Eur J Cardiothorac Surg 1999;16:324-330
© 1999 Elsevier Science NL
The effects of cardioplegia on coronary pressure–flow velocity relationships during aortic valve replacement
Xu Y. Jin,
Derek G. Gibson,
John R. Pepper
Departments of Cardiac Surgery and Cardiology, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK
Corresponding author. Tel./fax: +44-171-351-8530
e-mail: a.garrick{at}rbh.nthames.nhs.uk
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Abstract
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Objective: The acute physiological response of the coronary circulation to aortic valve replacement (AVR) has not been fully elucidated. This study aimed to characterize the changes in coronary perfusion pressure-flow velocity relationships, and to test whether this relationship is affected by cardioplegic method. Methods: Nineteen patients (mean age 67±12 (SD) years, 9 males) undergoing aortic valve replacement who received either cold blood cardioplegia (CBC, n=9) or warm blood cardioplegia (WBC, n=10), were prospectively studied before and 30 min after the operation, using transesophageal Doppler echocardiography combined with high fidelity left ventricular (LV) and aortic pressures. We thus determined: (1) Diastolic flow velocities in proximal anterior descending coronary artery (LAD), and simultaneous aorta to LV pressure differences. (2) The slope (LAD proximal linear resistance) and pressure intercept (zero flow pressure) of this relationship. (3) Overall LAD linear resistance as the ratio of mean diastolic flow velocity to mean pressure difference between aorta and left ventricle. (4) LV myocardial stroke work. Results: Following operation, myocardial stroke work fell from 5.2±2.7 to 3.0±1.7, mJ cm-3 (P=0.001), LAD mean diastolic flow velocity increased from 47±19 to 74±21, cm s-1 (P=0.0002). LAD overall linear resistance fell (0.75±0.24 vs. 1.26±0.26, mmHg cm-1 s, P=0.001). LAD proximal linear resistance, however, remained unchanged (P=0.21), but the zero flow pressure fell (18±12.6 vs. 27±12.2, mmHg above LV end diastolic pressure, P=0.013). With similar fall in myocardial work postoperatively, there was a greater fall in zero flow pressure after WBC than CBC (48±28 vs. 19±13,% of pre-op, P=0.012), and a greater increase in flow velocity time integral (127±81 vs. 53±59,%, P=0.039). Conclusion: Instantaneous diastolic LAD pressure-flow velocity relations in the early postoperative period can be explained more satisfactorily in terms of zero flow pressure and proximal linear resistance than simple resistance alone. The fall in zero flow pressure alone explains the increase in LAD flow velocity immediately after aortic valve replacement. The extent of this fall is greater after warm rather than cold blood cardioplegia.
Key Words: Coronary pressure–flow velocity relationship • Aortic valve replacement • Cardioplegia • Doppler echocardiography
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1. Introduction
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The acute response of the coronary circulation to cardiopulmonary bypass has been extensively investigated [1–4]. Coronary resistance, calculated as the simple ratio of perfusion pressure to its flow rate, has variably been found to rise [2] or fall [3,4] immediately after cardiac surgery. These changes may be related to the diverse nature and extent of coronary vascular injury by cardioplegia and reperfusion [5]. The precise mechanisms underlying changes in coronary resistance remain incompletely understood. It is possible that the simple ratio of pressure to flow may not adequately characterise coronary hemodynamics. Indeed, the existence of a finite coronary zero flow pressure [6,7], which is assumed to be zero in the orthodox definition of resistance, may play an important role in determining flow and thus the acute response of coronary circulation during cardiac surgery.
In the clinical setting, flow velocities in the proximal coronary arteries can be reliably measured by transesophageal echocardiography [8,9]. Changes in coronary flow velocity profile several weeks after aortic valve replacement have been documented [10,11], but few studies have been reported during the operation itself. We have previously found that retrograde warm blood cardioplegia resulted in a less satisfactory protection of hypertrophic myocardium than cold blood cardioplegia [12]. However, it is not clear whether the cardioplegia method also has an independent effect upon the coronary hemodynamic response. Taking advantage of the relative stability and accessibility of intra-operative conditions, we have combined measurements of coronary artery flow velocity with simultaneous perfusion pressure and myocardial stroke work, derived from aortic and left ventricular (LV) micromanometers and simultaneous LV echocardiogram. This approach enabled us to incorporate the waterfall approach in assessing the acute effects of aortic valve replacement on the coronary pressure-flow velocity relationship, and the possible influence of cardioplegic methods.
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2. Methods
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2.1. Subjects
We studied 19 patients undergoing elective isolated aortic valve replacement for predominant valvular aortic stenosis (16 patients) or regurgitation (3 patients), with a mean age 67±12 (mean±SD) years; 9 patients were male. LV mass index was 195±45g m-2 measured by M-mode echocardiography using standard criteria [13]. Patients with clinically significant coronary artery disease (>50% of stenosis in diameter) at prior coronary angiography, or in whom echocardiographic recordings were inadequate for analysis were not included. This study is a part of a clinical research project approved by the Ethics Committee of the Royal Brompton Hospital. Written informed consent was obtained from all participants. There was no early mortality, morbidity, or side effects due to this study.
Patients were studied under general anesthesia, maintained with fentanyl (20 to 50 µg kg-1), pancuronium oxide (0.1 mg kg-1). A Swan-Ganz thermodilution balloon tip catheter was positioned with its tip in the pulmonary artery after induction of anesthesia and used for hemodynamic measurements. Cardiopulmonary bypass was routinely established using membrane oxygenator and roller pump, with hemodilution (hematocrit value 20-25%), and systemic hypothermia (28°C nasopharyngeal temperature, when using cold blood cardioplegia, 9 patients), or with normothermia (37°C), in 10 patients in whom continuous retrograde warm blood cardioplegia was given by a randomised approach which has been reported previously in detail [12].
2.2. Protocols
2.2.1. Measurement of coronary blood flow velocity
A 5 MHz biplane transesophageal echocardiographic transducer (HP 21362C) interfaced with a Hewlett Packard 77025A Sonos 500 or 1500 Ultrasound System was positioned after induction of anesthesia. From the transesophageal horizontal view at aortic valve level, the proximal left anterior descending coronary artery (LAD) was located on the two dimensional colour flow image. LAD blood flow velocity was recorded by 5 MHz pulsed Doppler with the sample volume (1 mm) placed at its proximal one third, i.e. 2–3 cm distal to the bifurcation of anterior descending and circumflex arteries [8,9]. Records were made at a paper speed 100 mm s-1 with simultaneous electrocardiogram, LV pressure and aortic root pressure, before the onset of cardiopulmonary bypass in a stable hemodynamic state, and repeated 30 min after the cardiopulmonary bypass had been weaned off, with the chest still open (Fig. 1).
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Fig. 1. Simultaneous recordings of electrocardiogram, flow velocity of left anterior descending coronary artery, and high fidelity pressures in left ventricle and aortic root from a representative patient, with paper speed of 100 mm s-1. (A) Before cardiopulmonary bypass; (B) immediately after aortic valve replacement. Note that there was a significant increase in coronary flow velocity after the operation, particularly in mid and late diastole.
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2.2.2. Measurement of ascending aortic and LV pressures
Once the pericardium had been opened, a 4 F catheter tip pressure transducer (Gaeltec CTC/4F/USCI, Gaeltec Ltd, Isle of Skye, UK) was introduced into the left ventricle with its tip located in the mid-portion of the cavity via the roof of the left atrium and across the mitral valve [12,14]. Another similar 4 F catheter was introduced directly into the ascending aorta with its tip at coronary ostial level as confirmed on the echo image. Both signal outputs were filtered with an upper cutoff frequency of 1 kHz, pre-amplified (Gaeltec S7b, Gaeltec Ltd), and transferred to two auxiliary lines of the echocardiograph. The pressure transducer tipped catheters were calibrated electrically before the initial measurement at the same zero level. Zero pressure was taken as atmospheric. The pulmonary artery wedge pressure was used to identify the LV end-diastolic pressure.
2.2.3. Measurement of LV dimension and wall thickness
M-mode echocardiogram of LV minor axis and anterior wall thickness was recorded with simultaneous cavity pressure and electrocardiogram [12,14].
Baseline measurements of coronary flow velocity, pressures and LV dimension were made before the cannulation of cardiopulmonary bypass, and these were repeated at immediately after weaning off cardiopulmonary bypass (approximately 25–30 min reperfusion) prior to any requirement of inotropic drug was administrated. After the study, the catheters were removed, and checked against an air-operated dead-weight balance (Budenberg Gauge Co. Ltd, London, UK) [12,14].
2.3. Digitizing and calculations of coronary flow velocities and hemodynamics
We measured values of early, end, and mean diastolic aortic pressure, of early (minimum) and end diastolic LV pressure, and of LAD early (peak), end diastolic flow velocity. The time integral of LAD flow velocity was computed and expressed in per beat and per minute. We also digitized aortic and LV diastolic pressures with simultaneous LAD flow velocity. The orthodox LAD linear resistance was calculated as the ratio of mean diastolic pressure difference between aorta and left ventricle to the mean diastolic LAD flow velocity. We continuously plotted LAD flow velocity against the pressure drop between aorta and left ventricle during diastole (Fig. 2). From these plots, we measured the slope which defines LAD proximal linear resistance (mmHg cm-1 s-1), and its intercept on the pressure axis, zero flow pressure, in mmHg [6,7,15], and referenced to LV end-diastolic pressure.
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Fig. 2. Plots of flow velocities of left anterior descending coronary artery versus pressure differences between the aorta and left ventricle during mid-later diastole with every 10 ms from a representative patient are shown. Using linear regression analysis, the pre-operative (circles) and post-operative (triangles) relationship of pressure differences (X) and flow velocities (Y) were: X=22.2+0.78Y (r=0.96) and X=-1.7+0.88Y (r=0.95), respectively. The major change of flow velocity-pressure relation was a significant fall in pressure intercept (zero flow pressure), from 22.2 mmHg to -1.7 mmHg, while the proximal linear resistance showed little change.
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We have previously described methods of measuring myocardial stroke work in detail [12,14]. In brief, left ventricular circumferential wall stress and shortening velocity were determined by digitising the simultaneous M-modes of the left ventricle to derive cavity dimension and anterior wall thickness along with cavity pressure. Myocardial power was defined as the product of instantaneous circumferential wall stress and shortening velocity throughout systole. Myocardial stroke work was calculated as the time integral of instantaneous myocardial power during systole. Values of myocardial stroke work were indexed to a cubic centimetre of myocardium.
2.4. Statistical methods
Data are presented as mean±1 standard deviation. Minitab statistical software (PC Version, Release 8, 1991, Minitab Inc., USA) [16] was used for statistical analysis. Normal distribution of data was checked using normal probability plots and was within 95% confidence interval. Plots of coronary flow velocity against pressure drop were analysed by linear regression. Paired t-tests were used to compare changes in these characteristics of coronary flow-velocity pattern before and after valve replacement. Unpaired t-tests were performed to define the difference between orthodox linear resistance and proximal linear resistance, the difference in LAD hemodynamics between the two cardioplegia groups, expressed in absolute and percentage terms. Between-patient interrelations were examined by stepwise regression analysis. The reproducibility of measurements of LAD flow velocity and zero flow pressure was assessed by inter-beat variation. This was first examined by a paired t test of the values of two beats taken from same patient and same study, and then the root mean square of the inter-beat difference was expressed as the percentage of the mean, representing the coefficiency variation. P<0.05 was taken as being statistically significant.
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3. Results
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3.1. Patients
Age, gender and aortic valve disease (stenotic/regurgitation: 8/2 vs. 8/1) did not differ between the groups, nor did the LV mass index (190±46 vs. 194±68, g m-2) or intraoperative aortic cross clamp time (102±15 vs. 97±16 min), all P>0.05 (insignificant). The aortic valve was replaced with a bioprosthesis with a mean size 25±2.4 mm. Normal performance of the bioprostheses was confirmed by transesophageal echocardiography post-operatively. The mean cardiopulmonary bypass time was 129±17 min.
3.2. Changes in myocardial wall stress and stroke work (Table 1)
There was a prompt fall in ventricular peak systolic stress after the operation, and a significant fall in myocardial stroke work.
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Table 1. Changes in LAD flow velocity, aortic and left ventricular diastolic pressures after aortic valve replacement (mean±SD)a
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3.3. LAD flow velocity
Typical recordings of proximal LAD blood flow velocity before and immediately after the operation are shown in Fig. 1. Peak LAD flow velocities occurred during early diastole, those during systole being considerably less, and often retrograde in direction. Preoperatively, the peak diastolic blood velocity had a mean value of 56 cm s-1, falling to 37 cm s-1, at end diastole. Thirty minutes after the reperfusion and weaning off cardiopulmonary bypass, both early diastolic and end diastolic flow velocities were significantly higher than the corresponding values before, each by approximately 20 cm s-1. There was thus a significant increase in velocity time integral expressed as centimetre per beat (Table 1).
3.4. Coronary pressures
There was no significant change in peak aortic diastolic pressure. Due to the fall of aortic diastolic pressure became greater after the operation (from 16 mmHg to 22 mmHg), the mean aortic diastolic pressure fell by 6 mmHg correspondingly. Left ventricular minimum pressure pre-operatively was 9 mmHg, increasing to 14 mmHg at end diastole. These values were not consistently different 30 min after operation (Table 1).
3.5. Interrelations between LAD flow velocity and driving pressure (Table 1)
LAD overall linear resistance calculated in the orthodox way fell by more than 40% (P=0.0001) immediately after operation, but the slope of instantaneous LAD flow velocity against the difference between aortic and LV pressure did not change significantly. Instead, their intercept on pressure axis fell in all patients from its mean value of 27 mmHg above left ventricular end diastolic pressure to 18 mmHg (P=0.013) after operation. As the standard deviation of the intercept remained approximately 40% of the mean value, the pressure intercept approached towards zero in individual patients after operation. The comparison of LAD overall linear resistance (by orthodox calculation) and the proximal linear resistance (by waterfall approach) also revealed that the former was consistently greater both before operation (1.26±0.36 vs. 0.56±0.27, mmHg cm-1 s, P<0.001) and afterwards (0.75±0.24 vs. 0.46±0.24, mmHg cm-1 s, P=0.006).
3.6. Determinants of LAD flow velocity
Independent determinants of mean LAD diastolic flow velocity between patients were defined by stepwise regression analysis, against mean aortic diastolic pressure, LAD proximal linear resistance, and pressure intercept (LAD zero flow pressure), preoperatively and post-operatively. Before operation, aortic mean diastolic pressure, LAD linear resistance and pressure intercept all proved to be independent determinants of flow velocity in individual patients. In total, these three factors accounted for about 82% of the variance of mean LAD flow velocity both before and after operation (Table 2). There was no univariant linear correlation between left ventricular mass and any aspect of coronary flow velocity.
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Table 2. Stepwise regression analysis of determinants of mean LAD diastolic flow velocity before and after aortic valve replacement (n=19)
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3.7. Effects of cardioplegia method
Before operation, there was no statistically significant difference between the patients who were to receive cold or warm blood cardioplegia with regard to aortic and left ventricular diastolic pressures, LAD flow velocity, linear resistances, zero flow pressure, or myocardial stroke work. Following surgery, however, the percentage fall in zero flow pressure, with respect to LV end diastolic pressure, was greater with warm, compared with cold, blood cardioplegia (P=0.012). Warm blood cardioplegia was also associated with a larger percentage increase in LAD flow velocity time integral (P=0.039) than cold blood cardioplegia. Peak LAD flow velocity, proximal and overall coronary resistances, and myocardial peak wall stress and stroke work did not differ between the two groups (Table 3).
3.8. Reproducibility
There was no consistent inter-beat difference in measuring LAD flow velocity or zero flow pressure when examined by paired t-test. The corresponding coefficiencies of variation were 5.7% and 4.0%, respectively.
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4. Discussion
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Flow velocities from proximal LAD have previously been recorded using transesophageal echocardiography [8] and have been validated against invasive methods [9]. Since Bellamy's [6] first proposal of using waterfall approach in elucidating the hemodynamics of coronary vascular bed, similar LAD pressure-flow velocity interrelations in humans with normal coronary arteries have been recorded using flow velocity measurements derived by intra-coronary Doppler [7]. In recent years, coronary pressure-flow velocity relationship has been applied to assess the effects of coronary artery stenoses [17,18]. However, simultaneous high fidelity pressures in left ventricle and aorta have not been recorded along with LAD flow velocity in aortic valve disease or during aortic valve replacement, nor in previous studies of coronary flow velocity profiles observed weeks or months after the valve replacement [10,11]. Our results demonstrate that immediately after correcting aortic stenosis, blood flow velocity is greatly increased in the proximal LAD, while regional myocardial wall stress and stroke work have both fallen. In order to investigate the mechanism for this increase, we also recorded high fidelity aortic and LV pressures, so that instantaneous values of flow velocity could be correlated with the corresponding pressure difference, representing driving pressure. In the range that we measured, a linear relation between the two was demonstrated (Fig. 2), but this relation was associated with a positive pressure, with a mean value of 27 mmHg above LV end-diastolic pressure, the zero flow pressure. These finding are similar to previous studies involving pressure–flow relation [6,7], allowing for the difference between LV end diastolic and atmospheric pressure. The presence of such an intercept has been taken to imply that extrapolation beyond the measured range leads to flow velocity falling to zero at finite driving pressure [6,7]. Blood flow in the proximal LAD can thus be considered to behave resistively in that there is a linear relation with pressure throughout diastole within the physiological range, whose slope defines proximal linear resistance [15]. Direct demonstration that flow does, in fact, fall to zero at the predicted pressure in the beating heart presents obvious difficulties under clinical conditions; the long diastolic pause necessary for flow to fall might alter the properties of the micro circulation, while the use of vasodilators, such as adenosine, to slow the heart [7,9,17,18] would add a further complication. The mechanism underlying the positive pressure intercept remains uncertain. It has been explained in terms both of a vascular waterfall, and also a large intra myocardial capacitance with a long time constant [15,17]. From practical point of view, therefore, we regard slope and intercept simply as potentially independent descriptors of the observed linear relation between diastolic flow velocity and pressure.
4.1. Limitations of the study
This study has limitations. For obvious reasons, we did not investigate normal subjects, though all our patients had normal coronary arteriograms, and all were under general anesthesia. We deliberately chose patients with aortic valve disease, since left ventricular hypertrophy provides an exacting test of myocardial preservation, and since the unequivocal fall in regional myocardial work [12,14] with operation allows the effect of loading to be clearly dissociated from the increased coronary flow velocity. We avoided patients with coronary artery disease since the presence of regional stenosis, and subsequent bypass grafting would have made the interpretation of proximal LAD velocities problematic and since the effect of operation on ventricular loading in such patients would have been less decisive. Clinical investigation imposes constraints. The number of patients studied was small, but the protocol was highly invasive, so we used the minimum to support our conclusions. The aortic pressure sensor had to be removed before the sternum was closed, so the study period was correspondingly reduced. As with all Doppler measurements, flow velocity rather than volume flow was recorded, so we did not need to make assumption about flow profile or arterial cross sectional area. Any changes in the flow are likely to be in the same direction as those in flow velocity [19], therefore, when flow velocity is zero in epicardial vessels, so is volume flow. Information about flow velocities in more distal vessels would clearly have been of interest, but this is beyond the capability of the methods we used. We defined driving pressure using left ventricular diastolic pressure as the base line to minimise the effects of variation in the latter [20]. Using atmospheric pressure would not have altered our conclusion. In order to determine the more physiological reference pressure however it would have been necessary to study patients in whom heart rate was slower, end-diastolic pressure higher, and proximal resistance lower than in the present study.
4.2. Clinical implications
Our results demonstrate that immediately after the termination of cardiopulmonary bypass following aortic valve replacement, blood flow velocities are conspicuously increased in the proximal LAD. This increase cannot be attributed to increased hemodynamic demand, since regional work in the myocardium subtended by the LAD has fallen, or to the effects of general anesthesia or inotropic drug administration. We believe, therefore, that it represents a direct effect of cardioplegia which leads to loss of the normal balance between myocardial flow and function [21]. Such an increase occurring at effectively constant aortic perfusion pressure might well be attributed to a fall in classical overall coronary vascular resistance. However, analysis in terms of instantaneous pressure-flow velocity indicates that it is, in fact, mediated by a fall in the pressure intercept. Paradoxically, proximal vascular resistance defined as the slope of the driving pressure-flow velocity relation remained unchanged. In contrast, inter-patient variance in pre- and postoperative flow velocities depended on perfusion pressure and proximal resistance and only partially correlated to zero flow pressure. We therefore hypothesised that a fall in zero flow pressure might be used as a marker of the disturbance caused by cardioplegia, thus to distinguish it from other mechanisms accounting for the increase of proximal coronary flow velocity.
In order to test this idea, we investigated differences between warm and cold blood cardioplegia, since we have previously shown that in similar patients, departures from normal physiology were greater with the former [12]. In the present study, it was apparent that with similar changes in myocardial loading and stroke work, the fall in zero flow pressure was more than twice as greater with warm blood cardioplegia, although the two cardioplegic regimes could not be differentiated in terms of simple coronary linear resistance alone. The increase in flow velocity time integral was also larger with warm blood cardioplegia, where it amounted to 130% of baseline, suggesting that it approached the value of coronary reserve previously reported for hypertrophied myocardium [22]. Whether these increases represent a mechanism of disease or simply a marker of disturbed physiology, we have no definite evidence. The patients we studied were selected to be at low risk, and there was thus no mortality or detectable morbidity. However, we note that inappropriate coronary vasodilatation induced by dipyridamole or adenosine in the setting of myocardial perfusion imaging is a very predictable way of inducing regional ischemia in patients with coronary artery disease [23].
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5. Conclusion
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Immediately after aortic valve replacement, flow velocities are considerably increased in the proximal LAD coronary artery. This increase occurs in spite of a fall in regional myocardial work, and appears to represent a direct effect of cardioplegia. Analysis in terms of pressure-flow velocity relations show that, unlike the variances in flow velocity occurring before or after operation, it is mediated by a fall in zero flow pressure. This fall is greater with warm blood cardioplegia. Whether this greater departure from normality represents a detrimental effect of warm blood cardioplegia which we have previously shown to cause a less physiological myocardial response than cold blood cardioplegia [12], or whether it demonstrates more rapid correction of intraoperative ischemic stress occurs at a higher temperature we are still uncertain. Nevertheless, we suggest that these characteristic alterations in coronary hemodynamics may be a marker for disturbances associated with cardioplegia, allowing them to be quantified, and even giving information about their basic underlying mechanisms.
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Acknowledgments
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This study was supported by grants from the British Heart Foundation (New Clinical Initiative, 3014178), Wellcome Trust (ASW2, 1992) and the Royal Brompton Hospital Special Cardiac Fund, London, UK.
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Received December 21, 1998;
received in revised form May 31, 1999;
accepted June 7, 1999.
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Abstract
1. Introduction
