Skip Navigation

Cardiovascular Research 1997 36(3):377-385; doi:10.1016/S0008-6363(97)00195-8
© 1997 by European Society of Cardiology
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sloth, E.
Right arrow Articles by Hasenkam, J.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sloth, E.
Right arrow Articles by Hasenkam, J.M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1997, European Society of Cardiology

The impact of ischemic heart disease on main pulmonary artery blood flow patterns: a comparison between magnetic resonance phase velocity mapping and transesophageal color Doppler

Erik Slotha,c,*, Mary Kruseb,c, Kim C Houlindb,c, Erik M Pedersenb,c and J.Michael Hasenkamb,c

aDepartment of Anaesthesia, Aarhus Kommune Hospital and Skejby Sygehus, Aarhus University Hospital, 8200 Aarhus N, Denmark
bDepartment of Cardiothoracic and Vascular Surgery, Skejby Sygehus, Aarhus University Hospital, Aarhus, Denmark
cInstitute of Experimental Clinical Research and MR-Center, Skejby Sygehus, Aarhus University Hospital, Aarhus, Denmark

* Corresponding author. Tel. +45 89495615 (priv. +45 86173918); Fax: +45 89496014.

Received 14 April 1997; accepted 17 June 1997


    Abstract
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
Objective: To give a detailed evaluation on main pulmonary artery blood velocity patterns, in patients with ischemic heart disease and to provide recommendations for pulsed Doppler sample volume placement, in order to optimize cardiac output estimation. Methods: Using magnetic resonance phase and esophageal color Doppler velocity mapping in 12 patients with ischemic heart disease and undergoing coronary artery by-pass grafting, very similar data on pulmonary artery blood velocity patterns were provided for comparison with each other. Results: Peak blood velocities were located in the inferior half of the main pulmonary artery cross-sectional area. Early after peak systole the highest velocities shifted towards the superior/left (major curvature) with a simultaneous decrease in velocities inferiorly. The velocity decrease further evolved into retrograde flow to the inferior/right (minor curvature). This feature was significantly enhanced compared to earlier findings in healthy volunteers. The mean temporal blood velocity profiles were asymmetrically skewed, thereby giving unreliable cardiac output estimates based on single point Doppler blood velocity recordings. The error incurred may amount to more than 100% in extreme cases. According to our data, optimal assessment of cardiac output should be based on multiple sample volumes placed along the inferior/right to superior/left diameter. Conclusions: MR-phase velocity mapping and multiplane transesophageal color Doppler recordings provided similar blood velocity patterns in patients with ischemic heart disease. The skewness of the mean temporal blood velocity profile is enhanced compared with healthy subjects, resulting in error in the assessment of CO by means of pulsed Doppler echocardiography. By using multiple Doppler sample volumes, the error can be minimized.

KEYWORDS Pulmonary artery; Magnetic resonance velocity mapping; Blood velocity profile; Human; Color Doppler; Ischemic heart disease; Cardiac output


    1 Introduction
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
Cardiac output (CO) assessment today is still invasive and based on thermodilution [1, 2]or modifications of this technique [3]. Pulsed Doppler echocardiography has emerged with increasing attention and several application techniques have been described: transthoracic (TTE) [4, 5], transesophageal (TEE) [6–8]and intraluminal (ILM) [9–11]. Regardless of which acoustic window is used, information about the velocity profile is necessary if the vessel cross-sectional area exceeds the area of the Doppler sample volume (SV). Otherwise, errors in velocity estimation due to a non-flat mean temporal blood velocity profile may occur [12, 13]. This is particularly true when measuring CO in the human main pulmonary artery (PA) under pathological cardio-vascular conditions. Therefore, information about how main PA blood velocity profiles change in specific cardiac disorders can contribute to our understanding and handling of CO measurements.

Although detailed evaluations of blood velocity fields in the human main PA in healthy adults have recently been performed [13, 14], only a limited amount of information is available in relation to pathological conditions. Bogren et al. described the blood velocity patterns in patients with pulmonary artery hypertension as markedly irregular with a greater amount of retrograde flow as compared to healthy adults [15]. Increased retrograde flow was later confirmed by Kondo et al., who also found significantly lower peak velocities in patients with pulmonary hypertension [16]. Recently Mohiaddin et al. proved blood swirling in the main PA in patients with hypertension [17]. All these studies were based on magnetic resonance (MR) phase encoding techniques [13–17].

Patients with coronary artery disease constitute a greater part of those undergoing cardiac surgery and intensive care treatment. In this group of patients, CO monitoring is frequently used. MR imaging (MRI) can provide detailed velocity information from the human main PA [13–16]and it can also be used to evaluate the impact of placing a fictive SV during systole or diastole, simulating pulsed Doppler ultrasound where the SV is fixed relative to the moving PA. Based on this, we proposed that MR phase velocity maps could provide new information on main PA velocity fields in patients with ischemic heart disease (IHD) including Doppler specific data for CO measurement.

Therefore, the purpose of this study was to evaluate the main pulmonary artery blood velocity patterns and to provide recommendations for pulsed Doppler velocity measurements in patients with IHD. Furthermore, we wanted to compare the results with previously published data in healthy adults obtained with the same MRI technique [13, 14].


    2 Methods
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
2.1 Population
Twelve patients (3 female and 9 male) with an age range from 47 to 73 years (mean 58 years; s.d. 9.1 years) scheduled for coronary artery by-pass grafting (CABG) comprised the study group. MR phase velocity mapping was conducted at the level of the main PA 1 or 2 days before surgery. In 8 of the patients, main PA multiplane transesophageal color Doppler velocity mapping was performed preoperatively in the operating theater. The investigation was approved by the institutional committee on human research according to the Helsinki II declaration, and individual informed consent was obtained.

2.2 MR-phase velocity measurement and data analysis
Measurements were performed on a 1.5 Tesla 15S Gyroscan HP Philips system using a spin echo sequence for 2D imaging and a FLow Adjusted Gradients (FLAG) sequence for flow measurement [18]. The unsedated patients were placed in the supine position. In order to minimize respiratory induced PA movements and flow variations, all flow measurements were obtained during expiration using respiratory gating. In all measurements cardiac triggering started data acquisition for the flow measurements 8 ms after the R-wave in the ECG. The heart phase intervals depended on the heart rate and varied between 25 ms and 31 ms. From transversal and sagittal spin echo images, a double oblique plane of the mid-main PA was identified [13]for velocity measurements which were performed as two averages of 256 phase encoding steps. The velocity encoding was designed to measure the axial velocity components. The slice thickness was 8 mm and the pixel size was 1.87 mm2. The phase velocity measuring time ranged from 20 to 45 min (mean 34 min; s.d. 7 min). Arterial blood pressure and heart rate were measured at 5-min intervals to verify hemodynamic stability (Table 1).


View this table:
[in this window]
[in a new window]

 
Table 1 Clinical and hemodynamic parameters

 
The reconstructed and subtracted data were corrected for background phase error using a dedicated semiautomated software program [19]. Manual tracing of the main PA was done in order to distinguish PA flow from the surrounding cardiac structures. The MR velocity data were displayed as surface plots in order to provide two- and three-dimensional visualizations of the velocity fields at different times during the cardiac cycle. A dynamic interpretation of profile development was made possible by animation of consecutive velocity plots. Animation and graphical display was performed on a Macintosh computer using a commercially available software program (Spyglass, Champaign, IL, USA).

The nomenclature used in this paper refers to the anatomical orientation of the main PA as viewed in a plane perpendicular to the main axis of the main PA. All plots are seen from the downstream position.

2.2.1 Hemodynamic parameters
Using a standard spreadsheet program (Lotus 1-2-3, Middlesex, UK), the velocities from each voxel in each phase were integrated to compute the volume flow. The following hemodynamic parameters were calculated: mean Reynolds number (REmean), peak Reynolds number (REpeak) and Womersley's {alpha}-parameter (ALPHA) (see footnote of Table 2 for definitions).


View this table:
[in this window]
[in a new window]

 
Table 2 Hemodynamic parameters calculated from MR blood velocity data

 
In order to quantify the shape of the velocity profiles, a spatial distribution index (Vmax(peak)/Vmean(peak)) for the peak systolic velocity in the main PA was calculated as the maximum peak systolic value in the velocity matrix divided by the spatial mean velocity during peak systole.

2.2.2 Retrograde flow
To quantify the percentage of systolic retrograde flow in the main PA, the index (retrogsys/antsys) was calculated as the proportion of retrograde volume flow rate to antegrade volume flow rate in systole (systole defined as the first frame with net antegrade flow to the last frame before net retrograde flow occurred or to the frame before an increase in net antegrade flow if no net retrograde flow was seen). For the same time interval, an index (retrogmax/antmax) was calculated as the maximum retrograde volume flow as a percentage of the maximum antegrade volume flow.

2.2.3 Mean temporal blood velocity profile and point velocities
The ‘true’ mean temporal blood velocity profile in the main PA was computed by correcting for movements in the main PA cross-sectional plane. This was achieved by visually superimposing the center (square of 4 center pixels) of each traced area during averaging (for details see Fig. 1). When looking at single point mean temporal blood velocity estimates, this correction was not performed in order to obtain values analogous to pulsed Doppler measurements where the sample volume is fixed in space relative to the moving PA [14], see Fig. 1. Based on this latter method, a number of velocity indices were calculated for the assessment of the potential error in single point blood velocity derived CO calculations [14]. Thirteen different points (fictive Doppler sample volumes, 1–13) across the vessel area were chosen. Identification of the 13 points were conducted visually by superimposing a predefined template onto the computer screen during analysis [14]. Because the PA moves while the template is fixed, the position of these points within the vessel cross-sectional area vary with its timing during the heart cycle. In order to evaluate this, we superimposed the template onto a top systolic blood velocity map (frame 6 in Fig. 1A) and a diastolic blood velocity map (frame N in Fig. 1A) defining the center (point 1) from these two maps. Because the center of the template is different for each map, different pixel values will be extracted from the mean temporal velocity data (Fig. 1C2).


Figure 1
View larger version (20K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 1 Schematic illustration of the method used for processing of the MR mean temporal blood velocity data. A, velocity data for different time frames (1–N). Notice the movement of the main pulmonary artery during the heart cycle relative to the fixed data storing matrix. B1, averaging by visually superimposing the center of each traced area onto the data storing matrix revealing the ‘true’ mean temporal blood velocity profile, which takes into account the pulmonary artery movement, C1. B2 and C2, averaging without pulmonary artery movement reduction (fixed data storing matrix) simulating single-point Doppler velocity recordings where the transducer also represents a fixed reference in space. Center of the pulmonary artery is indicated by a dot.

 
A blood velocity index was calculated as the ratio of the time velocity integral (TVI) (extracted from Fig. 1C2) in each of the 13 measuring points to the mean time velocity integral (temporal and spatial mean velocity) (TVImean) (averaging all velocities in Fig. 1C2). An index value of 1 thus indicates that the true temporal and spatial mean blood velocity can be estimated from TVI in that measuring point. Velocity indices defined at top systole were calculated as:


Formula 1

(1)
Similarly for points defined at end diastole:


Formula 2

(2)

2.3 Transesophageal color Doppler mapping and data analysis
A 5-MHz multiplane transesophageal echocardiographic (MTEE) probe operated with a Vingmed CFM 800C echo Doppler machine was used for acquisition of reference color Doppler velocity data. After induction of anesthesia and endotracheal intubation, the MTEE probe was inserted. ECG and invasive arterial blood pressure was continuously monitored and a pulmonary artery catheter was available for measurement of pulmonary arterial pressure. Color Doppler measurements commenced pre-operatively and was conducted with the patient in the supine position. The color frame rate varied between 9 and 15 frames/s. Color Doppler signals from the main PA were continuously recorded on Super-VHS videotape. In addition, color cine-loops from selected scanning planes (30°, 45° or 60° from the standard transverse plane) going through the major area of negative velocities interpreted on two-dimensional color maps were stored digitally. Using EchoDisp (Vingmed, Horten, Norway), diameter velocity profiles from each frame of these color maps were displayed for a description of the temporal blood velocity field development. The diameter velocity profile from the first systolic frame where negative velocities occurred were then compared to the corresponding MR phase velocity map (selected from ECG and MRI flow curves).

2.4 Statistical methods
Non-paired t-tests were used for comparison of parameters (mean and peak Reynolds number, systolic velocity distribution, Womersley's {alpha}-parameter and the percentage of retrograde flow) from IHD patients and those previously published [13, 14], see Table 2. A P-value <0.05 was considered statistically significant.


    3 Results
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
3.1 MR data
Gross hemodynamic parameter values are shown in Table 2 as mean±standard deviations. Only the amount of retrograde flow differed statistically significantly (P<0.05) from values obtained in healthy subjects, see later.

3.1.1 Temporal development of cross-sectional velocity distribution
In the early systolic acceleration phase the velocity profiles appeared generally flat. Later during acceleration, the highest velocities developed predominantly towards the inferior wall (7 of 12 patients). In 4 patients it developed towards the inferior/right (minor curvature) and in one inferior/left. A clearly clockwise 20° to 45° rotation of the highest velocities until peak systole was seen in 4 patients. In the remaining patients no rotational pattern was obvious. In 5 patients there was a linear shift in velocities towards the superior left, and in the remaining 3 the highest systolic velocities stayed within the same cross-sectional area of the main PA. In all patients the highest peak systolic velocities were located in the inferior half of the main PA cross-sectional area (Fig. 2). In early deceleration the highest velocities shifted towards the superior/left (major curvature) part of the vessel with a simultaneous decrease in velocities inferiorly. In all patients these features continued throughout the late deceleration phase and early diastole, where a reverse flow area developed to the inferior/right. The late diastolic phase was predominantly characterized by antegrade flow without any consistent pattern.


Figure 2
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 2 Location in the cross-sectional area where the highest blood velocities in the cardiac cycle were found for each patient. S, superior; I, inferior; R, right; L, left.

 
Main PA systolic flow reversal was seen in all patients and varied between 0.38% and 4.14% of the total flow (mean 1.69%; s.d. 1.12%) (Table 2).

3.1.2 Mean temporal blood velocity profile and velocity indices
All patients had a consistently skewed mean temporal blood velocity profile with a well-defined low velocity region towards the inferior/right (Fig. 3). This general feature was reflected in the distribution of the quantitative velocity indices (Fig. 4). The average blood velocity index distribution (average of all 12 patients) for points defined in systole and diastole showed the same characteristics. Very low indices were found at the inferior/right wall compared with the rest of the cross-sectional area. The average blood velocity indices for the inferior/right to superior left diameter (mean of point 1, 2, 6, 10, 11, 12 and 13) yielded a blood velocity index of 1.03 (range: 0.78 to 1.45; s.d.: 0.2) and 1.02 (range: 0.84 to 1.45; s.d.: 0.17) for defining the points in systole and diastole, respectively.


Figure 3
View larger version (34K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 3 Example of a typical mean temporal blood velocity plot of the main pulmonary artery showing the low velocity area towards the inferior/right. The area of highest velocities are found in a crescent like area towards the superior/left. Red, high velocities; blue, low velocities. Left, surface plot; right, two-dimensional plot. S, superior; I, inferior; R, right; L, left.

 

Figure 4
View larger version (34K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 4 (Top) The distribution of the average blood velocity indices (square of four pixels) for all 12 patients. The points representing the fictive sample volumes are shown in the small circle for easy reference. Black typing indicates index values >1 in both systole and diastole. (Bottom) Corresponding graphs showing average blood velocity indices±standard deviations along the inferior/right to superior/left diameter (points 13->11). Notice the relatively large standard deviations. S, superior; I, inferior; R, right; L, left.

 
The mean values of the systolic and diastolic average velocity indices differed insignificantly with a P-value of 0.32.

3.2 Color Doppler velocity data
In all patients the early systolic inferior/right to superior/left diameter velocity profile was skewed with the highest velocities located towards the inferior/right wall. Later in systole, the velocity profile became more flat with a decrease in velocities inferior/right compared to superior/left. In late systole, negative velocities evolved at the inferior/right with augmentation of the negative velocities in early diastole (Fig. 5). Color Doppler- and MR-derived diameter profiles (inferior/right to superior/left) obtained in late systole were qualitatively very similar, as exemplified in Fig. 6.


Figure 5
View larger version (38K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 5 (Top) Color Doppler for one representative patient showing the temporal blood velocity development of the main pulmonary artery with scanning plane rotated 45° relative to the standard transverse plane. Red represents antegrade flow (towards the transducer placed in the top of each image), blue represents retrograde flow. Frames 4 to 7 of a total of 13 are presented. (Bottom-left) Color Doppler diameter mean velocity for each of the 13 frames. (Bottom-right) Frames 4 to 7 displayed as diameter blood velocity profiles. The measured diameter (white line between +-marks in each image) is going through the inferior/right (minor curvature) to superior/left (major curvature) part of the main pulmonary artery. AA, ascending aorta; RPA, right pulmonary artery; MPA, main pulmonary artery; I/R, inferior/right vessel wall; S/L, superior/left vessel wall.

 

Figure 6
View larger version (14K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 6 Typical diameter blood velocity profiles from one patient obtained in late systole by the two measurement techniques. Measured diameter is indicated in Fig. 5.

 

    4 Discussion
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
Different and inconsistent skewing of velocity profiles and rotation of the highest velocities have previously been described in the human main PA under normal and diseased conditions [13, 15, 20]. In this study, rotation of the highest velocities until peak flow was seen in only 4 patients. However, an obvious shift in the highest velocities from the inferior to the superior/left part of the vessel area in early deceleration phase was seen in all patients. Such velocity shifts have also been described in dogs [21]and healthy volunteers [13, 20]. In this study the velocity shifts were confirmed in all eight patients who had MTEE performed preoperatively, even though the measurements were carried out under quite different hemodynamic conditions. During MRI the patients were awake, while the MTEE took place 1 or 2 days later and during general anaesthesia with a potentially impact on the hemodynamic conditions. In spite of this, the presence of migrating highest velocities from the minor to the major PA curvature during the cardiac cycle was a consistent feature. We consider the observed rotation of the highest velocities as a reflection of this migration phenomenon finally determined by inter-individual anatomical and geometrical differences [22]. Because the anatomy and geometry vary among individuals, no unequivocal rotational pattern can be expected, in accordance with earlier findings of the blood velocity fields in the human PA [13, 15, 20]. The location of the highest velocities during peak systole predominantly at the inferior/left part of the vessel cross-sectional area is somewhat different from healthy individuals, in whom they were situated directly inferiorly [13]. Such migration of the highest blood velocities towards the outer curvature is expected under circumstances of a more parabolic inlet blood velocity profile rather than a flat one. Whether this caused this finding remains unclear. The highest velocities were found to be less consistent than those in healthy subjects [13], reflecting more irregular blood flow patterns as previously reported in patients with pulmonary hypertension [15–17].

The amount of retrograde flow was significantly increased (P = 0.04 for retrogsys/antsys and P = 0.03 for retrogmax/antmax) compared to what has been found in healthy volunteers using the same measurement and analysis technique [13]. The increased retrograde flow corresponds with the findings in three earlier studies in patients with pulmonary hypertension [15–17]. The mean main PA pressure of 18.4 mmHg in our patients (Table 1) does not fulfil the criteria for definite pulmonary hypertension [23]. On the other hand, it is indisputably increased compared to the value for healthy adults [23], and increased pulmonary artery pressure remains the most plausible explanation for the increased flow reversal. Whether right ventricular contraction pattern, anatomical or geometrical changes due to aging or as a consequence of pathological conditions play a role cannot be acknowledged from our data but must be addressed in future studies.

Except from the amount of retrograde flow, IHD does not seem to affect the hemodynamic parameters listed in Table 2. They correspond well (P-value >0.1) with those obtained in healthy subjects [13]. The peak systolic index calculated as the ratio of the maximum to mean velocity indicated a non-flat cross-sectional velocity distribution, since the values were different from unity.

4.1 Mean temporal blood velocity profile and velocity indices
Detailed knowledge about the mean temporal blood velocity profile is of paramount importance for the estimation of CO from measurements in the main PA using pulsed Doppler ultrasound techniques. We have shown that the common assumption of a flat mean temporal blood velocity profile [4, 6–8]is a serious oversimplification. The skewness of the mean temporal blood velocity profile seen in all patients is predominantly a consequence of the flow reversal at the inferior/right part of the main PA. The migration of the peak velocities may also contribute. The more pronounced skewness compared to healthy subjects [13, 14]is in agreement with our findings of a slightly (but not significant) elevated REpeak and lower REmean compared to our previously published data [13]. The mean Womersley's {alpha}-parameter in the two studies were almost identical, 18.5 [13]and 19.2, respectively. Differences in {alpha}-parameter (that are otherwise known to influence the development of the velocity profiles) cannot be claimed to be responsible for the differences seen between the two groups.

The skewness of the mean temporal blood velocity profile may lead to substantial errors in estimated mean velocity and consequently CO, Fig. 4. The index values vary considerably between the patients illustrated by high standard deviations (range 21–39 in systole and 22–47 in diastole) (Fig. 4). Thus CO estimates using a single sample volume are expected to be even more erroneous in individual cases. For example, in patient number 10 the central (point 1) velocity index value was 2.21, indicating an overestimation in velocity estimate of 121%. In this patient diastolic flow reversal was considerable. MR right ventricular outflow tract velocity mapping, which was performed when patient compliance allowed it (in 5 of the 12 patients without respiratory gating), confirmed pronounced diastolic retrograde flow in that particular patient. By studying the two- and three-dimensional MR velocity maps from patient no. 10, the centrally located positive velocities in diastole were surrounded by pronounced negative velocities, explaining the high central index obtained. Consequently, it seems that pathological flow patterns with extensive flow reversal may invalidate CO estimations from single-point Doppler velocity recordings. Compared to our previous work in healthy adults [14], the variation in average index values described here are more extreme. This indicates a more pronounced skewness of the mean temporal blood velocity profile in this patient group compared to healthy subjects [14]. Furthermore, there was more inter-individual variability reflected in the high standard deviations on blood velocity index calculations (Fig. 4). This finding highlights the difficulties in assessing main PA CO from single pulsed Doppler ultrasound in patients with IHD.

Since respiration influences the venous return to the right side of the heart, both cardiac and respiratory triggering were used to optimize the velocity acquisition. Without these features, further uncertainty is introduced when using mean velocity estimates to calculate single point Doppler CO. If single point Doppler is used, e.g. for intra-individual trend studies, we recommend the central point because indices from this location did not alter significantly between the systolic and diastolic definition. However, the central index value of 1.16 was associated with a considerable s.d. of 0.39 and 0.32 for systolic and diastolic defining of the central point, respectively.

The use of multiple sample volumes has earlier been recommended in healthy adults [14]and has been used especially for measurement of CO by means of a PA pulsed Doppler catheter [9–11]. Indeed, our study reveals that cross-sectional sampling from the inferior/right to superior left diameter (average of all 12 patients) yields a blood velocity index of 1.0. However, the limited number of patients and their inter-individual variability has to be taken into account. Sampling along this diameter is practicable using an MTEE probe and is also favorable in terms of aligning the two-dimensional scanning plane with the long axis of the main PA [20, 24]. Thus, multiple sample volumes along this diameter is highly recommended even though accurate assessment of CO cannot be expected. For intra-individual trend studies, however, this should minimize the inherent errors in velocity estimation from single pulsed Doppler due to the skewed mean temporal blood velocity profile. Increasing the sample volume area has earlier been found unhelpful for optimization of the blood velocity index values [14], and this topic was therefore not studied in the present work.

Future studies should be carried out under different pathological conditions, including supplementary measurement of in-plane velocities in order to fully uncover the three-dimensional nature of blood flow velocities in the main PA. For Doppler-based CO measurement, attention should be focused on the assessment of main PA cross-sectional area, as the Doppler insonation angle has recently been published [24].


    5 Conclusion
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 
MR-phase velocity mapping and multiplane transesophageal color Doppler recordings provided similar blood velocity patterns in patients with IHD. The skewness of the mean temporal blood velocity profile is more pronounced in patients with IHD than in healthy subjects. Ignoring the skewness of the mean temporal blood velocity profile may induce an error of more than 100% in Doppler-based CO estimates. By using multiple Doppler sample volumes, the error can be minimized.

Time for primary review 25 days.


    Acknowledgements
 
This work has been supported by The John and Birthe Meyer Foundation, The Karen Elise Jensen Foundation and The Danish Heart Foundation.


    References
 Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusion
 References
 

  1. Ganz W, Donoso R, Marcus H.S, Forrester J.S, Swan H.J.C. A new technique for measurement of cardiac output by thermodilution in man. Am J Cardiol (1971) 27:292–296.
  2. Moore F.A, Haenel J.B, Moore E.E. Alternatives to Swan-Ganz cardiac output monitoring. Surg Clin North Am (1991) 71:699–721.[Web of Science][Medline]
  3. Mihaljevic T, von Segesser L.K, Tönz M, Leskosek B, Jenni R, Turina M. Continuous thermodilution measurement of cardiac output: in-vitro and in-vivo evaluation. Thorac Cardiovasc Surg (1994) 42:32–35.[Web of Science][Medline]
  4. Labovitz A.J, Buckingham T.A, Habermehl K, Nelson J, Kennedy H.L, Willams G.A. The effects of sampling site on the two-dimensional echo-Doppler determination of cardiac output. Am Heart J (1985) 109:327–333.[CrossRef][Web of Science][Medline]
  5. Robson S.C, Hunter S, Boys R.J, Dunlop W. Serial changes in pulmonary haemodynamics during human pregnancy: a non-invasive study using Doppler echocardiography. Clin Sci (1991) 80:113–117.[Web of Science][Medline]
  6. Muhiudeen I.A, Kuecherer H.F, Lee E, Cahalan M.K, Schiller N.B. Intraoperative estimation of cardiac output by transesophageal pulsed Doppler echocardiography. Anesthesiology (1991) 74:9–14.[CrossRef][Web of Science][Medline]
  7. Savino J.S, Troianos C.A, Aukburg S, Weiss R, Reichek N. Measurement of pulmonary blood flow with transesophageal two- dimensional and Doppler echocardiography. Anesthesiology (1991) 75:445–451.[Web of Science][Medline]
  8. Gorscan J, Diana P, Ball B.A, Hattler B.G. Intraoperative determination of cardiac output by transesophageal continuous wave Doppler. Am Heart J (1992) 123:171–176.[CrossRef][Web of Science][Medline]
  9. Segal J, Pearl R.G, Ford A.J.J, Stern R.A, Gehlbach S.M. Instantaneous and continuous cardiac output obtained with a Doppler pulmonary artery catheter. J Am Coll Cardiol (1989) 13:1382–1392.[Abstract]
  10. Segal J, Nassi M, Ford A.J Jr., Schuenemeyer T.D. Instantaneous and continuous cardiac output in humans obtained with a Doppler pulmonary artery catheter. J Am Coll Cardiol (1990) 16:1398–1407.[Abstract]
  11. Segal J, Gaudiani V, Nishimura T. Continuous determination of cardiac output using a flow-directed Doppler pulmonary artery catheter. J Cardiothorac Vasc Anesth (1991) 5:309–315.[CrossRef][Medline]
  12. Sømod L, Hasenkam J.M, Kim W.Y, Nygaard H, Paulsen P.K. Three dimensional visualisation of velocity profiles in the normal porcine pulmonary trunk. Cardiovasc Res (1993) 27:291–295.[Abstract/Free Full Text]
  13. Sloth E, Houlind K.C, Oyre S, et al. Three-dimensional visualization of the velocity profiles in the human main pulmonary artery using magnetic resonance phase velocity mapping. Am Heart J (1994) 128:1130–1138.[CrossRef][Web of Science][Medline]
  14. Sloth E, Houlind K.C, Pedersen E.M, Hasenkam J.M. Where to place the Doppler sample volume in the human main pulmonary artery. evaluated from magnetic resonance phase velocity maps. Cardiovasc Res (1997) 33:156–163.[Abstract/Free Full Text]
  15. Bogren H.G, Klipstein R.H, Mohiaddin R.H, et al. Pulmonary artery distensibility and blood flow patterns: a magnetic resonance study of normal subjects and of patients with pulmonary arterial hypertension. Am Heart J (1989) 118:990–999.[CrossRef][Web of Science][Medline]
  16. Kondo C, Caputo G.R, Masui T, et al. Pulmonary hypertension: pulmonary flow quantification and flow profile analysis with velocity-encoded cine MR imaging. Radiology (1992) 183:751–758.[Abstract/Free Full Text]
  17. Mohiaddin R.H, Yang G.Z, Kilner P.J. Visualization of flow by vector analysis of multidirectional cine MR velocity mapping. J Comput Assist Tomogr (1994) 18:383–392.[Web of Science][Medline]
  18. Groen JP, van Dijk P, In den Kleef JJE. Design of flow adjustable gradient waveforms. New York: Society of Magnetic Resonance in Medicine, 6th Annual Meeting, 1987;868 (abstract).
  19. Walker P.G, Cranney G.B, Scheidegger M.B, Waseleski G, Pohost G.M, Yoganathan A.P. Semiautomated method for noise reduction and background phase error correction on MR phase velocity data. J MRI (1993) 3:521–530.
  20. Sloth E, Pedersen E.M, Nygaard H, Hasenkam J.M, Juhl B. Multiplane transesophageal Doppler-echocardiografic measurements of the velocity profile in the human pulmonary artery. J Am Soc Echocardiogr (1994) 7:132–140.[Medline]
  21. Lucas C.L, Henry G.W, Ferreiro J.I, Ha B, Keagy B.A, Wilcox B.R. Pulmonary blood velocity profile variability in open-chest dogs: influence of acutely altered hemodynamic states on profiles, and influence of profiles on the accuracy of techniques for cardiac output determination. Heart Vessels (1988) 4:65–78.[CrossRef][Medline]
  22. Lanzer P, Yoganathan AP. Vascular imaging by color Doppler and magnetic resonance imaging. Berlin: Springer, 1991;3–338.
  23. Braunwald E. Heart disease. A textbook of cardiovascular medicine, ed. 5. Philadelphia: WB Saunders, 1997;1–876.
  24. Sloth E, Pedersen EM, Egeblad H, Hasenkam JM, Juhl B. Transesophageal multiplane imaging of the human pulmonary artery. A comparison of MRI and multiplane transesophageal two-dimensional echocardiography. Cardiovasc Res. 1997;34:582–589.

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
L. R. Johnson and M. H. Laughlin
Chronic exercise training does not alter pulmonary vasorelaxation in normal pigs
J Appl Physiol, June 1, 2000; 88(6): 2008 - 2014.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sloth, E.
Right arrow Articles by Hasenkam, J.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sloth, E.
Right arrow Articles by Hasenkam, J.M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?