 2007; online publish-ahead-of-print 14 March 2008.
* Corresponding author: U833-Collège de France 11 place Marcelin Berthelot 75005 Paris, France. Tel: +33 144271581; fax: +33 144271591. E-mail address: nicolasbrechot{at}wanadoo.fr
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Aims: Systolic pulmonary artery pressure (sPAP) cannot always be assessed from Doppler-detected tricuspid regurgitation (TR), especially when sPAP is normal. The right ventricular isovolumic relaxation time (rIVRT) is related to sPAP, and assessment of rIVRT by tissular Doppler imaging (rIVRT') has recently been proposed as an alternative method for estimating sPAP in patients with pulmonary artery hypertension (PAH). We evaluated here its usefulness in everyday clinical practice.
Methods and results: We conducted a prospective Doppler vs. catheterization study in 26 patients. TR was undetectable in 6 patients (32%) with normal sPAP and in one patient (14%) from those with PAH. rIVRT' was recordable in all patients. We found a strong correlation between rIVRT' and sPAP (r = 0.87; P < 0.0001). rIVRT' had a high sensitivity in detecting PAH, and a rIVRT' of 40 ms or less excluded PAH with a negative predictive value of 100%. We also found that a prolonged rIVRT' is not specific to PAH and that the rIVRT'-evaluated sPAP did not agree well with the catheter-evaluated value.
Conclusion: Measurement of rIVRT' can help estimate sPAP in the absence of TR: A normal rIVRT' excludes PAH with a high negative predictive value. A prolonged rIVRT' is in favour of an elevated sPAP but cannot affirm it by itself.
Keywords: Doppler echocardiography; Right ventricular isovolumic relaxation time; Pulmonary artery pressure; Doppler tissular imaging; Cardiac catheterization; Prospective studies
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Non-invasive assessment of systolic pulmonary artery pressure (sPAP) is now a routine investigation in echocardiographic laboratories. The most common approach is to measure the peak velocity of a tricuspid regurgitant jet and apply the modified Bernouilli equation.1–4 However, the assessment of tricuspid regurgitation (TR) is thought to be problematic in
20% of healthy subjects5 and up to 70% of patients suffering from chronic obstructive pulmonary disease (COPD).6–8 Contrast agents can be used to enhance the TR signal, but require venous catheterization. Other less invasive tools are required to estimate sPAP. Forty years ago the right ventricular isovolumic relaxation time (rIVRT) was described as a tool to predict sPAP using phonocardiography.9 Although Hatle et al.10 characterized the parameter by Doppler ultrasonography its use remained technically demanding.3,4,8 Tissular Doppler imaging technique (TDI) rekindled interest in its use: In 2001, Caso et al.11 described rIVRT measured by TDI (rIVRT') as a reliable tool for predicting pulmonary artery hypertension (PAH) in COPD patients. Further simultaneous Doppler-catheterization studies showed that rIVRT' correlates well with sPAP.12,13 Recently, Dambrauskaite et al.14 described rIVRT' as an efficient tool to predict sPAP in patients with PAH. The aim of the present study was to evaluate the feasibility and accuracy of rIVRT' measurement for estimating sPAP in a population of unselected patients with a large range of sPAP levels.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
This prospective study was conducted from November 2004 to May 2005 in the University Hospital of Bordeaux-Pessac, France. Every patient referred for routine right heart catheterization was eligible for the study. Exclusion criteria were: age <18 years, non-sinus rhythm, prosthetic tricuspid valve, haemodynamic instability (infusion of vasoactive drugs, depletion by diuretics at the time of the study), left ventricular hypertrophy (rIVRT' was described to be increased in the absence of PAH during this condition15), history of myocardial infarction (regional wall motion hypokinesis may impair TDI recordings). The cut-off value of 40 mmHg was chosen to define PAH because it seemed to us to be the most clinically relevant: In 2001, Mc Quillian studied a population of 15 000 healthy subjects. A sPAP >30 mmHg was found in 28% of individuals.5
All patients gave their written consent to participate in the study, which was approved by the local ethics committee.
Cardiac catheterization
Right heart catheterization was performed using a Swan-Ganz catheter (Edward Life Sciences sas ref 131f7) inserted through the right femoral vein after local anaesthesia. Pressure measurements were calibrated before the study from the midaxillary line. Right atrial pressure (RAP), right ventricular pressures, pulmonary systolic, diastolic, and occlusive pressures were determined. Triplicate measurements of thermodilution cardiac output were averaged. Cardiac index, arteriolar pulmonary resistance (APR), and total pulmonary resistance (TPR) were calculated.
The physician performing the cardiac catheterization was unaware of the results of Doppler examination and vice versa. Patients were at rest and did not receive sedatives.
Echocardiographic and Doppler studies
The echocardiographic study was performed the day before cardiac catheterization, with a mean interval of 12 h between the two measurements, in stable clinical status, and with unchanged therapy. Doppler echocardiography was performed with a General Electrics Vivid 7 Expert equipped with a M4S transducer. Patients underwent a routine transthoracic echocardiographic examination with standard measurements including sPAP estimation using TR. Non-invasive RAP was estimated from the dimensions of the inferior vena cava and its respiratory motion as described previously.16,17 TDI measurements were conducted from the apical window at the lateral (right) corner of the tricuspid annulus, as described by Caso et al.11 This site has been shown to provide better correlation with sPAP than the apical segment of right ventricular (RV) free wall in Dambrauskaite's study14 with comparable results as those from the basal segment.
Sample size for pulsed TDI was 6 mm. rIVRT' was measured as the time between the end of the systolic S' wave (peak systolic tricuspid annular velocity) and the beginning of the diastolic E' wave (Figure 1). Recordings were made at a sweep speed of 100 mm/s. An average of five cardiac cycles was recorded. As rIVRT is heart rate (HR)-dependent, adjusted rIVRT' was calculated as rIVRT'/
RR.
|
RV systolic function was assessed using S' wave and RV systolic dysfunction was defined by a S' <11.5 cm/s, as previously described.18
All Doppler echocardiographic and TDI recordings were obtained at end expiration.
Reproducibility
Ten echocardiographic and TDI recordings were performed with offline data analysis (Echopac, GE vingmed Ultrasound). These studies were conducted in a blinded manner by a second observer and by the first observer a second time. Measurements variability was expressed as mean ± SD of the difference between the two sets of observations, and the mean percentage error was calculated as the absolute difference between observations divided by the mean observation.
Statistical analysis
Continuous variables are reported as means ± SD. Paired t tests were used to assess differences in HR between cardiac catheterization and echocardiographic examination, and unpaired t tests for the subgroup analysis. Correlations between invasive sPAP, APR, TPR, and the Doppler parameters were established using linear regression and are expressed as correlation coefficients; Bland–Altman analysis19 was used to evaluate the agreement between invasive sPAP and TDI-estimated sPAP. Receiver-operating characteristics (ROC) curves were constructed for the rIVRT' measurements for predicting sPAP of 40 mmHg or higher. Statistical significance was set at P < 0.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Patient characteristics
This study included 26 consecutive patients, 16 males and 10 females. The mean age was 62 ± 14 years (20–83) and mean sPAP was 37 ± 20 mmHg (15–98). Referral diagnoses were valvular heart disease (n=10), idiopathic pulmonary hypertension (n=4), cardiomyopathy (n=4), systemic sclerosis (n=2), heart transplant (n=2), coronary artery disease (n=1), syncope (n=1), congenital heart disease (n=1), COPD (n=1). Seven patients had a sPAP >40 mmHg, 13 patients had a sPAP ranging from 25 to 40 mmHg, and 6 had a sPAP <25 mmHg. Individual as well as subgroup echocardiographic and haemodynamic variables are listed in Tables 1 and 2, respectively. There was no difference between HR during Doppler examination and during haemodynamic measurements. Only 3 patients had a right bundle branch block (RBBB), 2 with a normal sPAP, and one in the PAH group (Table 1).
|
|
Tricuspid regurgitation
An analysable Doppler tricuspid diastolic signal could not be obtained in 7 patients (27%). Six of them were in the group of patients without PAH, which means that TR was not recordable in 32% of patients in this group. All but one patient (86%) of the PAH group had an analysable tricuspid regurgitant jet. None of our patients had a more than trivial TR.
When feasible, the Doppler-estimated sPAP showed a strong correlation with the catheter-measured sPAP (r = 0.94, P < 0.001).
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and systolic pulmonary artery pressure
rIVRT' was available in all patients. The mean rIVRT' was 16 ± 10 ms in patients with sPAP <25 mmHg, 31 ± 23 ms in patients with sPAP between 25 and 40 mmHg, and 83 ± 34 ms in patients with sPAP >40 mmHg. rIVRT' was significantly lower in the group without PAH than in the group with PAH (Table 2). Figure 2 shows the linear regression analysis between rIVRT' and invasive sPAP. There was a strong correlation between rIVRT' and invasive sPAP (r = 0.87; P < 0.0001). Correcting rIVRT' for HR did not improve this correlation (r = 0.83; P < 0.0001). There was also a significant correlation between rIVRT' and APR (r = 0.84; P < 0.0001), and between rIVRT' and TPR (r = 0.74; P < 0.0001).
|
Figure 3 shows the Bland–Altman analysis of the agreement between TDI-estimated and catheter-measured sPAP. The mean differences between measured and estimated pressures were 0.02 ± 9.89 mmHg (range –18.14 to 19.02) in the whole population, –2.22 ± 7.89 mmHg in the no PAH group (range –17.79 to 10.66) and 0.55 ± 14.05 mmHg in the PAH group (range –18.14 to 19.02). In the subgroup of patients with a rIVRT' <40 ms, the mean difference between the two was 1.21 ± 6.64 mmHg (–11.79 to 10.66). The ROC curve for predicting a sPAP of 40 mmHg or higher is shown in Figure 4. The area under the curve was 0.95 (95% confidence interval 0.88–1.03). In this study, a rIVRT' >59 ms predicted a PAH with a sensitivity of 86% and a specificity of 89.5%, and a rIVRT' <40 ms excluded it with a negative predictive value of 100%.
|
|
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and right ventricular function
S' was significantly reduced in PAH patients (Table 2), and the rate of RV dysfunction was higher in this group (5/7 vs. 4/19 in the no PAH group; P = 0.019). rIVRT' did not correlate well with S' values (r = 0.24; P < 0.0001). Correlation between rIVRT' and sPAP was reduced in patients with RV systolic dysfunction (r = 0.79; P = 0.0098) when compared with patients with a preserved RV systolic function (r = 0.90; P < 0.0001).
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and right atrial pressure
RAP was significantly higher in patients with PAH (Table 2), and we found a slight positive correlation between rIVRT' and RAP in our population (r = 0.39; P = 0.049).
Correlation between rIVRT' and sPAP was also improved when patients with elevated RAP were excluded (r = 0.89; P < 0.001; 16 patients). A trend towards a reduced S' wave in patients with elevated RAP was observed (11.6 ± 2.1 vs. 12.5 ± 1.1 cm/s in patients with normal RAP), but this did not reach statistical significance (P = 0.25). In contrast PAOP was significantly increased in patients with elevated RAP (16.8 ± 9.4 mmHg in this group vs. 10.3 ± 3.3 in patients with normal RAP; P = 0.01).
When patients with RV systolic dysfunction and elevated RAP were excluded, correlation between rIVRT' and sPAP reached r = 0.94 (P < 0.0001) in the 12 patients left.
Reproducibility
Measurements on recorded loops provided an intra-observer variability of 1.4 ± 7.8 mmHg (15 ± 15%, P = 0.53) and an inter-observer variability of 2.0 ± 8.9 mmHg (14.5 ± 21.4%, P = 0.51).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
In this Doppler-catheterization study, we found a strong correlation between right ventricular isovolumic relaxation time measured by TDI (rIVRT') and sPAP. This result is consistent with numerous studies conducted from 1967 to 2006.3,4,7–14). Such a correlation raises the question of evaluating sPAP using rIVRT'.
Usefulness of right ventricular isovolumic relaxation time measured by Tissular Doppler imaging in predicting systolic pulmonary artery pressure
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging is a reliable tool for excluding PAH in normal subjects
In particular we found that a rIVRT' <40 ms predicted a normal sPAP with a negative predictive value of 100%. This is in agreement with other studies, in which none of the patients with a rIVRT <40 ms had PAH, as long as HR remained <115 bpm.3,4,11,13,14 This is of particular interest because the proportion of patients with non-recordable TR increases with decreasing pulmonary artery pressure (rising from 5% in patients with PAH to 20% in healthy subjects in the most recent studies5,6), which makes it difficult to affirm the normality of sPAP in healthy subjects. In contrast, rIVRT' assessed by TDI was obtained in at least 96% of the patients in previous studies.13 In our study, TR was recorded in 70% of patients with normal sPAP and in 86% of patients with PAH, whereas rIVRT' was recorded in all patients. rIVRT' affirmed a normal sPAP in five out of the seven patients without recordable TR.
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging measurement is less efficient as a continuous marker of systolic pulmonary artery pressure
(i) A prolonged rIVRT' is not specific to PAH: It has been reported to be prolonged in patients with hypertrophic cardiomyopathy,15 right ventricular dysfunction,20,21 or right bundle branch block.22 On the contrary it was shown to be pseudo-normalized in patients with elevated RAP or tricuspid insufficiency.23 This may limit its use in patients with PAH, who are more likely to exhibit these conditions.4,6–8,11,18,20,24–27 (ii) Despite a strong correlation between rIVRT'-predicted sPAP and invasive sPAP, two standard deviations in our Bland–Altman analysis represent discrepancies between the two methods of up to 20 mmHg. (iii) Inter- and intra-observer variability was quite high, >10%.
In respect to these limitations, a prolonged rIVRT' may indicate an elevated sPAP in combination with other parameters, such as pulmonary flow acceleration time3,4,7,8,28 or pulmonary regurgitant flow velocity.4,29 We found in our population that a rIVRT' >59 ms predicted a sPAP of 40 mmHg or higher with a sensitivity of 86% and a specificity of 89.5%. Furthermore, correlation between rIVRT' and sPAP was improved when patients with RV dysfunction and elevated RAP were excluded. This finding should be investigated on a large effective.
Right ventricular isovolumic relaxation time pathophysiology
rIVRT duration is determined by: (i) The difference between sPAP and RAP: The interval required for RV pressure to decrease from the pulmonary valve closure pressure to the tricuspid valve opening level increases with increasing sPAP.9,10 (ii) Right ventricular diastolic function: RV dysfunction decreases the rate of fall of right ventricular pressures during relaxation, thus increasing rIVRT.15,20,21 This mechanism was in particular well described during hypertrophic cardiomyopathy.15 (iii) HR, inversely related to rIVRT.9,10 Other mechanisms have been proposed: Shaver et al. described a ‘hanged-out’ interval of 30 to 80 ms between the end of right ventricular systole and the pulmonary valve closure. The interval decreased with increasing dPAP, thus lengthening rIVRT.30,31 In an animal study, Myhre et al.32 described pulmonary artery impedance as being the principal determinant of rIVRT, as neither RAP nor HR were correlated with rIVRT.
Considering the pathophysiology of rIVRT, it appears clearly that HR, RV dysfunction and RAP may perturb the evaluation of sPAP with rIVRT'.
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and heart rate
Correlation between rIVRT' and sPAP was not improved by correcting rIVRT' for HR, as described by others.9–11,13,14 This is probably because HRs were in the same range in our population, and corrected rIVRT' may be useful in case of extreme HR.
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and right ventricular function
In this work we used S' wave to assess RV function. The rate of RV dysfunction was significantly higher in patients with PAH, as described previously.11,18,20,24–27 Interestingly, correlation between rIVRT' and sPAP was poorer in patients exhibiting RV dysfunction. This result is consistent with data published by Dambrauskaite et al.14 in PAH patients, showing that correlation between rIVRT' and sPAP was reduced in patients having a tricuspid annular plane systolic excursion <18 mm. rIVRT was also described to be prolonged during RV dysfunction in the absence of PAH.15 In our population, RV dysfunction may have been responsible for false positive results for rIVRT' measurement, in particular in Patients n°18 and 21 (Table 1). Taken together, theses results further indicate that RV dysfunction may perturb the evaluation of sPAP using rIVRT'.
Right ventricular isovolumic relaxation time measured by Tissular Doppler imaging and right atrial pressure
According to the above physiologic principles, an increase in RAP should shorten rIVRT. Abbas et al.33 in a Doppler-catheterization study in 21 patients noted an inverse relation between RAP and rIVRT', as expected. Yoshifuku et al.23 also described rIVRT' to be pseudo-normalized in patients with elevated RAP during acute right ventricular myocardial infarction. In our study, RAP was higher in patients with PAH and we found a slight positive correlation between RAP and rIVRT'. This is probably because the increase in RAP was a consequence of elevated left ventricular filling pressures and hypervolemia in our population, as opposed to Abbas' and Yoshifuku' patients where the principle mechanism was RV failure. Indeed we found only a trend towards a reduction of S' wave in patients with elevated RAP in our study, whereas they exhibited a PAOP significantly higher.
Correlation between rIVRT' and sPAP was further improved when patients with elevated RAP were excluded. We therefore believe that elevated RAP may also influence the evaluation of sPAP with rIVRT'.
Study limitations
In our study, rIVRT'-measured sPAP was compared with a reference method in a population of unselected patients exhibiting a large range of sPAP. We focused on the clinical usefulness of this parameter. To our knowledge it is the first time that rIVRT' was studied in patients with both normal and elevated sPAPs. This allowed to validate it as a good tool for identifying patients not having PAH, to highlight its limits as a continuous marker of sPAP and to detect the presence of false positive patients for this parameter. However, our study suffers from limitations: although our results were consistent with previous studies and reached statistical significance, our population was small, and in particular contained only 7 patients with PAH. Therefore conclusions on PAH patients are of limited value, as well as ROC curve, and the cut-off limit for normal and abnormal values of rIVRT' should be further confirmed in a larger effective.
Only one patient suffering from COPD was included in this study. TR assessment is particularly difficult in such patients,6,7,11 and rIVRT' may be of particular interest for assessing sPAP in these patients. Our cohort also contained only 3 patients with RBBB, so that we could not analyse the influence of RBBB on the evaluation of sPAP with rIVRT'. The Doppler examination and invasive measurements were performed within 12 h of each other, but patients were haemodynamically stable and the correlation between the two techniques remained close. As we focused on haemodynamically stable patients, it is unclear wether our conclusions would remain true in case of acute PAH, such as pulmonary embolism.
|
Conclusions |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
rIVRT' appears to be helpful in evaluating sPAP: a normal rIVRT' (<40 ms) can exclude PAH with a high negative predictive value. A prolonged rIVRT' is indicative of PAH but cannot affirm it by itself.
|
Acknowledgements |
|---|
We would like to thank Professor Alain Combes for his advice. We also would like to thank Drs Ania Nieszkowska, Raphaëlle Dumaine, Patricia Réant and Valerie Le Bouffos for their help in the study.
Conflict of interest: none declared.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
- Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation (1984) 70:657–62.
[Abstract/Free Full Text] - Currie PJ, Seward JB, Chan KL, Fyfe DA, Hagler DJ, Mair DD, et al. Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol (1985) 6:750–6.[Abstract]
- Chan KL, Currie PJ, Seward JB, Hagler DJ, Mair DD, Tajik AJ. Comparison of three Doppler ultrasound methods in the prediction of pulmonary artery pressure. J Am Coll Cardiol (1987) 9:549–54.[Abstract]
- Stevenson JG. Comparison of several noninvasive methods for estimation of pulmonary artery pressure. J Am Soc Echocardiogr (1989) 2:157–71.[Medline]
- McQuillan BM, Picard MH, Leavitt M, Weyman AE. Clinical correlates and reference intervals for pulmonary artery systolic pressure among echocardiographically normal subjects. Circulation (2001) 104:2797–802.
[Abstract/Free Full Text] - Laaban JP, Diebold B, Zelinski R, Lafay M, Raffoul H, Rochemaure J. Noninvasive estimation of systolic pulmonary artery pressure using Doppler echocardiography in patients with chronic obstructive pulmonary disease. Chest (1989) 96:1258–62.[CrossRef][Web of Science][Medline]
- Tramarin R, Torbicki A, Marchandise B, Laaban JP, Morpurgo M. Doppler echocardiographic evaluation of pulmonary artery pressure in chronic obstructive pulmonary disease. A European multicentre study. Working Group on Noninvasive Evaluation of Pulmonary Artery Pressure. European Office of the World Health Organization, Copenhagen. Eur Heart J (1991) 12:103–11.
[Abstract/Free Full Text] - Torbicki A, Skwarski K, Hawrylkiewicz I, Pasierski T, Miskiewicz Z, Zielinski J. Attempts at measuring pulmonary arterial pressure by means of Doppler echocardiography in patients with chronic lung disease. Eur Respir J (1989) 2:856–60.[Abstract]
- Burstin L. Determination of pressure in the pulmonary artery by external graphic recordings. Br Heart J (1967) 29:396–404.
[Free Full Text] - Hatle L, Angelsen BA, Tromsdal A. Non-invasive estimation of pulmonary artery systolic pressure with Doppler ultrasound. Br Heart J (1981) 45:157–65.
[Abstract/Free Full Text] - Caso P, Galderisi M, Cicala S, Cioppa C, D'Andrea A, Lagioia G, et al. Association between myocardial right ventricular relaxation time and pulmonary arterial pressure in chronic obstructive lung disease: analysis by pulsed Doppler tissue imaging. J Am Soc Echocardiogr (2001) 14:970–7.[CrossRef][Web of Science][Medline]
- Bolca O, Hobikoglu G, Norgaz T, Asilturk R, Unal S, Gurkan U, et al. The prediction of pulmonary artery systolic pressure and vascular resistance by using tricuspid annular tissue Doppler imaging. Anadolu Kardiyol Derg (2002) 2:302–6.[Medline]
- Lindqvist P, Waldenstrom A, Wikstrom G, Kazzam E. Right ventricular myocardial isovolumic relaxation time and pulmonary pressure. Clin Physiol Funct Imaging (2006) 26:1–8.[CrossRef][Web of Science][Medline]
- Dambrauskaite V, Delcroix M, Claus P, Herbots L, Palecek T, D'Hooge J, et al. The evaluation of pulmonary hypertension using right ventricular myocardial isovolumic relaxation time. J Am Soc Echocardiogr (2005) 18:1113–20.[CrossRef][Web of Science][Medline]
- Efthimiadis GK, Parharidis GE, Karvounis HI, Gemitzis KD, Styliadis IH, Louridas GE. Doppler echocardiographic evaluation of right ventricular diastolic function in hypertrophic cardiomyopathy. Eur J Echocardiogr (2002) 3:143–8.
[Abstract/Free Full Text] - Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol (1990) 66:493–6.[CrossRef][Web of Science][Medline]
- Nagueh SF, Kopelen HA, Zoghbi WA. Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation (1996) 93:1160–9.
[Abstract/Free Full Text] - Meluzin J, Spinarova L, Bakala J, Toman J, Krejci J, Hude P, et al. Pulsed Doppler tissue imaging of the velocity of tricuspid annular systolic motion; a new, rapid, and non-invasive method of evaluating right ventricular systolic function. Eur Heart J (2001) 22:340–8.
[Abstract/Free Full Text] - Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet (1986) 1:307–10.[CrossRef][Web of Science][Medline]
- Tei C, Dujardin KS, Hodge DO, Bailey KR, McGoon MD, Tajik AJ, et al. Doppler echocardiographic index for assessment of global right ventricular function. J Am Soc Echocardiogr (1996) 9:838–47.[CrossRef][Medline]
- D'Andrea A, Caso P, Sarubbi B, D'Alto M, Giovanna Russo M, Scherillo M, et al. Right ventricular myocardial activation delay in adult patients with right bundle branch block late after repair of Tetralogy of Fallot. Eur J Echocardiogr (2004) 5:123–31.
[Abstract/Free Full Text] - Henein MY, Gibson DG. Long axis function in disease. Heart (1999) 81:229–31.
[Free Full Text] - Yoshifuku S, Otsuji Y, Takasaki K, et al. Pseudonormalized Doppler total ejection isovolume (Tei) index in patients with right ventricular acute myocardial infarction. Am J Cardiol (2003) 91:527–31.[CrossRef][Web of Science][Medline]
- Florea VG, Florea ND, Sharma R, Coats AJ, Gibson DG, Hodson ME, et al. Right ventricular dysfunction in adult severe cystic fibrosis. Chest (2000) 118:1063–8.[CrossRef][Web of Science][Medline]
- Ueti OM, Camargo EE, Ueti Ade A, de Lima-Filho EC, Nogueira EA. Assessment of right ventricular function with Doppler echocardiographic indices derived from tricuspid annular motion: comparison with radionuclide angiography. Heart (2002) 88:244–8.
[Abstract/Free Full Text] - Burgess MI, Bright-Thomas RJ, Ray SG. Echocardiographic evaluation of right ventricular function. Eur J Echocardiogr (2002) 3:252–62.
[Free Full Text] - Burgess MI, Mogulkoc N, Bright-Thomas RJ, Bishop P, Egan JJ, Ray SG. Comparison of echocardiographic markers of right ventricular function in determining prognosis in chronic pulmonary disease. J Am Soc Echocardiogr (2002) 15:633–9.[CrossRef][Web of Science][Medline]
- Kitabatake A, Inoue M, Asao M, Masuyama T, Tanouchi J, Morita T, et al. Noninvasive evaluation of pulmonary hypertension by a pulsed Doppler technique. Circulation (1983) 68:302–9.
[Abstract/Free Full Text] - Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol (2003) 92:1373–6.[CrossRef][Web of Science][Medline]
- Shaver JA, Nadolny RA, O'Toole JD, Thompson ME, Reddy PS, Leon DF, et al. Sound pressure correlates of the second heart sound. An intracardiac sound study. Circulation (1974) 49:316–25.
[Abstract/Free Full Text] - Triffon D, Groves BM, Reeves JT, Ditchey RV. Determinants of the relation between systolic pressure and duration of isovolumic relaxation in the right ventricle. J Am Coll Cardiol (1988) 11:322–9.[Abstract]
- Myhre ES, Slinker BK, LeWinter MM. Absence of right ventricular isovolumic relaxation in open-chest anesthetized dogs. Am J Physiol (1992) 263:H1587–90.[Web of Science][Medline]
- Abbas A, Lester S, Moreno FC, Srivathsan K, Fortuin D, Appleton C. Noninvasive assessment of right atrial pressure using Doppler tissue imaging. J Am Soc Echocardiogr (2004) 17:1155–60.[CrossRef][Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||