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
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Abstract
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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.
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Introduction
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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 (
) (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.
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Materials and Methods
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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.
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Figure 1. Color M-mode Doppler propagation velocity (Vp) shown as the slope of the first aliasing velocity during early filling of the ventricle.
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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.
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Table 1. Table 1. Summary of Criteria for Diastolic Dysfunction Adapted from the Canadian Consensus on Diastolic Dysfunction
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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 
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.
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Results
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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).
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Table 2. Table 2. Demographic and Surgical Characteristics of Patients with Normal and Abnormal Diastolic Function
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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%.
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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.
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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.
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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).
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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
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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).
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Table 5. Table 5. Hemodynamic Variables Before and After Cardiopulmonary Bypass in Patients with Normal and Abnormal Diastolic Function
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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.
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Discussion
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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 (). 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.
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Acknowledgments
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Supported, in part, by National Center for Research Resources, Clinical Research Centers Program, National Institutes of Health grant MO1-RR-30.
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Accepted for publication May 13, 2002.
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Abstract
Introduction
