(Circulation. 1995;92:155-162.)
© 1995 American Heart Association, Inc.
Articles |
Early Changes in Regional and Global Left Ventricular Function After Aortic Valve Replacement
Comparison of Crystalloid, Cold Blood, and Warm Blood Cardioplegias
From the Academic Department of Cardiothoracic Surgery (X.Y.J., J.R.P.), National Heart and Lung Institute, and the Cardiac Department (X.Y.J., D.G.G.), Royal Brompton Hospital, London, UK.
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Abstract |
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Background The clinical effects of different cardioplegic methods on left ventricular (LV) function have not been fully elucidated, particularly in the setting of myocardial hypertrophy.
Methods and Results Sixty-four patients (mean age, 62±12 years; 41 men, 23 women) who were undergoing elective aortic valve replacement (stenosis, 49; regurgitation, 15; concomitant coronary artery bypass grafting, 22), with LV mass index 230±70 g/m2, were randomized to the following groups: antegrade crystalloid cardioplegia (CCP, 21 patients), antegrade/retrograde cold blood cardioplegia (CBP, 23 patients), or continuous retrograde warm (37°C) blood cardioplegia (WBP, 20 patients). Mean aortic cross-clamp and cardiopulmonary bypass times were 100±20 and 126±24 minutes. Positive inotropic drug therapy was required postoperatively in 9 patients after CBP, 14 after CCP, and 18 after WBP. Perioperative LV function was assessed using transesophageal M-mode echocardiography, combined with high-fidelity LV pressure recording and thermodilution cardiac output, before bypass and 0.5, 1, 3, 6, 12, and 20 hours after cross-clamp removal. There was a similar fall in LV peak circumferential wall stress at constant LV end-diastolic dimension in each group after aortic valve replacement. The increase in contraction velocity was significant from 0.5 hour with CBP; however, no significant increase occurred until 12 hours with CCP and until 20 hours with WBP. The rate and extent of LV pressure fall and early diastolic filling rate both increased with CBP, and only in this group did ventricular coordination improve. LV stroke work index was maintained with CBP throughout the postoperative period with less inotropic support than with the other two methods.
Conclusions In the hypertrophied LV, CBP offers the best preservation of myocardial physiological response and ventricular function with less inotropic support.
Key Words: cardioplegia • myocardial contraction • valves • echocardiography • surgery
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Introduction |
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Our ability to preserve myocardial function has continued to improve as cardiac surgery has developed. Over the past two decades, methods based on hypothermia have been generally used,1 2 3 but more recently WBP has attracted great interest.4 5 6 7 8 Differences among various animal models and protocols and the use of a wide range of outcome measures have made it difficult to extrapolate these experimental results to the clinical setting.9 10 11 12 13 14 15 16 17 18 19 The most satisfactory criterion would seem to be maintenance of normal or near-normal ventricular function,20 although assessing ventricular function early after surgery presents many practical problems. The simple measures of cardiac output and filling pressure that are usually used are insensitive. Changes in intrinsic ventricular function are frequently difficult to dissociate from those due to altered loading21 22 23 24 or due to the effects of catecholamine, both exogenous and endogenous. Loss of the normal homogeneity of ventricular function found in significant coronary artery disease or hypertrophy is a further confounding factor.25 In the present study, therefore, we used a more direct method to study LV function, both regional and global. We used transesophageal echocardiography and high-fidelity pressure measurements over the first 20 hours after surgery to study a clinically representative group of patients undergoing AVR.
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Methods |
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Subjects
From June 1992 to the end of July 1994, we studied 64 patients undergoing elective AVR (age, 62±12 years; range, 33 to 81 years; (41 men, 23 women). Forty-nine had aortic stenosis, and 15 had predominant regurgitation. LV mass index was 230±70 g/m2 as measured by M-mode echocardiography. Twenty-two patients with concomitant coronary artery disease (20 with aortic stenosis, 2 with aortic regurgitation) received full revascularization (2±1 grafts). Early after surgery, following our normal clinical practice, positive inotropic drugs were given when cardiac index fell below 2.0 L/m2 in spite of a pulmonary artery wedge pressure
15 mm Hg. On this
basis, 23 patients required no inotropic support
perioperatively (dose level=0), 27 patients received
dopamine in a dose of 3 to 4.9
µg · kg-1 · min-1
(dose level=1), and 14 who failed to respond to dopamine received
adrenaline in a dose of 0.02 to 0.10
µg · kg-1 · min-1
(mean, 0.06
µg · kg-1 · min-1;
dose level=2). These dose levels were determined by those in clinical
charge of the patients, without input from the investigators. No
patients required intra-aortic balloon pump assist after surgery.
This protocol was approved by the Ethics Committee of the Royal
Brompton Hospital, and written informed consent was obtained from each
participant. There were no side effects of this study.
Surgical Techniques
The patients were ventilated with 60%
oxygen. General
anesthesia was maintained with fentanyl (20 to 50 mg/kg),
pancuronium oxide (0.1 mg/kg), and enflurane. A radial artery catheter
and a Swan-Ganz thermodilution catheter were positioned after induction
and used for hemodynamic measurements; the
thermodilution catheter had its tip in the pulmonary artery.
Cardiopulmonary bypass was established (ascending aortic
and a single right atrial cannulation) with hemodilution (hematocrit,
20% to 25%) and systemic hypothermia (25°C nasopharyngeal
temperature) when using CBP or normotheria (37°C) when using WBP. The
extracorporeal circuit contained a membrane oxygenator primed with 1800
mL of crystalloid solution and 500 mL of albumin. The systemic
perfusion flow rate was 2.2
L · min-1 · m-2
at 37°C, decreasing to 1.6
L · min-1 · m-2
at 25°C. A DLP triple lumen catheter was positioned in the
coronary sinus and manually inflated, and its proximal pressure
was monitored and maintained at 30 to 40 mm Hg during retrograde
perfusion. Patients were randomized to CCP, CBP, or WBP. For CCP (20
mL/kg) St Thomas Hospital No. 1 solution, potassium 20 mEq/L at
4°C, was administered during antegrade arrest via each
coronary ostium and maintained with 10 mL/kg (potassium, 6 to 8
mEq/L) every 20 minutes by antegrade perfusion. CBP was accomplished
using a 4:1 dilution of systemic perfusion fluid and St Thomas
Hospital No. 1 solution, potassium 20 mEq/L at 6°C given by antegrade
combined retrograde arrest (20 mL/kg, first two thirds of the dose via
aortic root or coronary artery and the remaining one third via
coronary sinus), maintained by potassium-enriched
autologous blood 10 mL/kg (potassium, 6 to 8 mEq/L) via
coronary sinus every 20 minutes. A 10 mL/kg retrograde "hot
shot" (37°C), which consisted of potassium-enriched (6 to 8
mEq/L) autologous blood and no other additives, was given before
removal of the aortic cross clamp. For WBP, a 4:1 dilution of systemic
perfusion fluid and St Thomas Hospital No. 1 solution was used. The
arrest dose (20 mL/kg) was given antegradely in two thirds, and the
remaining one third, retrogradely, with potassium 20 mEq/L at 37°C
and a hematocrit of 20%. The maintenance dose of approximately
200 to 250 mL/min (potassium, 6 to 8 mEq/L; hemocratic, 20%; at
37°C) was administered continuously via the coronary sinus at
a pressure of 30 to 40 mm Hg. There was a 2- to 3-minute interruption
of retrograde WBP during suturing of the valve around each
coronary ostium. In one patient, complete cardiac arrest could
not be achieved after a full arrest dose of WBP, so another half arrest
dose of CBP was added antegradely, and the CBP protocol was therefore
substituted. All valve replacements were performed by the same surgeon
(J.R.P.). The aortic valve was replaced with an aortic homograft in 29
patients, with a Toronto stentless porcine valve in 23, and
with a stented valve in 12. The mean size of implanted valve was
25±2.5 mm. No patient had significant postoperative aortic
regurgitation as assessed using
transesophageal echocardiography.
Cardiopulmonary bypass time was 126±24 minutes, and aortic
cross-clamp time was 100±20 minutes. After surgery, patients were
transferred to intensive care under continuous sedation (morphine, 1
mg/h; propofol, 50 to 100 mg/h IV) and receiving controlled ventilation
(FIO2, 0.35 to 0.50; I-R ratio, 1:2; positive
end-expiratory pressure, 1 to 2 mm Hg).
Facilities and Protocol
A 5 MHz biplanar transesophageal
echocardiographic transducer (model HP 21362C,
Hewlett-Packard) 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–tipped
catheter (Gaeltec CTC/4F/USCI, Gaeltec Ltd) was introduced into the LV
with its tip located in the midportion of the cavity, via the roof of
the left atrium and across the mitral valve. The transducer had a
sensitivity of 5 µV · V-1 · mm
Hg-1, bridge resistance 2.0 K
.
Its signal output was filtered, preamplified (Gaeltec S7b, Gaeltec
Ltd), and transferred into the auxiliary line of the
echocardiographic system (with response frequency 0 to
1000 Hz). The calibration (to 100 mm Hg) of the pressure
transducer–tipped catheter was performed electrically before the
initial measurement and was checked with an air-operated
dead-weight balance (Budenberg Gauge Company Ltd) after the study,
when the catheter was removed. The mean left atrial pressure or
pulmonary artery wedge pressure (identical within 2 mm Hg to
mean left atrial pressure when the chest was open) was used to identify
the LV end-diastolic pressure. Zero pressure was taken
as atmospheric. After the final measurement, the
transesophageal echocardiographic
transducer and pressure transducer–tippedcatheter were removed,
sedation was discontinued, and the patient was weaned off ventilation
within 2 to 3 hours. No early mortality occurred in this group of
patients.
Using the transgastric LV short-axis view, a two-dimensional image-directed M-mode echocardiogram of the LV minor axis was recorded at the level of the tips of papillary muscles and printed on paper at a speed of 100 mm/s, with a simultaneous LV pressure trace and electrocardiogram. Once positioned, the transducer remained in situ throughout the study. The location of the M-mode cursor was checked with respect to the cross-sectional display before each measurement was made. Hemodynamic measurements including heart rate (HR), thermodilution cardiac output (CO), systolic and mean systemic pressures, mean and wedged pulmonary artery pressures (or mean left atrial pressure) were recorded simultaneously with each echocardiographic measurement. Baseline measurements were made before the institution of cardiopulmonary bypass when the patients were in a stable hemodynamic state and subsequently 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).
Measurements and Calculations
From the LV M-mode
echocardiogram and pressure trace, the minor
dimension, cavity pressure, and anterior wall thickness were digitized
off-line (sampling frequency, 100 Hz), along with depth and time
calibration, by computer.26 27 The onset of QRS
complex of
the electrocardiogram was used to identify end
diastole. The time from peak rate of pressure rise (peak
+dP/dt) to peak rate of pressure fall (peak -dP/dt) was taken as
LV ejection time.28 29 The time point of peak
-dP/dt
was checked with the closure of the aortic valve on M-mode
echocardiogram. Three successive heart beats were digitized at each
time interval, and mean values were recorded. From the digitized
output and hemodynamic data, the following
variables were derived: (1) LV dimension and wall thickness; (2) LV
pressure and wall stress; (3) myocardial power, work, and LV
coordination; and (4) hemodynamics of systemic
circulation.
LV Dimension and Wall Thickness
To determine
LV dimension and wall thickness, the
end-diastolic dimension, the peak rate of dimension
shortening and the lengthening during early diastole, and
the peak rate of anterior wall thickening were derived to assess LV
regional function.
LV Pressure and Wall Stress
From
LV pressure pulse, we determined mean ejection pressure
(MEP), peak +dP/dt normalized to maximal developed pressure (DP) (peak
+dP/dt/DP), peak -dP/dt normalized to end-systolic
pressure (peak -dP/dt/ESP), minimum diastolic
pressure at early diastole, and
end-diastolic pressure (EDP). We used the method of
Falsetti et al30 to calculate circumferential midwall
stress, and the peak value during systole was derived.
Myocardial Power, Work, and LV Coordination
In
systole, the rate at which the myocardium does
external work (ie, the power that it develops) is given as the
product of wall stress and circumferential shortening rate. Stress
was referred to a position in the midwall. Its circumference at this
point is given by 
(D+T/2), where T and D are instantaneous
values of dimension and wall thickness and the shortening rate is its
first differential with respect to time. Values of local power were
referred to in cubic centimeters of myocardium at end
diastole. The time integral of power during an entire
cardiac circle was derived to give the value of myocardial stroke
work.26 27 A significant change of dimension during
either
isovolumic period represents ventricular
incoordination. We used cycle efficiency, defined as the ratio of the
ventricular pressure dimension loop area to that of the
rectangle that just encloses it (ie, the ratio of useful external work
to the maximum possible for myocardium working over the
same range of pressure and dimension), to quantify these effects of
ventricular incoordination in terms of their influence on
energy transfer from myocardium to the
circulation.26 27
Hemodynamics of
Systemic Circulation
From thermodilution cardiac output measurements
and
simultaneous heart rate, LV ejection pressure, and mean
systemic artery pressure (BPm), we calculated LV stroke volume index
(LVSVI); LV stroke work index,
SWILV=LVSVIx(MEP-EDP)x0.0136x9.8 (in
mJ/m-2); and the stroke work index in the
systemic circulation,
SWISYS=LVSVIxBPmx0.0136x9.8
(in mJ/m2).31
Statistical Methods
Continuous data were presented as
mean±1 SD.
MINITAB statistical software (PC version, release 8, 1991,
Minitab Inc)32 was used for statistical analysis.
Clinical and surgical profiles among three groups were compared by
one-way ANOVA or a 
2 test as applicable.
Possible significant sources of variance of the
perioperative functional measurements with respect to
time, cardioplegic method, inotropic dose level, and their interactions
were first identified by multivariant ANOVA. For each
parameter thus demonstrated to be significantly affected by
cardioplegia or a related interaction, postoperative changes with
respect to prebypass level were further assessed by one-way ANOVA
combined with the multiple-pair comparisons of 95% CI (Dunnett's
method, family error rate 0.10 and individual error rate 0.020) within
each group, respectively. A value of P<.05 was taken as
statistically significant.
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Results |
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Comparison of Clinical Data and Prebypass Left Ventricular Performance Before Cardiopulmonary Bypass
With a randomized approach, there was a matched distribution among the groups with respect to age, sex, valve disease, LV hypertrophy, incidence of associated coronary artery disease, and extent of revascularization. The same was true for the valve substitutes implanted and for aortic cross-clamp and cardiopulmonary bypass times. However, the requirement for positive inotropic drugs after surgery was significantly different between groups, being highest after WBP (90%) and least after CBP (30%) (Table 1
).
Before cardiopulmonary bypass, there was no significant
difference between the groups with respect to LV loading conditions,
systolic or diastolic function,
ventricular coordination, or overall
hemodynamics.
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Significant Factors Affecting Perioperative LV
Loading and Function
The results of multivariant ANOVA are summarized
in Table 2. Time, cardioplegia, inotropic dose level, and their
interaction were all significant sources of variance for one or more
variable.
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Time
Time was not a significant source of
preload variance as assessed
by end-diastolic cavity dimension. It was, however, a
major source of variance in afterload, the peak systolic wall
stress, reflecting the valve replacement. Time also affected all other
hemodynamic measurements and LV function, except
myocardial power. Interactions with time were inconspicuous, the only
significant one being with cardioplegia for peak -dP/dt/ESP.
Cardioplegia and Inotropic Drugs
The different
requirement for positive inotropic drugs also
significantly influenced ventricular systolic
function, ventricular diastolic function, and
hemodynamics. Interactions between cardioplegia and
inotropic drugs were frequent. Neither time nor the isolated effects of
cardioplegia or inotropic drugs were significant sources of variance of
cycle efficiency, but the interaction between cardioplegia and
inotropic dose level was very significant (P<.001).
Comparison of Perioperative Changes in LV Loading,
Hemodynamics, and LV Function
LV Loading and Hemodynamics
The postoperative fall of LV afterload, as reflected by peak
systolic wall stress, was similar in each group. LV preload,
assessed by end-diastolic dimension, remained unchanged
in each group throughout the perioperative period. From
3 hours onward, LV stroke volume index and stroke work index in
systemic circulation, reflecting overall systemic
hemodynamics, both increased with CBP but not with
either CCP or WBP (Table 3).
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LV systolic function. As afterload fell, there was a
prompt and significant increase in contraction velocity with CBP,
reflected by the peak rates of circumferential dimension shortening
(Figure) and wall thickening regionally as well as by
peak +dP/dt/DP globally. In contrast, these changes were of a small
amplitude, showed larger scatter, and did not reach significance until
12 to 20 hours after CCP or WBP. Peak myocardial power had fallen
significantly at 6 hours with WBP. Both regional and global stroke work
were well maintained with CBP apart from a transient fall in regional
stroke work at 30 minutes. However, both fell consistently with
CCP and WBP, the largest changes occurring at 30 minutes (0.5 hour)
after CCP, and at 6 hours after WBP (Table 4).
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indicates cold blood cardioplegia; 
, warm blood cardioplegia;
, crystalloid cardioplegia; and CPB, cardiopulmonary
bypass. *Significance compared with prebypass level by Dunnett's
method.
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LV diastolic function and coordination. In
contrast to systolic function, there was no immediate change in
values of diastolic function with any cardioplegia
technique. Although, peak -dP/dt/ESP had increased significantly
by 6 hours in each group, peak rate of dimension lengthening during
early diastole had increased significantly by 12 hours with
CBP and CCP but not with WBP. Furthermore, LV minimum pressure during
early diastole fell significantly only with CBP at 12 and
20 hours. LV coordination, as assessed by cycle efficiency, had
increased significantly, above the prebypass level by 12 hours after
CBP, but showed no consistent change with CCP and actually fell
with WBP at 6 hours (Table 5).
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Discussion |
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Aortic valve replacement provides a unique opportunity to compare possible differences in the efficacy of myocardial preservation methods. Not only is the hypertrophied ventricle very susceptible to ischemia and reperfusion injury, particularly with a prolonged aortic cross-clamp time for a complex surgery, but also the benefits of normalization of ventricular afterload can be anticipated within the first 20 hours and readily assessed in the clinical setting.33 The randomization approach offered well-matched clinical and intraoperative data, and all three groups of patients had a similar incidence of concomitant revascularization. In contrast to animal models, current ethical surgical practice requires that myocardial dysfunction should be treated when present postoperatively. This involves the use of positive inotropic drugs, given according to standardized clinical indications, at Royal Brompton Hospital indications are a cardiac index of <2 L · min-1 · m-2 in spite of a pulmonary artery wedge pressure
15 mm Hg. In
the present study, this policy resulted in significantly different
dose levels among the three cardioplegic methods, the highest being
necessary with WBP and the lowest with CBP. It thus becomes necessary
not only to quantify the variance of LV function due to cardioplegic
method, along with time and inotropic agents, but also to look for
interactions between them. Our study clearly shows that cardioplegia,
inotropic dose level, and presence of an interaction between them are
all significant sources of variations of aspects of
perioperative LV function. It is thus justifiable to
look closely at the postoperative changes in these variables seen
over time that are significantly affected by cardioplegic method,
whether alone or in combination with inotropic drugs.
Correction of aortic stenosis causes peak LV wall stress to
fall, so that according to the myocardial force-velocity
relation34 35 myocardial shortening velocity should
increase. However, this response was found immediately after surgery
only with CBP (Figure
). With the other two methods, the
increase was
delayed until 12 and 20 hours. Myocardial relaxation is often impaired
in the hypertrophied ventricle,36 but this tends to
improve within 12 hours of relieving the aortic
stenosis.33 In our study, CBP was associated with
the most consistent improvement in both the rate and the extent
of ventricular pressure fall during early relaxation, as
well as in early diastolic filling rate. Furthermore, it
was only after CBP that ventricular coordination, assessed
by cycle efficiency, improved over the same time period. If one uses
all these aspects as functional end points, it can be seen that CBP
with its lower catecholamine requirement clearly offers
better myocardial preservation than either CCP or WBP in the
hypertrophied human ventricle. Although many experimental studies have
shown that positive inotropic drugs may restore the systolic
function of "stunned myocardium,"37 38
our clinical finding was that even with an increased dose of inotropic
drugs and using the techniques of CCP or WBP the expected response of
an increased shortening velocity predicted by the force-velocity
relations was not restored. However, the peak myocardial power was
nearly maintained. Thus, the mechanical dysfunction commonly seen after
cardiac surgery cannot be ascribed purely to impaired myocardial
contractility as defined by force-velocity
relations. Our observations in fact support the view that
diastolic function and ventricular
incoordination also play important roles.33
It is possible that the differences in the rate and extent of recovery of LV function we described were not only related to the cardioplegic regimens themselves but also to the methods of delivery. As has been pointed out by Menasche et al,19 the oxygen consumption of the hypertrophied myocardium during warm cardioplegic arrest is still quite significant. This implies that the hemoglobin concentration, perfusion flow rate, and transmural flow distribution are all likely to be critical in ensuring adequate delivery of oxygen to the myocardium and interstitial tissue. Although a flow rate of 80 mL/min with hemoglobin (Hb) 80 g/L at a perfusion pressure of 40 mm Hg has been recommended for continuous retrograde perfusion,39 and a 10-minute interruption or even multiple interruptions of perfusion have been demonstrated to be acceptable,40 41 we deliberately used at least 200 to 250 mL/min with Hb 70 to 80 g/L because we believe it to be more appropriate for the hypertrophied ventricle, and we limited interruption of perfusion to <5 minutes. The unfavorable effect of increased intercapillary distances on oxygen diffusion and the inhomogeneous distribution of myocardial perfusion in vivo have been well documented in the working hypertrophied ventricle.42 43 44 45 Similar problems may also occur during ventricular arrest, particularly the loss of intramyocardial pump function46 combined with a retrograde route may well result in regional perfusion deficits47 and microvascular maldistribution.48 The manipulation of retrograde perfusion pressure has failed to improve these shortcomings,49 but hypothermia seems to have favorable effects over normothermia on postischemic functional recovery.50 In the hypertrophied ventricle, therefore, unintentional ischemia is likely to be particularly significant during normothermia retrograde perfusion by the considerably high oxygen consumption associated with suboptimal nutrient distribution and, in particular, the subendocardium, which is the most susceptible area.51 Subendocardial ischemia results in LV dysfunction being more significant in longitudinal than in circumferential function.52 53 54 Compromised longitudinal function not only reduces the rate and extent of LV free wall thickening and thus of circumferential dimension shortening but is also a major cause of ventricular incoordination.55 A significant increase in wall thickening rate and cycle efficiency with CBP supports this hypothesis, although direct measurements are needed in a further study to confirm it.
There are several limitations to this study. We included patients with both aortic stenosis and regurgitation, and 30% had concomitant coronary artery disease. Although these factors were similarly distributed among the three groups by randomization, their presence will have caused increased baseline variances. Similarly, cardioplegia composition and its delivery time and temperature are not precisely controlled in routine clinical practice. Again, these factors are unlikely to have altered the overall results of the study, although they may have reduced its sensitivity in detecting more subtle differences between cardioplegia methods. We did not measure the oxygen saturation of the efflux during WBP, although flow rates were continuously monitored and kept well above the levels at which it has been demonstrated that significant acidosis does not occur and that residual oxygen saturation is well maintained.19 Preoperative LV stroke volume was calculated by pulmonary thermodilution catheter, so we will have underestimated its true value in 15 patients with aortic regurgitation. However, the prevalence of patients with aortic regurgitation was similar in the three groups. The validity of the techniques we used to study LV function may have been influenced by the echocardiographic transducer position. This was routinely checked and referenced to mitral valve anatomy before each determination. Mild or random variation in position among observations would increase error variance but would not lead to consistent differences between the groups. Furthermore, the change in ventricular properties with position around the ventricular circumference is small at mid-cavity level, so it is doubtful that transducer displacement by as much as 1 cm would significantly alter measured variables. The selection of measurements we made of LV systolic and diastolic function was based on the capability of the techniques we used and was thus to some extent arbitrary. We have documented their reproducibility elsewhere.33 The constancy of LV end-diastolic dimension after AVR made it unnecessary to allow for changes in preload, for example by determining preload recruitable stroke work, a technique that does not lend itself to repeated measurements in the postoperative situation. Instead, we used peak myocardial power to assess the change in contractility,35 which is quite insensitive even to the change in afterload caused by relief of aortic stenosis,33 and has clear physical dimensions, with measurements made direct rather than extrapolating. We did not construct a basic lagrangian stress-strain relation, since previous experience with identical methods has shown that in intact humans, it departs very significantly from the theoretical exponential on which it is based.56 Generally, the use of a higher dose of positive inotropes during reperfusion would not reflect favorably on the efficacy of myocardial preservation; however, we do not regard the differing doses of catecholamine used with the three cardioplegic methods as a confounding factor. Provided that their administration is based on clinically defined criteria, differing inotropic drug requirement must be regarded as an inseparable part of any cardioplegic method used in clinical practice. Attempts to dissociate the two are not, therefore, critical to the interpretation of our results.
In summary, perioperative transesophageal echocardiography together with high-fidelity ventricular pressure recording and thermodilution cardiac output offers a comprehensive and practical approach to the study of LV function in the cardiac surgical setting. The data in this study have shown that better, although still not optimal, preservation of physiological function in the hypertrophied LV can be obtained by using CBP. The theoretical advantages of WBP under currently used techniques have yet to be realized, and a full understanding of retrograde myocardial perfusion of the hypertrophic LV during arrest is needed. In the clinical setting, therefore, the hypothermia technique may still be the method of choice for preserving the hypertrophied myocardium during retrograde perfusion until a truly homogeneous and aerobic arrest can be easily and predictably achieved. To reach this ideal situation, further investigations such as modifying the composition and delivery techniques in retrograde WBP are required.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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Supported by grants from the Wellcome Trust (ASW2, 1992), British Heart Foundation (New Clinical Initiative 3014178), Garfield Weston Trust, and Royal Brompton Hospital Special Cardiac Fund, London, UK.
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Footnotes |
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Reprint requests to John R. Pepper, FRCS, the Academic Department of Cardiothoracic Surgery, National Heart and Lung Institute, Sydney Street, London SW3 6NP, UK.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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