JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (13)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Djaiani, G. N.
Right arrow Articles by Mathew, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Djaiani, G. N.
Right arrow Articles by Mathew, J. P.
Related Collections
Right arrow Surgery
Right arrow Heart

Anesth Analg 2002;95:524-530
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Mitral Flow Propagation Velocity Identifies Patients with Abnormal Diastolic Function During Coronary Artery Bypass Graft Surgery

George N. Djaiani, MD DEAA, FRCA, Brian J. McCreath, MBChB BSc, FRCA, Lian K. Ti, MD, Burkhard G. Mackensen, MD, Mihai Podgoreanu, MD, Barbara Phillips-Bute, PhD, and Joseph P. Mathew, MD

Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina

Address correspondence and reprint requests to Joseph P. Mathew, MD, Department of Anesthesiology, PO Box 3094, Duke University Medical Center, Durham, NC 27710. Address e-mail to mathe014{at}mc.duke.edu


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Flow propagation velocity (Vp) is a new method of assessing left ventricular (LV) diastolic (D) function that seems to be insensitive to heart rate and preload changes. We hypothesized that Vp <50 cm/s identifies patients with D dysfunction and that Vp provides an assessment of D function when standard Doppler techniques are uninterpretable. We conducted a prospective Doppler echocardiographic assessment of D function in 63 patients undergoing coronary artery bypass graft surgery. Doppler derivatives of mitral inflow and pulmonary vein flow profiles as well as isovolumic relaxation time were compared with Vp before and after cardiopulmonary bypass. A Valsalva maneuver was used to decrease preload. All patients with D dysfunction had Vp <50 cm/s. A Valsalva maneuver did not affect Vp. Vp remained a reliable measure of LV D function when mitral flow profiles could not be determined because of changes in heart rate and rhythm. LV filling patterns did not change significantly after cardiopulmonary bypass. We conclude that Vp is a simple measure of D function during coronary artery bypass graft surgery that correlates with standard, load-dependent Doppler echocardiographic techniques to identify D dysfunction. Vp <50 cm/s identifies abnormal D function in this patient population.

IMPLICATIONS: Mitral propagation velocity (Vp) is a simple, reproducible measure of diastolic function during coronary artery bypass graft surgery that correlates with standard Doppler echocardiographic techniques to identify dysfunction in the setting of a rapid heart rate or variable preload. Vp <50 cm/s identifies abnormal diastolic function in this patient population.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Left ventricular (LV) diastolic (D) dysfunction, present when ventricular filling is impaired either by abnormal relaxation or decreased compliance, is a common manifestation of heart disease and is associated with significant morbidity and mortality (1). Because of its noninvasive nature and ease of application and reproducibility, Doppler evaluation of mitral and pulmonary vein flows has emerged during the past two decades as the preferred clinical tool for the diagnosis and long-term evaluation of D function (2,3). Three abnormal ventricular filling patterns are usually identified by Doppler echocardiography: impaired relaxation, pseudonormalization, and restrictive filling. However, heart rate (HR), preload, afterload, and age (4,5) may also influence these Doppler derivatives. A rapid HR may result in velocity wave fusion, whereas varying loading conditions can change the filling patterns and mask the baseline D state of the ventricle. Furthermore, accurate diagnosis of D dysfunction requires the interrogation of both the mitral and pulmonary vein flows.

Flow propagation velocity (Vp), as determined by color M-mode Doppler echocardiography, has been proposed as a single measurement that reveals the true nature of LV D function (6). Closely related to the time constant of isovolumic relaxation ({tau}) (7), in animal models, Vp has been shown to be independent of HR (8). This new Doppler echocardiographic application also seems to be a preload insensitive index of LV relaxation (9) that is able to differentiate the pseudonormal mitral flow profile from the normal filling pattern (10). A Vp >55 cm/s is associated with normal D function in young healthy subjects (6). However, impaired D function associated with advancing age or a variety of pathophysiological conditions, including dilated and hypertrophic cardiomyopathy, hypertension, aortic stenosis, myocardial ischemia and infarction, LV hypertrophy, and diabetes, has been reported to generally reduce Vp to <50 cm/s (7,11–13).

In patients undergoing coronary artery bypass graft (CABG) surgery, LV D dysfunction is common (14). Although analysis of the combination of mitral and pulmonary vein flow profiles often helps in making the diagnosis of D dysfunction, Vp may be a simpler method for assessing D function. We therefore hypothesized that during CABG surgery, Vp <50 cm/s would identify patients with D dysfunction when compared with standard Doppler techniques, and Vp measurement would provide an assessment of D function when standard Doppler techniques were uninterpretable.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
With IRB approval, we conducted a prospective echocardiographic assessment of D function in 63 patients undergoing CABG surgery with cardiopulmonary bypass (CPB) and cardioplegic arrest. Patients with valvular heart disease and chronic atrial fibrillation were excluded.

All routine cardiac medications were continued up to the morning of surgery. Patients were premedicated with diazepam 10 mg 1–2 h before surgery. Routine monitoring included continuous direct arterial blood pressure and central venous pressure or pulmonary artery pressure measurements. Anesthesia was induced with midazolam 0.05–0.1 mg/kg, fentanyl 5–8 µg/kg, thiopental 1–2 mg/kg, and pancuronium 0.1 mg/kg. Maintenance of anesthesia was accomplished with isoflurane 0.5%–1.5%, fentanyl 3–6 µg/kg, and midazolam 0.05–0.1 mg/kg. After intubation, mechanical ventilation was instituted, and the end-tidal CO2 was maintained within the normal range. CPB was conducted according to a standardized institutional protocol that included systemic cooling to 32°C, intermittent cold blood cardioplegia, mean flow rate of 2.2 L · min-1 · m-2, perfusion pressure between 50–70 mm Hg, and active rewarming to 37°C. Management of the separation from CPB and, in particular, the choice of inotropes was at the discretion of the anesthesia care team.

Echocardiographic data were acquired using a Phillips Sonos 5500 (Andover, MA) ultrasound system equipped with a multiplane transesophageal probe. Peak early (E) and late (A) mitral inflow velocities and deceleration time were obtained from a midesophageal four-chamber view with the pulsed sample volume placed at the tips of the mitral leaflets. Isovolumic relaxation time (IVRT) was acquired from a deep transgastric long-axis view with the pulsed sample volume placed between the mitral valve inflow and LV outflow tract and the gate length set to maximum. Peak systolic (S) and D velocities of left or right upper pulmonary vein flow profiles were interrogated by withdrawing the probe from a midesophageal four-chamber view or using modified bicaval views, respectively, with the pulsed sample volume placed 1–2 cm into the vein.

From a midesophageal four-chamber view, the color Doppler sector map of the mitral inflow was also displayed and adjusted to obtain the longest column of color flow from the mitral annulus to the apex. A M-mode cursor was aligned in the direction of the inflow jet and placed through the center of the flow. The color velocity map was adjusted to alias at 75% of the peak E mitral inflow velocity, and the color M-mode Doppler Vp was measured as the slope of the first aliasing velocity during early filling from the mitral annulus to 4 cm into the LV cavity (Fig. 1). Before the start of the study, the two investigators obtaining Doppler data were trained in the technique of recording Vp by acquiring sample data in a series of 10 patients.



View larger version (84K):
[in this window]
[in a new window]
  		Figure 1. Color M-mode Doppler propagation velocity (Vp) shown as the slope of the first aliasing velocity during early filling of the ventricle.

 
All measurements were acquired during apnea using a sweep speed of 100 mm/s and stored onto videotape. Peak mitral E and A velocities, peak pulmonary vein S and D velocities, IVRT, and Vp were measured before the skin incision and repeated after sternal closure. Mitral E and A velocities and Vp were also measured before and after CPB during the Valsalva maneuver (VM), defined as a sustained positive airway pressure to 30 cm H20 for a period of 10 s. The VM is a relatively simple method of reducing venous return to the heart, thereby reducing left atrial pressure (i.e., changing loading conditions). An effective VM tends to produce at least a 10% reduction of E velocities (15). All E/A and S/D ratios were calculated. D dysfunction was diagnosed according to criteria adapted from the Canadian Consensus on Diastolic Dysfunction (16) (Table 1). A normal appearing filling pattern changing to a pattern of delayed relaxation with VM was considered a pseudonormalized pattern.


View this table:
[in this window]
[in a new window]
  		Table 1. Table 1. Summary of Criteria for Diastolic Dysfunction Adapted from the Canadian Consensus on Diastolic Dysfunction
 
To test the intraobserver variability, Vp was mea-sured twice from the data obtained from 10 randomly selected patients by a single observer. To observe the interobserver variability, two observers independently measured Vp in the same 10 patients. Intraobserver and interobserver variability were expressed as the percentage difference.

Mean arterial, pulmonary artery D, or central venous blood pressures and HR were recorded at the time of D function assessment. Ejection fraction (EF) was visually estimated before and after CPB from the transgastric short axis view of the left ventricle. The administration of inotropes for separation from CPB and the need for temporary pacemaker support was also recorded.

Based on mitral inflow and pulmonary vein flow patterns, patients were divided into normal and abnormal function groups. Patients with abnormal D function were subdivided into those with delayed relaxation, pseudonormalization, and restrictive filling. Demographic data were analyzed using two-tailed t-test and {chi}2 test as appropriate.

Vp was compared between patients with and without D dysfunction using the two-tailed t-test. The effect of VM on mitral inflow velocities and Vp was also examined before and after CPB. Bonferroni correction was applied for multiple testing, and P <= 0.025 was considered significant.

A receiver operator curve (ROC) was constructed to determine the best cutoff of Vp to correspond to the normal versus abnormal groupings. A univariate logistic regression model was performed to examine the relationship between Vp and D dysfunction.

D function in patients with absent A or fused E and A was analyzed with Mann-Whitney U-test. Inotrope use between patients with normal and abnormal D function was compared with Fischer’s exact test; P <= 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Two patients were excluded because of uninterpretable Doppler data at baseline. D dysfunction diagnosed by standard Doppler criteria in the pre-CPB period was present in 42 (69%) of the remaining 61 patients. Twenty-six patients displayed a delayed relaxation pattern, and one had restrictive filling. In these patients, the E velocity declined from 57 ± 13 cm/s to 51 ± 12 cm/s with the application of the VM. Use of the VM revealed that 15 patients had a pseudonormalized pattern. In patients with a pseudonormal LV filling pattern, E/A ratio was significantly decreased during VM but did not change during VM in patients with normal, delayed relaxation and restrictive LV filling patterns. Patients with normal and abnormal D function were similar in age, sex, LV EF, history of myocardial infarction, preoperative co-morbidities, use of ß-adrenergic blockers and calcium channel blockers, CPB and aortic cross-clamp time, and the number of bypass grafts performed (Table 2).


View this table:
[in this window]
[in a new window]
  		Table 2. Table 2. Demographic and Surgical Characteristics of Patients with Normal and Abnormal Diastolic Function
 
All patients with D dysfunction diagnosed by standard Doppler techniques had a Vp <50 cm/s. Vp identified patients with normal and abnormal D function before and after CPB (Fig. 2). Furthermore, Vp was not affected by the VM (Fig. 3). Intraobserver variability for the measurements of Vp was 8%. Interobserver variability was 10%.



View larger version (11K):
[in this window]
[in a new window]
  		Figure 2. Comparison of propagation velocity (Vp) between patients with normal and abnormal diastolic function before and after cardiopulmonary bypass (CPB). *P < 0.0001. DF = diastolic function.

 


View larger version (12K):
[in this window]
[in a new window]
  		Figure 3. Comparison of propagation velocity (Vp) and ratio of early (E) to late (A) mitral inflow velocity (E/A) in patients with normal (n = 19) and pseudonormal (n = 15) patterns of diastolic filling before and after Valsalva maneuver before cardiopulmonary bypass. *P < 0.0001.

 
Although LV filling patterns did not change significantly after CPB and cardioplegic arrest (Table 3), the E/A ratio could not be calculated in eight patients after CPB because of atrial fibrillation (n = 1), nodal rhythm (n = 1), or tachycardia-induced E/A fusion (n = 6). In these patients, abnormal D function was determined using S/D ratio (patients without atrial fibrillation) and IVRT. Vp (<50 cm/s) identified patients with abnormal D function even when E/A ratio, S/D ratio, and deceleration time could not be determined (Table 4).


View this table:
[in this window]
[in a new window]
  		Table 3. Table 3. Left Ventricular Diastolic Filling Patterns
 

View this table:
[in this window]
[in a new window]
  		Table 4. Table 4. Diastolic Function in Patients in Whom Early/Late Ratio Could Not Be Calculated With Absent Late or Fused Early and Late Mitral Flow Profile Ventricular Filling Velocities
 
For the hemodynamic variables, mean arterial blood pressure was significantly lower and HR marginally higher after CPB only in patients with normal D function. There was no difference between normal and abnormal D function groups in EF and central venous blood or pulmonary artery D pressure (Table 5). Twelve patients required inotropic support after CPB. Dopamine 3–6 µg · kg-1 · min-1 was required in 2 patients with normal and 8 patients with abnormal D function. Epinephrine 0.04–0.05 µg · kg-1 · min-1 was used in two patients with abnormal D function. However, there was no statistically significant difference in inotrope use between the two groups (P = 0.25).


View this table:
[in this window]
[in a new window]
  		Table 5. Table 5. Hemodynamic Variables Before and After Cardiopulmonary Bypass in Patients with Normal and Abnormal Diastolic Function
 
The c-index for the univariate regression model (examining the relationship between Vp and D dysfunction), which corresponds to the area under the ROC, was 1.0, indicating that the model had perfect predictive ability. The estimated event probability cutoff point, which maximizes both the sensitivity and the specificity of the model, corresponded to a Vp value of >46 and <52 cm/s. No patients had a Vp value between these two numbers. In other words, any value between 46 and 52 cm/s had 100% predictive ability and could be considered the best cutoff point. For the sake of completeness, we examined two other potential cutoffs. A logistic regression model using a Vp of 40 cm/s as a cutoff value had a c-index (or area under the ROC) of 0.854. A model using 55 cm/s as a cutoff value had a c-index of 0.895. Each model showed very good predictive ability, but our choice of 50 cm/s stood as the better discriminator of D dysfunction.

A simple kappa coefficient in 61 patients testing the agreement between abnormal D dysfunction and a classification based on the Vp <50 cm/s indicates that kappa is 0.96, with 95% confidence intervals ranging from 0.90 to 1.05. These confidence intervals are fairly narrow, very high, and do not include 0.50. Therefore, we can express confidence that our sample size and our data are sufficient to support the hypothesis that a Vp <50 cm/s identifies patients with D dysfunction.


   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
D dysfunction is common in patients presenting for CABG surgery (14). Traditional Doppler measures of D function have had limited success in the operating room because of the dramatic effect of changing HR and loading conditions upon these measures. Using a newer Doppler-derived index of LV filling in 61 patients, we have demonstrated that mitral flow Vp <50 cm/s identifies patients with D dysfunction before and after CPB. In addition, we found that Vp could differentiate the pseudonormal from the normal LV filling pattern. Although analysis of pulmonary vein flow profiles may help identify pseudonormalization, these profiles are also affected by rhythm, HR, and respiration (17). Similarly, IVRT may be used to distinguish between LV filling patterns, but its routine use can be technically challenging (17).

Color M-mode Doppler-derived Vp may be favored because it examines the spatio-temporal distribution of blood flow velocities along an entire portion of the LV cavity. Unlike the traditional measure of mitral inflow velocities, Vp provides information equivalent to multiple simultaneous pulsed-wave Doppler echocardiographic measurements obtained at different levels from the mitral orifice to the LV apex (6). Several clinical studies have evaluated the efficacy of Vp in nonsurgical populations. Brun et al. (7) used the transition from no color to color as the determinant of Vp, demonstrating a significant negative correlation between Vp and the gold standard for assessing LV D function, the time constant of relaxation ({tau}). Using the slope of the first aliasing velocity as the determinant of Vp, Takatsuji et al. (10) confirmed this finding. Subsequently, Garcia et al. (6) demonstrated that Takatsuji’s method was more reproducible and permitted a consistent measurement when the color M-mode echocardiographic recordings are curvilinear.

Two mechanisms have been proposed as determinants of Vp: the presence of pressure gradients and the formation of flow vortices (18). In patients with normal D function, rapid LV relaxation generates a pressure gradient that, according to Bernoulli’s equation, results in the flow of blood from the mitral orifice deep into the left ventricle (10). This pressure gradient is diminished in patients with abnormal D function, leading to slower propagation of early LV filling flow and a reduced Vp. Alternatively, vorticity is generated by shear between inflowing blood and the stationary blood already in the ventricle. Abnormal D function results in increased vortex formation and a reduced Vp (7).

LV filling abnormalities have been detected in as many as 90% of patients with coronary artery disease (19). In our study, abnormal D function was present in nearly three-quarters of patients undergoing CABG surgery. This finding is consistent with recent reports identifying D dysfunction in more than 74% of subjects undergoing cardiac surgery (20). Although myocardial revascularization may improve D function weeks to months after surgery (21,22), its immediate impact on D function is less clear. The potential improvement in D function may be offset by global ischemia during the cardioplegic arrest. Current evidence suggests that LV D function may deteriorate (23,24), improve (25), or remain unchanged (26) after CPB and cardioplegic arrest. This controversy surrounding the status of LV D function may be due to changing LV loading conditions, difficulty in differentiating between normal and pseudonormal mitral flow profiles, differences in the technique used to identify D dysfunction, or different approaches to myocardial protection. In our study using Vp, the prevalence of LV D dysfunction was unchanged after CPB and cardioplegic arrest. However, our post-CPB data are confounded by the use of inotropes in those patients most likely to demonstrate deterioration in D function. A larger sample in which no patients received inotropic therapy may have revealed either an improvement or a deterioration of D function in selected patients.

A primary limitation to our study is that comparisons are made to standard Doppler techniques that are themselves limited in capacity. However, these techniques currently serve as the gold standard for the clinical diagnosis of D dysfunction. Our measurements of Vp and mitral and pulmonary velocity profiles were conducted consecutively during a period of hemodynamic stability thus diminishing the likelihood of adverse effects from varying HR, preload, or afterload. When considering the effects of increased HR, standard Doppler measures are limited by their inability to distinguish the E from the A wave because of fusion. Such a scenario was not present in the pre-CPB period, wherein the ROC was constructed to define cutoffs. The adverse effects of varying preload and afterload are a primary concern in the sequential assessment of a patient (i.e., the Doppler patterns can vary across different time points during surgery as loading conditions change). However, even when these patterns change, they are accurately reflecting the influence of loading conditions upon D function. For example, a patient with a reversible restrictive disease pattern may move to a pseudonormalized pattern with preload reduction. The filling pattern changes because D function has changed. At the instant the measurement is made, the true D state of the ventricle has improved to pseudonormalization because of reduced preload. Thus, the chronic (preoperative) D state of the ventricle may be misdiagnosed because of altered load, but the acute D state is accurately measured. Because our Vp and mitral and pulmonary flow measurements were made in quick succession during periods without change in hemodynamic variables, it is likely that both Vp and mitral/pulmonary velocities were measuring the same D state of the ventricle.

Second, because we identified only one patient with restrictive filling, we were unable to determine the ability of Vp to discriminate between the three abnormal LV filling patterns. The incidence of a restrictive LV filling pattern in adult cardiac surgical patients has been estimated at <4% (20), and as a result, a larger sample size would be required to demonstrate Vp’s discriminative power. Similarly, Vp is limited in that whereas it detects relaxation abnormalities, it may not detect compliance abnormalities. Third, in this small study, we did not attempt to establish a link between D dysfunction and an increase in mortality. Whereas restrictive LV filling patterns predict increased mortality after myocardial infarction (27,28), in congestive cardiac failure (29), in dilated cardiomyopathy (30), and in cardiac amyloidosis (31), this issue has not been addressed in adult cardiac surgical patients. Although intriguing, the infrequency of a restrictive LV filling pattern in our patients prevented us from examining this issue. Finally, this study was limited to patients undergoing CABG surgery. Although our findings may not be applicable to every patient population, several clinical studies have established the validity and utility of Vp (9,10,27,32).

In conclusion, Vp is a simple, reproducible measure of D function during CABG surgery that correlates with standard, load-dependent Doppler techniques. Our study provides the first evidence that Vp <50 cm/s identifies abnormal D function in this patient population. Vp may overcome many of the limitations of standard Doppler echocardiographic techniques because it seems to be relatively preload independent (9) and unaffected by HR increases (8). It is yet to be determined whether Vp can discriminate between different abnormal LV filling patterns, between relaxation and compliance abnormalities, and whether it is associated with postoperative morbidity and mortality.


   Acknowledgments
 
Supported, in part, by National Center for Research Resources, Clinical Research Centers Program, National Institutes of Health grant MO1-RR-30.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Vasan RS, Benjamin EJ, Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol 1995; 26: 1565–74.[Abstract]
  2. Oh JK, Appleton CP, Hatle LK, et al. The noninvasive assessment of left ventricular diastolic function with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 1997; 10: 246–70.[Web of Science][Medline]
  3. Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician’s Rosetta Stone. J Am Coll Cardiol 1997; 30: 8–18.[Abstract]
  4. Choong CY, Herrmann HC, Weyman AE, Fifer MA. Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans. J Am Coll Cardiol 1987; 10: 800–8.[Abstract]
  5. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988; 12: 426–40.[Abstract]
  6. Garcia MJ, Thomas JD, Klein AL. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol 1998; 32: 865–75.[Abstract/Free Full Text]
  7. Brun P, Tribouilloy C, Duval AM, et al. Left ventricular flow propagation during early filling is related to wall relaxation: a color M-mode Doppler analysis. J Am Coll Cardiol 1992; 20: 420–32.[Abstract]
  8. Stugaard M, Smiseth OA, Risoe C, Ihlen H. Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography. Circulation 1993; 88: 2705–13.[Abstract/Free Full Text]
  9. Garcia MJ, Smedira NG, Greenberg NL, et al. Color M-mode Doppler flow propagation velocity is a preload insensitive index of left ventricular relaxation: animal and human validation. J Am Coll Cardiol 2000; 35: 201–8.[Abstract/Free Full Text]
  10. Takatsuji H, Mikami T, Urasawa K, et al. A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography. J Am Coll Cardiol 1996; 27: 365–71.[Abstract]
  11. Nishihara K, Mikami T, Takatsuji H, et al. Usefulness of early diastolic flow propagation velocity measured by color M-mode Doppler technique for the assessment of left ventricular diastolic function in patients with hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2000; 13: 801–8.[Web of Science][Medline]
  12. Steine K, Flogstad T, Stugaard M, Smiseth OA. Early diastolic intraventricular filling pattern in acute myocardial infarction by color M-mode Doppler echocardiography. J Am Soc Echocardiogr 1998; 11: 119–25.[Web of Science][Medline]
  13. Moller JE, Poulsen SH, Sondergaard E, Egstrup K. Preload dependence of color M-mode Doppler flow propagation velocity in controls and in patients with left ventricular dysfunction. J Am Soc Echocardiogr 2000; 13: 902–9.[Web of Science][Medline]
  14. Casthely PA, Shah C, Mekhjian H, et al. Left ventricular diastolic function after coronary artery bypass grafting: a correlative study with three different myocardial protection techniques. J Thorac Cardiovasc Surg 1997; 114: 254–60.[Abstract/Free Full Text]
  15. Hurrell DG, Nishimura RA, Ilstrup DM, Appleton CP. Utility of preload alteration in assessment of left ventricular filling pressure by Doppler echocardiography: a simultaneous catheterization and Doppler echocardiographic study. J Am Coll Cardiol 1997; 30: 459–67.[Abstract]
  16. Rakowski H, Appleton C, Chan KL, et al. Can consensus recommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. J Am Soc Echocardiogr 1996; 9: 736–60.[Medline]
  17. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity components: new insights from studies in lightly sedated normal dogs. J Am Coll Cardiol 1997; 30: 1562–74.[Abstract]
  18. Garcia MJ, Palac RT, Malenka DJ, et al. Color M-mode Doppler flow propagation velocity is a relatively preload-independent index of left ventricular filling. J Am Soc Echocardiogr 1999; 12: 129–37.[Web of Science][Medline]
  19. Bonow RO, Bacharach SL, Green MV, et al. Impaired left ventricular diastolic filling in patients with coronary artery disease: assessment with radionuclide angiography. Circulation 1981; 64: 315–23.[Abstract/Free Full Text]
  20. Lappas DG, Skubas NJ, Lappas GD, et al. Prevalence of left ventricular diastolic filling abnormalities in adult cardiac surgical patients: an intraoperative echocardiographic study. Semin Thorac Cardiovasc Surg 1999; 11: 125–33.[Medline]
  21. Miller RR, DeMaria AN, Amsterdam EA, et al. Improvement of reduced left ventricular diastolic compliance in ischemic heart disease after successful coronary artery bypass surgery. Am J Cardiol 1975; 35: 11–6.[Web of Science][Medline]
  22. Natsuaki M, Itoh T, Ohteki H, et al. Evaluation of left ventricular early diastolic function after coronary artery bypass grafting relating to myocardial damage. Jpn Circ J 1991; 55: 117–24.[Medline]
  23. McKenney PA, Apstein CS, Mendes LA, et al. Increased left ventricular diastolic chamber stiffness immediately after coronary artery bypass surgery. J Am Coll Cardiol 1994; 24: 1189–94.[Abstract]
  24. Samuelsson S, Brodin LA, Broman M, et al. Comparison between transesophageal Doppler echocardiography and nuclear cardioangiography for the evaluation of left ventricular filling during coronary artery bypass grafting. Anesth Analg 1995; 80: 41–6.[Abstract]
  25. De Hert SG, Rodrigus IE, Haenen LR, et al. Recovery of systolic and diastolic left ventricular function early after cardiopulmonary bypass. Anesthesiology 1996; 85: 1063–75.[Web of Science][Medline]
  26. Houltz E, Hellstrom A, Ricksten SE, et al. Early effects of coronary artery bypass surgery and cold cardioplegic ischemia on left ventricular diastolic function: evaluation by computer-assisted transesophageal echocardiography. J Cardiothorac Vasc Anesth 1996; 10: 728–33.[Web of Science][Medline]
  27. Moller JE, Sondergaard E, Seward JB, et al. Ratio of left ventricular peak E-wave velocity to flow propagation velocity assessed by color M-mode Doppler echocardiography in first myocardial infarction: prognostic and clinical implications. J Am Coll Cardiol 2000; 35: 363–70.[Abstract/Free Full Text]
  28. Giannuzzi P, Imparato A, Temporelli PL, et al. Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction. J Am Coll Cardiol 1994; 23: 1630–7.[Abstract]
  29. Xie GY, Berk MR, Smith MD, et al. Prognostic value of Doppler transmitral flow patterns in patients with congestive heart failure. J Am Coll Cardiol 1994; 24: 132–9.[Abstract]
  30. Werner GS, Schaefer C, Dirks R, et al. Prognostic value of Doppler echocardiographic assessment of left ventricular filling in idiopathic dilated cardiomyopathy. Am J Cardiol 1994; 73: 792–8.[Web of Science][Medline]
  31. Klein AL, Hatle LK, Taliercio CP, et al. Prognostic significance of Doppler measures of diastolic function in cardiac amyloidosis: a Doppler echocardiography study. Circulation 1991; 83: 808–16.[Abstract/Free Full Text]
  32. Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001; 87: 86–94.[Web of Science][Medline]
Accepted for publication May 13, 2002.




This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
Y. Shi, A. Y. Denault, P. Couture, A. Butnaru, M. Carrier, and J.-C. Tardif
Biventricular diastolic filling patterns after coronary artery bypass graft surgery
J. Thorac. Cardiovasc. Surg., May 1, 2006; 131(5): 1080 - 1086.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
B. W.L. De Boeck, J. K. Oh, P. M. Vandervoort, J. A. Vierendeels, R. P.L.M. van der Aa, and M.-J. M. Cramer
Colour M-mode velocity propagation: a glance at intra-ventricular pressure gradients and early diastolic ventricular performance
Eur J Heart Fail, January 1, 2005; 7(1): 19 - 28.
[Abstract] [Full Text] [PDF]

Home page
 Card Surg AdultHome page
J. A. Fox, V. Formanek, A. Friedrich, and S. K. Shernan
Intraoperative Echocardiography
Card. Surg. Adult, January 1, 2003; 2(2003): 283 - 314.
[Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (13)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Djaiani, G. N.
Right arrow Articles by Mathew, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Djaiani, G. N.
Right arrow Articles by Mathew, J. P.
Related Collections
Right arrow Surgery
Right arrow Heart

Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2002 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press