Ann Thorac Surg 1999;67:705-710
© 1999 The Society of Thoracic Surgeons
Original Articles
The relationship of myocardial stroke work to coronary flow velocity immediately after aortic valve replacement
Xu Y. Jin, MD, PhDa,
Derek G. Gibson, FRCPa,
John R. Pepper, FRCSa
a Departments of Cardiothoracic Surgery and Cardiology, Royal Brompton Hospital, London, England, USA
Accepted for publication August 26, 1998.
Address reprint requests to Dr Pepper, Department of Cardiac Surgery, Royal Brompton Hospital, Sydney St, London, SW3 6NP, England
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Abstract
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Background. The interrelations between myocardial stroke work and coronary flow velocity have not been fully defined during aortic valve replacement or with different cardioplegias.
Methods. Twenty-six patients (15 men age 63 ± 13 years) who had elective isolated aortic valve replacement were studied by transesophageal Doppler echocardiography with simultaneous high fidelity left ventricular pressure. Fifteen patients received cold blood cardioplegia and 11 had warm blood cardioplegia. Myocardial stroke work and flow velocities in proximal left anterior descending coronary artery were quantified simultaneously before cardiopulmonary bypass and at 1, 6, 12, and 20 hours afterwards.
Results. Myocardial stroke work decreased postoperatively in both groups (160 ± 19 versus 228 ± 19 mJ/cm3 per minute, with cold blood cardioplegia; 135 ± 22 versus 227 ± 22 mJ/cm3 per minute with warm blood cardioplegia; both p < 0.001 versus time, but p > 0.05 versus cardioplegia, by two-way analysis of variance). Left anterior descending artery flow velocity-time integral per minute increased significantly in both groups (26.1 ± 2.1 versus 15.0 ± 2.1 m/min with cold blood cardioplegia; 32.8 ± 2.5 versus 14.4 ± 2.5 m/min with warm blood cardioplegia; both p < 0.001 versus time, but p > 0.05 versus cardioplegia). Thus, at 1 hour postoperatively the mJ · cm-3 · m-1 · min ratio of myocardial stroke work to left anterior descending artery flow velocity-time integral decreased significantly in both groups (4.3 ± 1.6 versus 16.3 ± 1.7 mJ · cm-3 · m-1 · min with warm blood cardioplegia, and 7.4 ± 1.4 versus 17.9 ± 1.4 J · cm-3 · m-1 · min with cold blood cardioplegia; both p < 0.001 versus time). Warm blood cardioplegia was also associated with a lower mean ratio perioperatively than that with cold blood cardioplegia (7.8 ± 0.9 versus 10.9 ± 0.7 mJ · cm-3 · m-1 · min, p = 0.014).
Conclusions. Coronary hyperemia occurs for at least 20 hours postoperatively when myocardial stoke work has decreased. The ratio of myocardial stroke work to coronary flow velocity appears to be more sensitive than either alone in differentiating the effect of warm versus cold blood cardioplegia.
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Introduction
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Physiologic quantification of myocardial injury after aortic valve replacement remains difficult because of the striking decrease in myocardial stroke work that follows relief of pressure or volume overload of the ventricle [1–4]. Against this background, it is hard to define small differences between the effects of various cardioplegic methods on the basis of postoperative myocardial function. Furthermore, although stroke work is reduced, myocardial blood flow and oxygen consumption do not usually decrease after cardioplegia and reperfusion [5, 6]. Detailed assessment of mechanical performance of the left ventricle early after aortic valve replacement suggests that protection of the hypertrophic myocardium by warm continuous blood cardioplegia might be less satisfactory than protection by intermittent cold blood cardioplegia [4], and that after 1 hour of reperfusion, coronary hemodynamics can be significantly different [7]. It is still unknown, however, whether differences in coronary response to the cardioplegia affect interrelations between myocardial work and coronary flow velocity over a longer period. Flow velocity in the proximal left coronary artery, and the function of the myocardium it supplies can both be studied by transesophageal echocardiography [7–9]. We therefore assessed changes in left ventricular myocardial stroke work, left anterior descending coronary artery flow velocities, and the ratio of the two during and up to 20 hours after aortic valve replacement, to elucidate any possible differences between the two cardioplegic methods.
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Patients and methods
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We studied 26 patients who had elective isolated aortic valve replacement for predominant valvular aortic stenosis. Subjects had a mean age of 63 ± 13 years; 15 were male. Left ventricular mass index was 225 ± 95 g/m2 measured by M-mode echocardiography [10]. No patient had significant coronary artery disease at preoperative coronary angiography. This study is a part of a clinical research project and was approved by the Ethics Committee of the Royal Brompton Hospital. Written informed consent was obtained from all participants. There were no side effects of this study.
General anesthesia was used (fentanyl [20 to 50 µg/kg] and pancuronium oxide [0.1 mg/kg]). After induction of anesthesia a Swan-Ganz thermodilution balloon tip catheter was positioned with its tip in the pulmonary artery and used for hemodynamic measurements. Cardiopulmonary bypass was routinely established using a membrane oxygenator and roller pump, with hemodilution (hematocrit value 20% to 25%) and systemic hypothermia (28°C nasopharyngeal temperature) using cold blood cardioplegia in 15 patients or normothermia (37°C) in 11 patients in whom continuous retrograde warm blood cardioplegia was given, by a randomized approach [4]. The aortic valve was replaced with a stentless biologic valve in 23 patients and a stented bioprosthesis in 3 patients. The mean valve size was 25 ± 2.4 mm. Normal performance of the new valves was confirmed by transesophageal echocardiography. Cardiopulmonary bypass time was 129 ± 17 minutes, and aortic cross clamp time was 102 ± 17 minutes. Postoperatively, the patients were transferred to the intensive care under continuous sedation (morphine 1 mg/h and propofol 50 to 100 mg/h, intravenously) and controlled ventilation (fraction of inspired oxygen 35%, inspiration to expiration ratio 1:2, positive end-expiratory pressure 1 to 2 mm Hg). A positive inotropic drug (dopamine 
5 µg/kg per minute) was administered to 6 patients when cardiac output decreased to less than 2.0 L/m2 per minute with a mean left atrial pressure of 15 mm Hg or more, early after weaning off bypass. Eight patients were given dopamine at a renal dose (2 to 3 µg/kg per minute); in the remaining 12 patients, no inotropic drug was used.
Echocardiography and left ventricular pressure recording
A 5-MHz biplane transesophageal echocardiographic transducer (HP 21362C) was positioned after induction of anesthesia and interfaced with a Hewlett Packard 77025A Sonos 500 or 1500 Ultrasound System (Hewlett-Packard, Andover, MA). Once the pericardium was opened, a 4-F catheter tip pressure transducer (Gaeltec CTC/4F/USCI, Gaeltec Ltd, Isle of Skye, Scotland) was introduced into the left ventricle with its tip located in the midportion of the cavity, by way of the roof of the left atrium and across the mitral valve. Signal output was filtered with an upper cutoff frequency of 1 kHz, preamplified (Gaeltec S7b, Gaeltec Ltd, Isle of Skye, Scotland) and transferred to an auxiliary line of the echocardiographic system. The pressure-transducer-tipped catheter was calibrated electronically before the initial measurement, and checked, after final removal, against an air-operated dead-weight balance (Budenberg Gauge Company Ltd, London, England). Zero pressure was taken as atmospheric. The mean left atrial pressure or pulmonary artery wedge pressure was used to identify the left ventricular end-diastolic pressure [2, 11].
From the transgastric left ventricular short axis view, a two-dimensional image–directed M-mode echocardiogram of the minor axis was recorded at the level of the tips of papillary muscles and printed on paper at a speed of 100 mm/second with simultaneous left ventricular pressure trace, and electrocardiogram. Coronary blood flow velocities were recorded from transesophageal horizontal view at aortic valve level. The proximal left anterior descending coronary artery (LAD) was located on the two-dimensional color flow image. Blood flow velocity was recorded by 5-MHz pulsed Doppler echocardiography with the sample volume (1 mm) placed at its proximal one third, ie, 2 to 3 cm distal to the bifurcation of the anterior descending and circumflex arteries [8, 9]. Records were made at a paper speed of 100 mm/second with simultaneous electrocardiogram and left ventricular pressure (Fig 1). Hemodynamic measurements, including cardiac output recorded by thermodilution, heart rate, mean systemic artery pressure, and pulmonary wedge pressure or mean left atrial pressure, were obtained with each echocardiographic observation.
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Fig 1. Simultaneous recordings of electrocardiogram (ECG), flow velocity of left descending coronary artery (LAD FV), and high fidelity left ventricular pressure (LVP) from a patient after aortic valve replacement, with paper speed of 100 mm/s.
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Protocols
Initial measurements, including M-mode echocardiography, LAD flow velocity, left ventricular pressure, and hemodynamics were made before the institution of cardiopulmonary bypass under a stable hemodynamic state, and postoperative measurements of all variables were repeated at 1 (after weaning from bypass), 6, 12, 20 hours after removal of the aortic clamp. The transesophageal transducer, left ventricular pressure catheter, and pulmonary thermodilution catheter were left in situ until the final measurement. Sedation was then discontinued and the patient weaned from ventilation within 2 to 3 hours.
Digitization and calculations
From the left ventricular M-mode echocardiogram and pressure traces, the minor dimension, cavity pressure, and anterior wall thickness were digitized offline (sampling frequency 100 Hz) along with depth and time calibration [2, 4, 12]. The onset of the QRS complex of the electrocardiogram was used to identify end diastole. The timing of peak dP/dt was checked against the closure of aortic valve on the M-mode aortic echogram. Three successive beats were digitized at each time interval and mean values used.
Cavity size, wall thickness
From the digitized records, we measured cavity dimension and anterior and posterior wall thickness at end diastole.
Pressure and stress
Mean left ventricular pressure during ejection and peak rates of pressure increase or decrease were determined. Left ventricular circumferential mid-wall stress was calculated by Falsetti’s method [13] and was plotted continuously throughout the cardiac cycle, from which peak systolic wall stress was measured [12].
Regional myocardial stroke work
Mid-wall circumferential myocardial power was given by the instantaneous product of circumferential wall stress and mid-wall dimensional shortening rate. The mid-wall circumference at this point was taken as 
(D + T) (where D and T represent transverse cavity dimension and wall thickness, respectively), and the shortening rate as its first differential with respect to time. Myocardial stroke work was defined as the time integral of power over the systolic period, which was normalized to refer to a cubic centimeter of myocardium at end diastole [2, 11].
Left ventricular hemodynamics
From simultaneous measurements of cardiac output (CO), heart rate (HR), left ventricular mean ejection pressure (LVMEP), and left ventricular end-diastolic pressure (LVEDP), along with body surface area (BSA), we calculated left ventricular stroke volume index LVSVI = (CO/HR) · BSA-1, in mL/m2), and left ventricular stroke work index LVSWI = LVSVI · (LVMEP - LVEDP) · 0.0136 · 9.8, in mJ/m2 [11].
Coronary flow velocities
We measured peak LAD flow velocity during early diastole, the velocity at end diastole (the onset of QRS complex), and the time integral of LAD flow velocity during diastole (from second heart sound, or peak negative dP/dt when the chest was open, to the onset of QRS complex of the next beat), as well as that during systole (from onset of QRS to the second heart sound). Thus, the time integral of flow velocity per beat and per minute were determined [8].
Statistical methods
Data are presented as mean ± one standard deviation. Minitab statistical software (PC Version, Release 8, 1991, Minitab Inc, Philadelphia, PA) [14] was used for statistical analysis. A one-way analysis of variance with respect to time was used to identify significant changes in any perioperative measurements, combined with multiple comparisons of the 95% confidence interval (Dunnett’s method, family error rate, 0.05; individual error rate, 0.014) with respect to precardiopulmonary bypass data. A multivariant analysis of variance (general linear model) was used to identify any effects of time (preoperation, 1, 6, 12, and 20 hours afterwards), cardioplegic method (cold or warm blood cardioplegia), and positive inotropic drug (none, renal dose, or cardiac dose) on myocardial stroke work, LAD flow velocity time integral, and the ratio of the two. A value less than p < 0.05 was taken as statistically significant.
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Results
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Changes in left ventricular loading conditions, hemodynamics, and systolic function
With operation, left ventricular stroke volume index did not change significantly, although the increase in heart rate early after operation resulted in a higher cardiac index (Table 1). A prompt decrease in systolic wall stress with aortic valve replacement was not associated with any significant change in ventricular preload, as assessed by end-diastolic cavity dimension, or the peak rates of cavity pressure increase or decrease. Left ventricular stroke work index decreased immediately after operation and did not return to baseline by 20 hours postoperatively. Regional myocardial stroke work also decreased significantly immediately after operation.
Changes in LAD flow velocities
LAD early and late diastolic flow velocities increased 1.6-fold and 2.0-fold, respectively, compared with prebypass levels. The flow velocity time integral per beat or per minute also increased to 1.5 and 1.9 times of the baseline, respectively (Table 2). Not only were higher flow velocities maintained throughout diastole, but the time available for diastolic forward flow also increased due to a shorter ejection time. The time integral of systolic flow velocity, which accounted for only about 10% of the total for the cardiac cycle, did not change significantly. The increased diastolic flow velocity and its time integral per beat both regressed toward baseline over 6 to 20 hours. Left anterior descending artery flow velocity time integral per minute increased in a similar manner in the early postoperative period but still remained above baseline at 20 hours postoperatively. To integrate the reciprocal changes in myocardial stroke work and coronary flow velocity, as well as the changes in heart rate, we calculated the ratio of minute myocardial stroke work to minute flow velocity time integral. This ratio decreased profoundly after early reperfusion, with incomplete recovery by 20 hours.
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Table 2. Perioperative Changes in Flow Velocities of the Left Anterior Descending Artery and Its Relation to Myocardial Stroke Worka
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Effects of cardioplegic method and inotropic drug
We further analyzed the possible effects of cardioplegia and inotropic drugs by taking these factors along with the time effects, using multivariant analysis of variance (Table 3). We thus found that the cardiac cycle was consistently shorter when an inotropic drug was administrated, and the peak rate of ventricular pressure decrease was greater. Cardioplegic method did not affect heart rate or myocardial stroke work, either per beat or per minute. Warm blood cardioplegia was associated with a higher LAD flow velocity than that of cold blood cardioplegia at a borderline significance (p = 0.060). The most striking difference that we demonstrated between the two forms of cardioplegia was the ratio of myocardial stroke work to LAD flow velocity time integral, which was significantly lower with warm blood cardioplegia (p = 0.014) (Fig 2).
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Table 3. Results of Multivariant Analysis of Variance of Perioperative Myocardial Function, Left Anterior Descending Artery Flow Velocity, and Their Interrelationshipa
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Fig 2. The percentage changes (mean ± standard error of the mean), from prebypass measurement, in the ratio of myocardial stroke work to left anterior descending artery flow velocity time integral (SW/VTI) were plotted against time within each cardioplegic group. There was a significant decrease in this ratio immediately after aortic valve replacement (AVR) in both groups (p < 0.001 vs time), and the decrease was greater with warm continuous (filled triangle) than cold intermittent (open circle) cardioplegia (p = 0.014), by two-way analysis of variance.
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Comment
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Flow velocities can be measured readily in the proximal LAD by transesophageal echocardiography during the perioperative period [7–9]. Before valve replacement, we noted values similar to those previously recorded in patients with aortic valve disease and normal coronary arteries [15, 16]. During the perioperative period of observation, there was a clear pattern of change in coronary flow velocity with aortic valve replacement in our patients. Systolic coronary flow velocities were low, ill-sustained, and did not change consistently with operation. Peak early diastolic flow velocity, however, had increased by 60% and that at end-diastole had almost doubled by 1 hour postoperatively. There were similar changes in flow velocity time integral, whether expressed per beat or per minute. Over the next 20 hours, both early and late diastolic flow velocity values decreased toward their preoperative levels. These increased coronary flow velocities were not associated with any corresponding increase in local stroke work in the region of myocardium supplied by the LAD; whether expressed per beat or per minute, local stroke work consistently decreased, mainly as the result of correcting aortic valve disease [2, 3].
Myocardial function and blood flow are normally well matched both at rest and during stress [18]. The association of an increase in coronary flow velocity-time integral with a decrease in myocardial stroke work, rather than the increase that might have accounted for the increased flow velocities early after operation, thus represents a clear departure from normality, which needs to be explained. Disturbed flow-function relations are well recognized during myocardial ischemia and with reperfusion, particularly in the setting of stunning [5, 17, 18]. The disturbance found in the present study differed from those in that there was striking hyperemia, as shown by a substantial increase in velocity-time integral as well as a great decrease in myocardial mechanical output, which resulted from correcting the aortic valve disease. The increase in velocity-time integral was approximately 1.5 to 1.9-fold, which is compatible with its being limited by the coronary reserve (1.6 fold) of hypertrophic myocardium associated with aortic valve disease [19]. In 20 hours follow-up, both the extent and the time course of resolution of the disturbance to flow velocity was mirrored by that of the function. Relative changes in either flow velocity or function were similar between the cold and warm blood cardioplegia, although the extent of change in the ratio was greater after the latter, which we previously have shown to be associated with less satisfactory preservation of myocardial physiologic response to the correcting of aortic valve disease [4]. We were thus unable to dissociate the changes in coronary flow velocity and myocardial function; therefore, we conclude that the disturbance of coronary flow velocity should be regarded as a manifestation parallel to the depressed mechanical activity, which has been well documented as occurring after reperfusion of hypertrophic myocardium after a period of cardioplegia [4]. If this is the case, it follows that the increased flow velocities are an additional marker of myocardial injury; whether their presence is in itself harmful, or whether they are a compensatory mechanism, our observations provide no definite answer.
This study has a number of limitations. We have assumed that changes in the relatively small region of myocardium studied by M-mode echocardiography represent the entire region supplied by LAD flow. In the absence of significant coronary artery disease, major regional differences would not be expected. Nevertheless, we were unable to estimate the myocardial mass perfused by the LAD in individual patients, although it is unlikely to have changed during the operation. Differences in absolute values of the stroke work to velocity– time integral ratio between patients are thus subject to corresponding variation, but proportional changes with operation less so. The requirement for inotropic drug administration, although higher in patients randomly assigned to warm blood cardioplegia, was determined by purely clinical considerations. An increased inotropic requirement must, therefore, be regarded as a consequence of the warm blood cardioplegic regimens, as it applied clinically to patients with left ventricular hypertrophy, and not as a confounding factor. In fact, the analysis of variance demonstrated that inotropic drug administration itself was not a determinant of the disturbed flow-function relationship. The absence of difference in measurements of inotropic state between patients given inotropic agents and those who were not bears witness to the general effectiveness of the clinical criteria that governed their use in individual patients. Reliable measurements of flow profile and transverse diameter of the proximal LAD are beyond the capability of current transesophageal echocardiographic techniques, but any changes in the flow are likely to be in the same direction as changes in flow velocity [20], although the flow velocity might have underestimated flow itself during reperfusion when the coronary arteries usually dilate [21]. The series of patients we studied was relatively small and thus might have insufficient power to detect differences in flow velocity alone between cold and warm blood cardioplegia, which approached but did not attain statistical significance. However, even with the number of patients studied, the ratio of stroke work to the flow velocity, which combined both components of the response to cardioplegia, readily discriminated between them. As myocardial blood flow and coronary sinus saturation were not quantified, we did not define whether the decrease in the ratio of stroke work to velocity time integral could in part be explained by a reduction in myocardial mechanical efficiency [5], which is obviously an important subject for future study.
In summary, the well-known depression of myocardial function that immediately follows cardiopulmonary bypass is accompanied, in the hypertrophic left ventricle, by abnormally increased coronary flow velocities. These two disturbances move in parallel with one another, both in their development and in their spontaneous partial recovery in the first 20 hours after the reperfusion. We believe, therefore, that both should be regarded as components of the myocardial response to a period of cardioplegia, and we suggest that considering them together and using the simple ratio of the two could be a more sensitive means than measuring either stroke work or flow-velocity time integral alone for detecting and quantifying myocardial injury. This is particularly true after correcting heart valve disease, when the operation itself has a major effect on ventricular loading and thus myocardial work. By using flow velocity in addition to function, it was possible to detect even subtle differences between warm and cold blood cardioplegia on cardiac function, when measurements of flow velocity or function alone were inconclusive. This approach might provide a sensitive means of monitoring the quality of myocardial preservation and the effectiveness of pharmacologic and other procedures used to maintain cardiac function, as well as providing insight into basic mechanisms underlying myocardial injury.
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Acknowledgments
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Supported in part by grants from British Heart Foundation (New Clinical Initiative 3014178), Wellcome Trust (ASW2, 1992), and the Royal Brompton Hospital Special Cardiac Fund.
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Abstract
Introduction
