(Circulation. 1998;98:2598-2607.)
© 1998 American Heart Association, Inc.
Basic Science Reports |
Location of Diastolic Potentials in Reentrant Circuits Causing Sustained Ventricular Tachycardia in the Infarcted Canine Heart
Relationship to Predicted Critical Ablation Sites
From the Departments of Pharmacology (C.C., H.S., G.M., A.L.W., M.M.S.) and Medicine (J.C.), College of Physicians and Surgeons of Columbia University, New York, NY, and Department of Medicine, University of California, San Francisco (M.M.S.).
Correspondence to Andrew L. Wit, PhD, Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 W 168th St, New York, NY 10032. E-mail alw4{at}columbia.edu
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Background—The complete reentrant circuit for ablation of reentrant ventricular tachycardia (VT) in humans can rarely be localized by mapping. As a result, surrogate markers, such as diastolic electrical activity, subsequently confirmed by entrainment, have been used. However, ablation at those sites has had variable efficacy. The reasons for this variability are not clear.
Methods and Results—We correlated activation maps of reentrant circuits in the epicardial border zone of 4-day old infarcted dog hearts with the corresponding ECGs for 45 VTs to determine the regions of the reentrant circuits activated during diastole. In VTs with a figure-8 reentrant pattern, the center point of the central common pathway, the part of the circuit critical for the maintenance of reentry, was activated in early diastole in 32 of 35 VTs (91.4%), in late diastole in 1 (2.9%), and in systole in 2 (5.7%). Regions outside the circuit were rarely activated in diastole. In 10 VTs, the reentrant circuit was characterized by a single reentrant loop. In these circuits, no one region was predicted to be critical for maintenance of reentry, and a segment of the circuits was activated during diastole. However, regions peripheral to the circuit were also activated during diastole.
Conclusions—The pattern of reentrant activation determines the specificity of diastolic activity for locating critical sites for ablation of VT.
Key Words: ablation • myocardial infarction • mapping • reentry • tachycardia
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Introduction |
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Ablation of reentrant sustained ventricular tachycardias (VTs) associated with ischemic heart disease has not been uniformly successful because localization of the complete reentrant circuit cannot always be accomplished by mapping.1 2 3 As a result, surrogate markers, such as fractionated electrograms and continuous electrical activity4 or the timing of activation with respect to the ECG, have been used as guidelines for locating the circuits, subject to confirmation by entrainment at these sites.2 3 5 For example, sites activated at various times during diastole, either early, mid, or late, have been designated as indicating activity in the circuit.1 4 In addition, even when the circuit is located successfully, termination of reentry may require ablation of a critical region of the circuit, whereas ablation of other regions in the circuit might not be effective. This may account for the variable efficacy of ablating sites with diastolic activity in stopping VT even when entrainment has suggested that ablation should be successful.1 3 The reason for this variability is not completely understood but was investigated in this study in a canine infarct model of VT.6
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Methods |
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Experimental Model
Reentrant circuits were mapped in the epicardial border zone (EBZ) of 29 healing canine infarcts,7 during sustained monomorphic VT (>30 seconds' duration), 4 days after surgical occlusion of the left anterior descending coronary artery (LAD). Tachycardias were induced by standard programmed stimulation protocols. All our methods, mapping electrode arrays with 196 or 312 bipolar electrodes and recording instrumentation for these studies, have been described in previous publications.7 8 9
Data Processing
Our methods for determining local activation times and drawing
isochronal maps have been described in detail
previously.7 8 9 The time of activation of each
region of the reentrant circuits was then correlated with the surface
ECG (leads I and II) to determine which part of the circuits were
activated during electrical systole (during the QRS complex)
and which parts were activated during electrical
diastole (the remaining cardiac cycle that is not during
the QRS). Although it is often difficult to determine the onset and end
of the QRS with precision during VT, when there was an isoelectric
segment between the end of the T wave and the beginning of the
subsequent QRS, the onset of the QRS was taken as the earliest
reproducible deviation from the isoelectric baseline in either lead I
or II. The end of the QRS was taken as the time of return of the last
wave of the complex to baseline in both leads (example in Figure 7
). In
cases in which there was no isoelectric segment between the end of the
T wave and the subsequent QRS, the onset of the QRS was indicated by a
negative deflection superimposed on the T wave (example in Figure 1). In cases in which no isoelectric
segment was evident between the QRS complex and the T wave, the end of
the QRS was selected at the inflection point that separates the convex
QRS wave returning to baseline from the concave T wave departing from
baseline (example in Figure 2). In cases
of rapid tachycardias, the onset of the QRS could be
determined on the first tachycardia beat occurring after
premature stimulation when it had the same morphology as during the
sustained tachycardia (example in Figure 3). The diastolic period was
further subdivided by designating the midpoint of the
diastolic interval as middiastole, the time
between the end of the QRS complex and this midpoint as early
diastole, and the time between the midpoint and the onset
of the subsequent QRS as late diastole. The time resolution
of these measurements on the ECG was 4 ms. In addition, the exit route
from the EBZ to the rest of the ventricles was determined as previously
described.8 This is the region of the electrode
array margin activated within 10 ms before the onset of the QRS
of the surface ECG during tachycardia.
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Results |
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Reentrant Circuits With a Figure
-8 Activation PatternBecause ablation of the central common pathway (CCP) in figure-8 reentrant circuits is predicted to be the vulnerable region for termination of tachycardia because it is the only region that is part of both reentrant circuits, we determined whether its time of activation in 35 tachycardias (mean cycle length±SD, 216±39 ms) had a consistent relationship to the ECG.
Figure 1A shows the pattern of activation of 1 of the figure-8
reentrant circuits during a VT with a cycle length of 233 ms. The
reentrant wave front at the beginning of the time window is moving from
the left lateral margin (LL) toward the LAD margin of the
electrode array (isochrones 0 to 60 ms). The sequence of
isochrones shows that it progresses in this direction between 2
lines of functional conduction block, indicated by the thick black
lines (not present during sinus rhythm or ventricular
pacing), that are parallel to each other and to the long axis of the
myocardial fiber bundles.7 At the ends of these
lines of block, the wave front splits into 2, 1 moving to the left
around the end of the left line of block and then back toward the LL
margin to complete 1 loop of the figure-8 circuit, the other moving to
the right around the end of the right line of block and then back to
the LL margin to complete the other loop of the circuit. These 2 wave
fronts coalesce at the LL margin. The region of the circuit between the
2 lines of functional block that is common to both reentrant wave
fronts is the CCP, and the regions of the circuit lateral to the lines
of block are designated the outer pathways. In this example, the CCP
extends from isochrone 0 (the same as isochrone 230) to
isochrone 70, a time of 70 ms, 
30% of the activation time for
the complete circuit. The exit route to the ventricles for the
reentrant impulse is shown by the asterisks in Figure 1A. The time
interval from the exit from the CCP (70 ms) to the exit point to the
ventricles (120 ms) was 50 ms.
Figure 1B shows the relationship of the time of activation of different
regions of the circuit to the ECG. Because the entire reentrant circuit
is in the EBZ, electrograms occur both during electrical systole and
diastole. Systole corresponds to isochrones 120 to 210
(90 ms) on the map, in the outer pathways of the figure-8 circuit.
Electrograms a through d, which were recorded from this region,
occur during the QRS complex (Figure 1B). Diastole
corresponds to isochrones 210 to 230 ms and 0 to 120 ms (140-ms
duration). Electrograms e through m (Figure 1B) are activated
during diastole. During 70 ms of the 140-ms
diastolic interval, there is activation of the CCP
(isochrones 0 to 70); electrograms f through k, which were
recorded in the CCP, were activated during
diastole. Therefore, in this example, activation of the CCP
occurs during early (electrodes f through i) and late (electrodes j and
k) diastole. Regions outside the CCP are also
activated during diastole: isochrones 210 to
230, which include electrode e, and isochrones 70 to 120, which
include electrodes l and m.
Figure 2 shows another relationship between activation of a figure-8
reentrant circuit and the ECG during a tachycardia with a
cycle length of 216 ms. The curved arrows in Figure 2A indicate 2 wave
fronts moving clockwise and counterclockwise around 2 lines of
functional block (thick black lines). The exit route to the ventricles
is at the LAD margin (asterisks), activated at 210 ms. In this
example, it is more difficult to designate the exact time of activation
of the CCP because of the transverse orientation of the left line of
block. In the strictest definition, the wave front passes between the 2
lines of block between isochrones 120 to 150, which is the CCP.
Activation of this region requires only 30 ms of the 216-ms cycle
length of the tachycardia. In Figure 2B, in which
electrograms from the circuit around the right line of block are
displayed along with the ECG, it can be seen that the time of
activation between electrograms h and i, which designate approximately
the beginning and end of the CCP, occurs during only a small portion of
the early diastolic interval. Regions of the circuit
outside the CCP, between isochrones 100 to 120 (electrogram g) and
150 to 220 (electrograms j and k), are also activated during
early and late diastole. Systole corresponds to
isochrones 0 to 100 (electrograms a through f in Figure 2B).
Therefore, in this example, the very short CCP is activated
during only a very small part of early diastole, with
activation outside the CCP occurring during most of
diastole.
Figure 3A shows the activation map of another circuit during a VT with
a cycle of 148 ms. Two reentrant wave fronts, shown by the curved
arrows, are moving clockwise and counterclockwise around 2 parallel
lines of functional block (thick black lines). Another short and mostly
transverse line of block is located above the right line of block but
is not an integral part of the circuit. As a consequence of the short
cycle length, the duration of the QRS of 108 ms (systole) was 73% of
the cycle length, and diastole (40 ms) was only 27% of the
cycle length (diastole was 61% and 54% of the cycle
lengths for the tachycardias shown in Figures 1 and 2,
respectively). A large part of this reentrant circuit, extending from
isochrones 110 to 150 and 0 to 70 (108 ms), was activated
during systole, and only a small part of the circuit, extending from
isochrones 70 to 110 (40 ms), was activated during
diastole. Activation of the CCP between the 2 lines of
block begins at isochrone 20 and extends to isochrone 50.
Therefore, electrodes c, d, and e are in the CCP and occur during
systole. Electrograms f and g, at the exit from the CCP, are
activated at the end of systole. Electrogram h occurs during
diastole but is not within the CCP.
To compare the location of the time of activation of the CCP in the
tachycardia cycle from all tachycardias with
different cycle lengths, we normalized the beginning and the end of the
activation of the CCP (and consequently the time of activation of the
CCP) with respect to the cycle length of the tachycardia
(Figure 4). For each
tachycardia (labeled 1 to 35), the thin horizontal line
represents activation of the entire CCP with respect to the
onset of the QRS (dashed vertical line at the left) and the entire
cycle length (ie, to the onset of the subsequent QRS,
represented by the dashed vertical line at the right). The
solid circle is the midpoint of the CCP. The location of the early
diastolic interval for each tachycardia is
indicated by the horizontal shaded bar. Therefore, the time between the
dashed vertical line at the left and the beginning of each shaded bar
indicates QRS (systole) duration. The time between the end of the
shaded bar and the dashed vertical line at the right indicates the late
diastolic interval. For example, activation of the CCP for
tachycardias 2 through 5 begins before the onset of early
diastole (end of systole) and ends before the onset of late
diastole. Conversely, activation of the CCP of
tachycardias 27 through 29 begins after the onset of early
diastole and extends into late diastole.
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The total time for activation of the complete CCP occurred over >1 ECG
segment (systole and early and late diastole) in 29 of the
35 tachycardias (Figure 4). In 8 of the
tachycardias, activation of the CCP occurred during systole
and early diastole (2–5, 7, 9, 22, 30); in 17
tachycardias, it occurred during early and late
diastole (10, 13–15, 17–19, 21, 24–29, 31, 34, 35); and
in 4 tachycardias, it occurred during systole and early and
late diastole (12, 20, 32, 33). In 1
tachycardia, the CCP was activated entirely during
systole (1), and in 5 it was activated entirely during early
diastole (6, 8, 11, 16, 23). Despite this variability, the
midpoint of the CCP (black dot in Figure 4) was located in early
diastole (shaded area in Figure 4) in 32 of the 35
tachycardias (91.4%), whereas in 1 tachycardia
(2.9%, tachycardia 28 in Figure 4), it was located in late
diastole and in 2 tachycardias (5.7%,
tachycardias 1 and 30 in Figure 4), it was located in
systole. Figure 4 also shows the time elapsed from the end of
activation of the CCP to the exit point to the ventricle, which occurs
at the onset of the QRS (1.00 in Figure 4). Significant variability
occurred, ranging from experiments in which the exit to the ventricles
occurred long after activation of the CCP (experiments 2 through 9 in
Figure 4) to experiments in which the exit to the ventricles occurred
almost immediately after activation of the CCP (experiments 32 and 35
in Figure 4).
Significant variability also occurred in the time for activation of the
entire CCP for all 35 tachycardias, which ranged from 20 to
140 ms (mean±SD, 57±24 ms). The time for activation of the CCP was
directly proportional to the tachycardia cycle length
(Figure 5A;
r2=0.53). However, the percentage of the
tachycardia cycle length during which the reentrant impulse
activated the CCP was not related to the
tachycardia cycle length (Figure 5B; range, 9% to 44%;
mean, 26±8%), because there was an increase in activation time in
other regions of the circuit as well as the CCP as the cycle length
increased.
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During the time interval of activation of the CCP, the electrical
activity on the EBZ was restricted to the CCP in 27 of the 35
tachycardias (77%); no other region of the EBZ was being
activated at the same time as the CCP (Figures 1 and 2). In the
other 8 tachycardias (23%), activity at sites not located
in the CCP was occurring at the same time as the activation of the CCP.
The time of overlap ranged from 7 to 20 ms (mean±SD, 13±5 ms) (Figure 3). Those sites were unrelated to the maintenance of the
reentrant circuit responsible for the tachycardia.
Reentrant Circuits With a Single Reentrant Loop Activation
Pattern
In 10 VTs, the reentrant circuit on the EBZ was characterized by a
single reentrant loop (mean cycle length±SD, 184±23 ms), although
this does not eliminate the possibility that another reentrant loop
occurred outside the mapped region that involved normal
myocardium. An example of 1 of these circuits with a cycle
length of 190 ms is shown in Figure 6.
The sequence of isochrones from 10 to 190 ms is around a central
fulcrum of functional block (thick black line), as shown by the curved
arrows (Figure 6A). There are 2 exit routes to the ventricles from the
EBZ at the LAD and the LL margins of the electrode array
(asterisks in Figure 6A). Additional short lines of block are also
located at the bottom right of the map. Figure 6B shows the ECG and
electrograms recorded from the circuit (circled sites on the
activation map). The region of the circuit activated during
isochrones 120 to 190 and 190 to 10 (electrograms g through i and
a) was activated in systole, and the region between
isochrones 10 and 120 (electrograms b through f) was
activated during diastole, with the region between
isochrones 10 and 65 activated during early
diastole. Figure 6C shows electrograms recorded at the
boxed sites in Figure 6A, indicating that large regions of the EBZ
located at a distance from the central region of block are also
activated during the systolic and diastolic
intervals (both early and late diastole) because of the
centrifugal spread of the wave front away from the central region.
Therefore, in circuits caused by single reentrant wave fronts rotating
around a central region of block, it might not be possible to locate a
specific region of the circuit on the basis of the timing of
electrograms with relation to the ECG, and regions distant from the
circuit can be activated throughout the diastolic
interval.
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In 8 of the 10 reentrant circuits, in addition to the central
fulcrum of block around which activation rotated, other lines of block
were present in close proximity to the circuit. The effect of the
additional lines of block was often to confine the electrical activity
to smaller regions (close to the central line of block) during a
specific time in the cardiac cycle than would be expected if only the
central line were present. In Figure 7A, the reentrant wave front (arrows)
rotates around a central region of block, the vertical thick black
line, surrounded by circled electrodes. In addition to this central
line of block, another line of block having an inverted U shape is
present above it. As a result, activity in the EBZ between
isochrones 60 and 200 (60% of the 230-ms
tachycardia cycle) is confined to the region between this
line and the line of block forming the central fulcrum; activation
cannot spread centrifugally away from the circuit as in Figure 6A. The
additional line of block resulted in the creation of a bystander
pathway3 (at the top of the inverted U) from
isochrones 110 to 150 (open arrow). In Figure 7A, isochrones 0
to 80 correspond to systole (see ECG and electrograms a through f in
Figure 7B), isochrones 80 to 160 to early diastole
(electrograms g through i), and isochrones 160 to 230 to late
diastole (electrograms j and k). Electrogram l was
recorded in the bystander pathway, which was located in an area
that was activated every other reentrant beat (2:1 conduction).
Therefore, the time between both lines of block (the time of confined
electrical activity in the EBZ) corresponds to early and part of late
diastole on the ECG. In the other 6
tachycardias with a single reentrant loop and additional
lines of block, the areas of confined epicardial electrical activity
occurred during early diastole in 3
tachycardias and during late diastole in the
other 3.
During figure-8 reentrant circuits (Figures 1 to 3), the 2
reentrant wave fronts arrive at the entrance to the CCP at
approximately the same time, and both complete a reentrant excursion.
This requires that each wave front has a similar revolution time around
each of the 2 lines of block. However, 1 of the wave fronts may arrive
at the entrance much earlier than the other to complete its circuit. We
have classified these circuits as having a single reentrant loop. An
example is shown in Figure 8A. The
completed circuit is shown by the black curved arrows; the reentrant
wave front rotates in a clockwise direction around the vertical line of
block, surrounded by circled electrodes a through i, in 170 ms (cycle
length of the tachycardia). There is also a longer
horizontal line of block around which another wave front rotates in the
counterclockwise direction (open arrows). However, at 160 to 170 ms,
when the clockwise circuit is completed, the counterclockwise circuit
is turning around the left end of the line of block and then collides
with the clockwise wave front but does not complete its circuit. The
counterclockwise pathway, therefore, is a bystander pathway. There is a
narrow region between the 2 lines of block at the right, between
isochrones 10 and 40, which might be a vulnerable site for
ablation, although a lesion here might also serve to enlarge the
circuit. Electrodes j, f, and g are located in this region, with only
site g activated in (early) diastole, whereas sites
j and f are activated at the end of systole (Figure 8B).
Isochrones 10 to 30 also extend away from this narrow region
between the lines of block, toward the apex (at the left) and LL
margins. Other recording sites within these isochrones (k
and l), which are not in the narrow region, are also activated
at the end of systole and beginning of diastole (Figure 8B). Sites h and i, which are activated in mid and late
diastole, are also not within the possible vulnerable
region (Figure 8B). Therefore, diastolic activity does not
seem to be suggestive of an effective ablation site.
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Discussion |
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A major challenge for the ablation of reentrant VTs has been to locate the reentrant circuit, and more specifically, a region of the circuit that is crucial for maintenance of circulating activity. This is particularly problematic in the infarcted ventricles, because circuits may have different sizes and shapes, be caused by different mechanisms (anatomic or functional), and involve different regions in different hearts (reviewed in Reference 1111 ). Current electrical mapping techniques used clinically are often inadequate to map complete ventricular reentrant circuits.1 3 4 Therefore, surrogate markers of reentrant circuit location have been sought. One such marker has been the timing of local electrical activity with respect to the ECG during tachycardia. Whereas during normal sinus rhythm, activation of the ventricles occurs mainly during the QRS complex, during reentrant excitation, activation of the circuit has to occur throughout the cardiac cycle, including diastole, leading to the suggestion that regions of continuous4 or isolated1 3 12 diastolic activity represent all or part of the reentrant circuit. Thus, these regions became targets for ablation of VT with variable success. Sites of earliest activation (at least 50 ms presystolic13 ) have also been postulated to represent exit routes from the circuit to the ventricles and were assumed to be close to regions necessary for the maintenance of reentry.4 13 However, the success rate of ablation at these exit sites has been modest. Subsequently, stimulation at sites of diastolic activity (concealed entrainment) have proved to be very useful for identifying which of those sites are truly integral parts of the reentrant circuit.2 3 5 12 Sites that are activated during diastole but do not meet the criteria determined to indicate localization in the circuit by stimulation techniques have been designated as bystander pathways.3 Conversely, the application of radiofrequency energy at sites that meet the criteria for concealed entrainment is not always effective in the elimination of the tachycardia.2 3 12
Despite the differences between the experimental model of VT used in
our study and clinical tachycardia, examination of our data
can provide a conceptual framework for understanding the different
relationships between circuit activation and the ECG that may be a
cause of the variable efficacy of ablation of diastolic
sites. An important concept that can be derived from our experimental
results is that the pattern of reentrant activity is an important
determinant of the relationship between reentrant circuit activation
and the ECG. In figure-8 reentrant circuits, there is a specific region
of the circuit that must be ablated to terminate
tachycardia. This vulnerable region is the CCP, which is
activated by both reentrant wave
fronts.10 Our results show that at least part of
this region is almost always activated during
diastole (34 of 35 circuits), although segments of this
region can also be activated during systole. More specifically,
we consistently found that the midpoint of the CCP was
activated during early diastole, a time during
which, in most cases, no other region of the EBZ was activated.
Activity during late diastole most often occurred between
exiting the CCP and the exit route to the ventricles. The specificity
of early diastolic activity coinciding with CCP activation
occurred because the lines of block that form the boundaries of the CCP
prevent the reentrant wave front from exiting to the ventricles and,
therefore, prevent the onset of the QRS until the impulse leaves this
region. This is expected whether the lines of block are functional, as
in anisotropic reentry,7 or anatomic, as proposed
in the model of Stevenson et al.3 However, our
results show that variability of activation patterns, even when the
circuit is figure-8, can influence the ease at which such
diastolic activity might be located. Whereas the
"textbook" figure-8 pattern involves rotation of 2 reentrant wave
fronts around long parallel lines of block, with a long CCP between the
2 (Figure 1), Figure 2 shows that sometimes when the lines of block
have different directions, the vulnerable CCP may be quite small and
contribute to only a small segment of diastolic activity.
This may explain some clinical observations in which critical sites in
the circuit have been difficult to identify from stimulation in regions
of diastolic activity.2 3 The
vulnerable region of the circuit might also be activated
entirely during systole, when tachycardia cycle length and
the diastolic interval are short (Figure 3). In addition,
the variable distance between the location of the exit route and
the vulnerable region of the circuit in this model is also noteworthy
and may provide a reason for the variable efficacy of ablation at
exit routes in the termination of VT.13 In
figure-8 reentry (Figures 1 to 3), regions not in the CCP were also
activated during early and late diastole, showing
why diastolic activity alone is not always an accurate
predictor of CCP location.3
Sometimes only a single reentrant circuit could be mapped,
although we cannot rule out the presence of an additional circuit
outside the mapped region. Nevertheless, analysis of these
circuits provides possible explanations for the lack of specificity of
diastolic activity, and pacing at sites of
diastolic activity, for pointing out crucial regions for
ablation during some VTs. When there is only a central fulcrum of block
(Figure 6), there can be centrifugal spread of activity away from the
reentrant circuit. When this occurs, large regions that are not crucial
for reentry are activated simultaneously with the
circuit (considered to be that part of the reentrant wave front closest
to the central region of block). Indeed, in general, even when the
location of the reentrant circuit is clearly seen from high-resolution
maps as in Figure 6, a localized vulnerable region for effective
ablation that is critical for the maintenance of reentry is not
obvious. Also, stimulation at sites of diastolic activity
even within the reentrant circuit might not cause exact entrainment in
this pattern of reentry. Single-loop reentry, however, can be modified
by lines of block that are not part of the circuit and that can prevent
the reentrant wave front from spreading outward to all regions of the
EBZ (Figure 7). Activation in part of the circuit may be confined to
narrow regions by the additional lines of block, which might be
vulnerable to an ablation lesion (Figure 7). The region delineated by
the additional line of block in Figure 7 formed a bystander pathway,
which, although activated early in diastole, was
not activated every beat and therefore could not be a crucial
part of the reentrant circuit.14 Similarly,
regions of diastolic activity that are not
activated 1:1 with each QRS complex during
tachycardia have been described during clinical
studies,14 as have bystander pathways with more
consistent activation patterns.3 In
addition, pacing at sites in bystander pathways such as sites j, k, and
l in Figure 8, which are activated during early
diastole, might result in concealed entrainment but not be
effective sites for ablation.3
Limitations
Our results must be considered in light of the limitations
of the relationship of this animal model to human VT, including the
epicardial location of the reentrant circuits and the role of
anisotropy in causing functional reentry. An additional limitation is
the probability of inaccuracies in defining the onset and termination
of the QRS complex. Had more than 2 ECG leads, including precordial
leads, been recorded, an earlier QRS onset and a longer QRS
duration might have been evident and no clear diastolic
interval been located in more of the tachycardias with
short cycle lengths. Even when multiple leads are used, however,
precise determination of the beginning and end of the QRS may not be
possible.
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Acknowledgments |
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This study was supported by grant R37-HL-31393 and program project grant HL-30557 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Received December 29, 1997; revision received July 6, 1998; accepted July 21, 1998.
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Masters G, Cabo C, Schmitt H, Costeas C, Ciaccio E,
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