Ann Thorac Surg 1999;67:139-145
© 1999 The Society of Thoracic Surgeons
Original Articles
Early changes in the time course of myocardial contraction after correcting aortic regurgitation
Xu Y. Jin, MDa,
John R. Pepper, FRCSa,
Derek G. Gibson, FRCPb,
Magdi H. Yacoub, FRCSa
a Departments of Cardiac Surgery, Royal Brompton Hospital and Lung institute, London, England United Kingdom
b Cardiology, Royal Brompton Hospital and National Heart and Lung Institute, London, England United Kingdom
Accepted for publication June 28, 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. Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function.
Methods. We studied 18 patients (mean age, 59 ± 12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured.
Results. Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58 ± 31 mL versus 80 ± 30 mL, p = 0.004) and stroke work index (250 ± 86 mJ/m versus 401 ± 198 mJ/m, p = 0.005), but systemic arterial pressure (79 ± 11 mm Hg versus 65 ± 10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0 ± 1.3 mJ/cm versus 4.8 ± 2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475 ± 91 ms versus 543 ± 67 ms, p < 0.001). Diastolic time increased from 34% ± 18% to 71% ± 33% of systolic pulse duration (p < 0.001).
Conclusions. Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.
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Introduction
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Since the early 1960s [1], aortic valve replacement has become well established as a means of managing aortic regurgitation. It corrects left ventricular volume overload, allows cavity size to decrease, and in particular, prevents the development of left ventricular disease [2, 3]. Although the hemodynamic rationale for its correction can readily be appreciated in patients with a significantly dilated ventricle and impaired systolic function, for patients with moderately severe aortic regurgitation and mildly impaired systolic function, optimal timing of valve replacement is harder to define [4, 5]. This is partly because the physiologic changes in the left ventricle after valve replacement remain incompletely understood, and partly because of the suboptimal performance of some valve prostheses. The aortic homograft or the recently introduced porcine stentless valve offers least resistance to ventricular ejection [6]. Therefore, we have undertaken a prospective study of the changes in left ventricular function in terms of force–velocity relationship and timing of myocardial contraction in response to correcting aortic regurgitation with a stentless valve.
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Material and methods
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Patient population
Eighteen patients undergoing elective aortic valve replacement for aortic regurgitation in the Royal Brompton Hospital were investigated; these patients had satisfactory recordings of transesophageal echocardiograms and high fidelity left ventricular pressure. The ages ranged from 24 to 75 years (59 ± 12 years, mean ± standard deviation) and 14 were men. Preoperatively, all patients had significant clinical symptoms, with New York Heart Association functional class II or III. The grade of aortic valve regurgitation was moderately severe (in 12 patients) or severe (in 6 patients) defined by either aortic angiogram or echocardiogram. No patient had a previous myocardial infarction. Preoperative coronary angiography revealed greater than 75% stenosis in the circumflex or right coronary in 4 patients and they received aortocoronary bypass grafting. Preoperative ejection fraction of the left ventricle was 45% ± 16%; those who had significant hypokinetic wall motion on left ventricular angiograms or echocardiogram were not included in this study. Left ventricular mass index was 222 ± 76 g/m measured by M-mode echocardiography [7], with a mean body surface area of 1.84 ± 0.25 m2. All patients were in sinus rhythm throughout the study, although atrial pacing was temporally used in 3 patients when the heart rate decreased below 60 beats/min. No patients required significant dosage of a positive inotropic drug (defined as intravenous dopamine infusion over 5 µg · kg-1 · min-1). This study was part of a clinical research program, approved by the Ethics Committee of Royal Brompton Hospital. Written informed consent was obtained from all participants. There were no side effects of this study.
Operative techniques
The patients were ventilated with 100% oxygen. General anesthesia was maintained with fentanyl (20 to 50 µg/kg) and pancuronium oxide (0.1 mg/kg). A radial artery catheter and a Swan-Ganz thermodilution balloon tip catheter with its tip in the pulmonary artery were positioned after induction and used for hemodynamic measurements. Cardiopulmonary bypass was established with routine techniques. The heart was arrested and preserved using blood cardioplegia. All valve replacements were performed by J.R.P. or M.H.Y. The aortic valve was replaced with an aortic homograft valve in 12 patients, a Toronto stentless porcine valve in 6. The mean size of valve prosthesis was 25 ± 2.4 mm. No patient had significant postoperative aortic regurgitation. Cardiopulmonary bypass time was 115 ± 25 minutes and aortic cross-clamp time was 105 ± 23 minutes. After the operation, the patients were transferred into the intensive care unit under continuous sedation (morphine 1 mg/h and propofol 50 to 100 mg/h, intravenously) and controlled ventilation (oxygen concentration 40% to 50%, inspiration and expiration ratio 1:2, with 1 to 2 mm Hg of positive end expiration pressure).
Facilities and protocols
A 5-MHZ biplane transesophageal echocardiographic transducer (HP 21362C, Hewlett-Packard, Andover, MA) was positioned in the esophagus after induction and connected to a Hewlett Packard 77025A Sonos 500 Ultrasound System. Once the pericardium was opened, a 4F pressure transducer tip catheter (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 ventricle, through the right superior pulmonary vein and across the mitral valve. The transducer has a sensitivity of 5 µV/V per mm Hg, bridge resistance 2.0 K
. Its signal output was filtered and preamplified (Gaeltec S7b; Gaeltec Ltd) and transferred into the auxiliary line of the echocardiographic system. The transducer tip pressure catheter was calibrated before the initial measurements were made and checked with an air-operated dead-weight balance (Budenberg Gauge Company Ltd, London, England) after the study when the catheter had been removed [8, 9]. The diastolic pulmonary artery wedge pressure was used to identify the left ventricular end-diastolic pressure. Zero pressure was referenced to atmosphere. After the final measurement, the transesophageal echotransducer and transducer tip pressure catheter were removed, sedation was discontinued, and the patients were weaned off ventilation within 2 to 3 hours.
Using a transgastric short axis view of the left ventricle, a two-dimensional-directed M-mode echocardiogram of the minor axis at the level of the papillary muscle tips was used to display cavity dimension and myocardial thickness and printed on paper at a speed of 100 mm/s, with a simultaneous left ventricular pressure trace and electrocardiogram (Fig 1 ). Systemic and left ventricular hemodynamic measurements, including heart rate, pulmonary artery wedge pressure, and cardiac output, were recorded simultaneously with each echocardiographic study. Baseline measurements were made before cannulation for cardiopulmonary bypass when hemodynamic state was stable. Further measurements made at 0.5, 1, 3, 6, 12, and 20 hours after the final removal of the aortic cross-clamp (taken as zero time for postoperative measurements).
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Fig 1. Serial recordings of transesophageal M-mode echocardiograms (ECG) of left ventricular minor axis with simultaneous high fidelity left ventricular pressure (LVP) and electrocardiogram from a patient undergoing aortic valve replacement (AVR) for aortic regurgitation. Note that the significant decrease in the duration of systolic pressure pulse immediately after the valve replacement, with little change in peak systolic pressure, cavity size, or heart rate by 14 hours after the operation.
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Measurements and calculations
From the left ventricular short axis M-mode echocardiogram and pressure trace, the dimension, anterior and posterior wall thicknesses, and left ventricular pressure were digitized offline along with the same cardiac cycle and time calibration [8, 9]. At least three successive heart beats were digitized at each time interval and mean values derived. From the digitized output and hemodynamic data, the following variables were determined.
Left ventricular dimension and wall thickness
Left ventricular short axis dimension, anterior and posterior wall thickness at end-diastole; peak velocity of dimension shortening, and the ratio of wall thickness to the radius were determined.
Left ventricular pressure and stress
From the left ventricular pressure pulse, we determined peak systolic pressure, mean ejection pressure (mLVEP), end-diastolic pressure (LVEDP), peak rate of ventricular pressure increase (peak +dP/dt) and decrease (peak -dP/dt). Left ventricular ejection time was defined as the time interval between the two peaks. The timing of peak LV -dP/dt was checked against aortic valve closure (A2) on the M-mode aortic echogram. We used the method of Falsetti and colleagues [10] to calculate circumferential mid-wall stress. This relates to an annulus of myocardium perpendicular to the long axis of the ventricle, which is assumed to be circular in cross-section, with an internal diameter equal to the echocardiographic dimension. The long axis of the ellipsoid was predicted from the echocardiographic dimension using regression equations derived from a previous study [11]. The average circumferential stress is given by:
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where P = ventricular pressure, L = major axis, D = minor axis, and T = wall thickness. Wall stress was plotted continuously throughout the cardiac cycle, and its peak value during systole was measured.
Time course of left ventricular pressure development
From the trace of the first differential of left ventricular pressure with respect to the time (dP/dt), we measured (1) early systolic period: the time from the onset of the positive deflection of left ventricular +dP/dt to its peak value; (2) late systolic period: from the peak systolic pressure to the time when the ventricular pressure decreased to the level of end-diastolic pressure; and (3) diastolic period: the whole cardiac cycle minus the sum of early and late systolic period and QRS duration. From these determinations, the ratio of diastolic time to RR interval and to systolic period was calculated. In addition, the values of ejection time index were calculated from the measured values taking into account heart rate and gender according to established regression equations [12], and differences between these indices and the corresponding normal values were determined in individual patients at each study time point.
Regional myocardial power and stroke work
In systole, the rate at which the myocardium does external work (ie, the power that it develops) is given by the product of instantaneous circumferential wall stress and shortening rate. Stress was referred to a position in the mid-wall. Its circumference at this point is given by
and the shortening rate as its first differential with respect to time. Values of local power were normalized to refer to a cubic centimeter of myocardium at end-diastole and plotted continuously throughout the cardiac cycle. The time integral of power during systole gives the stroke work [8, 9].
Systemic and left ventricular hemodynamics
In the presence of aortic regurgitation, thermodilution cardiac output measured in the pulmonary artery reflects net systemic forward flow rate (systemic cardiac output), from which systemic stroke volume index was determined, and systemic stroke work index (SWIsys) were calculated as SVIsys x mBP x 0.0133 x 9.8, in millijoules per meter squared [13], where mBP is mean systemic blood pressure. Total left ventricular stroke volume was estimated by the changes in left ventricular short axis dimension between end-diastole and end-systole as measured by echocardiography. The corresponding left ventricular volumes, and thus the stroke volume (LVSVI) and ejection fraction was calculated by the Teichholz formula [14]. Left ventricular stroke work index was calculated by
in millijoules per meter squared [13]. Finally, aortic regurgitant volume was defined as the positive balance between ventricular stroke volume and systemic stroke volume.
Reproducibility
Left ventricular ejection time and the total duration of systolic pressure pulse were remeasured in a random sample of 30% of the patients. The reproducibility of other measurements derived using identical methods has been reported previously [9].
Statistical methods
Data were presented as mean ± 1 standard deviation. Minitab statistical software (PC version, release 8, 1991; Minitab Inc, Philadelphia, PA) was used in the data analysis. A one-way analysis of variance was used to test the possible significance of the differences in mean values after the operation with respect to time. If the p value was less than 0.10, further paired multiple comparisons with 95% confidence interval (Dunnett’s method) were performed to identify significant differences between before bypass and each postoperative measurement, with a family error rate 0.050 and individual error rate 0.010. To examine reproducibility, the significance of differences between duplicate measures was first tested by a paired Student’s t test to exclude consistent discrepancies. Reproducibility was then calculated as the root mean square difference between the two determinations divided by their mean value, and expressed as a percentage. A p value of less than 0.05 was considered statistically significant.
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Results
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Changes in left ventricular and systemic hemodynamics
Immediately after aortic valve replacement, there was a slight decrease (with borderline statistical significance) in left ventricular preload assessed both by cavity dimension and volume at end-diastole. However, left ventricular stroke volume and stroke work decreased immediately after the operation, and the regurgitant volume across the aortic valve approached zero. Mean systemic blood pressure had increased at 3 hours after the operation, as did systemic stroke work index at 20 hours, although heart rate and systemic cardiac index remained unchanged (Table 1 ).
Changes in left ventricular regional and global systolic function
Correcting aortic regurgitation did not cause any early change in peak systolic pressure, wall thickness ratio, systolic wall stress, peak circumferential fibre shortening rate, or peak myocardial power. Although myocardial stroke work, in line with the global stroke work, decreased immediately after the operation and remained below baseline level for the rest period of the study, peak +dP/dt and ejection fraction of the left ventricle showed no early change with operation (Table 2 ).
The time course of left ventricular contraction
When compared with established normal values, left ventricular ejection time was prolonged by more than 30 ms preoperatively, whereas by 20 hours, it was 35 ms less than predicted. Further analysis of the time course of the systolic pressure pulse revealed that correction of aortic regurgitation did not alter the timing of early systole, including both isovolumic contraction and early ejection. However, the late systolic time was shortened consistently, a change effectively established by 1 hour after operation. The shortening of systolic pressure pulse and ejection time resulted in a significant increase of diastolic time, therefore the percentage of diastolic time at a given cardiac cycle increased by around 60% of baseline, and its ratio to systolic pressure pulse had doubled by 20 hours after operation (Table 3 ).
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Table 3. Changes in the Time Course of Left Ventricular Contraction, and the Time Ratio of Diastole to Systole (Mean ± Standard Deviation)
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Reproducibility
A random sample of timing measurement was repeated in 30% of the patients. A paired Student’s t test showed there was no significant difference between the two measures. The variability of the measurement, presented as the percentage of root mean square of the difference to the mean value, was 4.1% and 6.1% for the duration of systolic pressure and the ejection time, respectively.
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Comment
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The present study demonstrated that early after correcting aortic regurgitation there is a striking decrease in regional and global stroke work in the absence of significant regional change in cavity size or systolic wall stress, or globally, in peak systolic or end-diastolic pressure or in heart rate. In addition, our findings confirmed many previous results in demonstrating the favorable effects of correcting aortic regurgitation on overall left ventricular and systemic hemodynamics [2]. The prompt and significant decrease in left ventricular stroke volume appears to be mediated by variable changes in end-diastolic and end-systolic dimensions, which was accompanied by consistent change in myocardial stroke work.
Intensity of myocardial contraction
The aim of correcting aortic regurgitation is to reduce the mechanical work of the left ventricle to prevent ventricular disease. The failure of ventricular stress to decrease immediately after correcting aortic regurgitation has been reported previously [15] using crystalloid cardioplegia. Our study not only confirmed that correcting the regurgitation did not consistently lead to any early decrease in systolic wall stress even when ventricular systolic function was well maintained by using blood cardioplegia, but further demonstrated that myocardial power did not change either. Unaltered peak positive dP/dt and ejection fraction associated with a constant end-diastolic dimension and peak wall stress, respectively, also exclude significant early change in the intensity of myocardial contraction defined in terms of global left ventricular function. Nevertheless, there was a very consistent early decrease in regional and global myocardial stroke work. Because stroke work represents the time integral of myocardial power, a decrease in work at constant peak power strongly suggests that the time course of power development must have altered with operation.
Time course of myocardial contraction
Classic force–velocity relationships are concerned with the peak value of shortening rate when systolic load is varied or extrapolated to zero [16] and not with the duration of contraction. Examination of the time course of ventricular pressure development showed that the total duration of systolic ejection in fact did decrease by 20% to 30% immediately after the operation, which is fully in line with the decrease in stroke work. The idea that ventricular contraction might be prolonged in patients with aortic valve disease is not new but was explored more than 70 years ago by Katz and Feil [17] and has been investigated later by other investigators [18, 19]. Our study has demonstrated that changes in the time course of contraction form a major component of the early response of the myocardium to correcting aortic regurgitation. When the time course of ventricular pressure development was analyzed in terms of early and late systole using peak pressure as a landmark, it appeared that only the latter half was prolonged preoperatively and that only this component shortened after operation. It appears that correcting aortic regurgitation with a nonobstructive biological valve does not alter the peak value of regional wall stress or shortening rate but does cause a prompt decrease in the duration of ventricular systole and thus in stroke work (Fig 2 ). Although this shortening of left ventricular mechanical systole is likely to have been caused by the decrease in stroke volume [20], its underlying mechanism, in terms of local myocardial function is not entirely clear [21]. The time course of ventricular pressure decline is known to be very sensitive to loading conditions early in contraction [22]. In the present study changes in preload or afterload were insignificant, whereas the modest increase in arterial pressure would be expected to lengthen rather than shorten ejection time. It is possible that there was an increase in sympathetic activity but the absence of change in heart rate or peak positive dP/dt would be against this explanation. Furthermore, the promptness of shortening of mechanical systole cannot be attributed to changes in heart rate, whereas myocardial injury attributable to ischemia and reperfusion seems unlikely to have played a significant role when peak myocardial power and positive dP/dt remained unchanged. Finally, altered muscle protein expression appears inconceivable in such a short period. We conclude that, in general terms, the shortening of the latter half of systole seen in our patients was the early consequence of the sudden reduction in stroke volume ejected through a nonobstructive valve by a ventricle adapted to a volume overload and contracting with unchanged speed and intensity. However, further study is needed to define more specific mechanisms.
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Fig 2. The mean percentage of myocardial peak power (open circle), late systolic time (filled square), and stroke work (filled wedge), with respect to the baseline measurements were plotted over the first 20 hours after correcting aortic regurgitation, respectively. Note that although the changes in the peak myocardial power was insignificant (p > 0.05), there was a significant decrease in late ejection time as well as in myocardial stroke work (analysis of variance versus time, both p < 0.01). (AVR = aortic valve replacement; NS = not significant.)
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Limitations of the study
Our study has potential limitations. Values of myocardial stress were based on Laplace’s law, and thus subject to well-known limitations [23]. Left ventricular stroke volume estimated from M-mode measurements has well recognized potential errors. However, regional disturbances of wall motion were not prominent in our patients, and the finding that mean regurgitant volume approached zero after operation suggests a major discrepancy between echocardiography and thermodilution in estimating mean stroke volume is unlikely. These echo-based estimations thus appear valid [14] and their application in serial measurements justified. The requirement of left ventricular pressure recording in the present study meant that baseline measurements could not be made before induction, and were delayed until after the chest was opened (before cardiopulmonary bypass). General anesthesia, by lowering systemic vascular resistance [24], may well have reduced the severity of the aortic regurgitation and been responsible for the mean value of left ventricular diastolic dimension in such patients, being approximately 0.5 to 0.8 cm less than that derived by transthoracic echo 24 to 48 hours before the operation (Jin XY, unpublished data). The present results refer to correcting aortic regurgitation with a stentless valve, and therefore cannot necessarily be assumed to apply when a prosthesis causing significant resistance to ejection is used. Including 4 patients with additional coronary artery disease may have increased overall clinical heterogeneity, but is unlikely to have led to consistent error. From the nature of our protocol, we studied only the very early effects of correcting aortic regurgitation on left ventricular function. Ventricular remodeling continues for many months after operation, but the stimulus underlying this is likely to be the early changes we have described. The reproducibility of the measurements of dimensional shortening, wall stress, and power have been reported elsewhere [9]; and together with that of the timing, as shown in the present study, are adequate to support our conclusions. There are obvious difficulties in defining normal values of time intervals in the presence of aortic regurgitation. Therefore, we regard the increase in the duration of ejection time before valve replacement in our patients merely as a means of recognizing the abnormality of the disease, and not as a direct measure of disturbed physiology.
Clinical implications
From the point of view of myocardial function, correction of aortic regurgitation with a nonobstructive biological valve reduces regional as well as global stroke work at a constant myocardial power by abbreviating the latter half of mechanical systole. At the same time, diastolic time increases significantly to occupy a greater proportion of a given cardiac cycle. When the intensity of contraction is unaltered, the shortening of late systole and the lengthening in diastolic time is likely to be an important underlying mechanism by which successful correction of aortic regurgitation will contribute to preventing the progression of ventricular disease as well as to the recovery of myocardial function.
In conclusion, in addition to its well-established effects on global left ventricular hemodynamics, correction of aortic regurgitation with an aortic homograft or stentless porcine valve can effectively reduce regional and global stroke work and significantly increase diastolic time, even if systolic wall stress and myocardial power do not change immediately. The physiologic benefits of the valve replacement are achieved by reducing the duration rather than altering the peak intensity of myocardial contraction. Careful reexamination of the time course of myocardial contraction may improve our understanding and management of aortic regurgitation.
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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 Royal Brompton Hospital Special Cardiac Fund, London, England.
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Abstract
Introduction
