Detection of Latent Function in Acutely Ischemic
Myocardium in the Dog
COMPARISON OF PHARMACOLOGIC INOTROPIC STIMULATION AND
POSTEXTRASYSTOLIC POTENTIATION
By Stephen H. Dyke, Charles W. Urschel, Edmund H. Sonnenblick. Richard Gorlin,
and Peter F. Cohn
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ABSTRACT
In poorly perfused myocardium with resultant ischemic dysfunction, augmentation of
contractility can, under certain conditions, be used to detect viable but ordinarily
noncontracting muscle. Two methods of inotropic augmentation, pharmacologic inotropic
stimulation and postextrasystolic potentiation (PESP), were studied in acutely ischemic
canine myocardium with controlled coronary blood flow. A caliper length gauge to record
segmental shortening and left ventricular pressure was used to construct pressure-length
loops. Acute regional ischemia depressed segmental function: early segmental shortening
decreased (-20 ± 0.02%[SE]) and frequent dyskinesia occurred. Restoring coronary blood
flow corrected segmental shortening to control levels. During acute regional ischemia,
PESP consistently augmented segmental function (+49 ± 0.03%) and abolished dyskinesia. Pharmacologic inotropic stimulation with isoproterenol or calcium administered
into the coronary arteries did not produce a comparable improvement in segmental
function (+9 ± 0.05%). Although early shortening markedly increased with pharmacologic
stimulation, there was no consistent change in total shortening, and the area of the
pressure-length loop decreased. Due to late dyskinesia, there was a decrease in injection
shortening. Systemically administered pharmacologic agents accentuated early dyskinesia but caused no consistent change in total shortening. Unlike PESP, pharmacologic
agents either worsened segmental function or caused responses that were minimum and
inconsistent; such responses clearly cannot be used to identify viable ischemic myocardium.
KEY WORDS
pressure-length loops
contractility
segmental shortening
• Present evidence indicates that coronary revascularization may correct segmental dysfunction in
some patients with coronary artery disease (1, 2).
This correction of a functional deficit implies that
flow is restored to areas of myocardial muscle that
are viable although ischemic. Detection of such
areas of viable but poorly perfused myocardium
may be critically important to the optimization of
the benefits of coronary bypass surgery.
Pharmacologic inotropic stimulation has been
proposed as a method of detecting viable ischemic
myocardium in man (3). In dogs, systolic bulging of
the left ventricle following occlusion of the left
anterior descending coronary artery can be reduced
by the administration of isoproterenol or calcium
(4). However, in ischemic muscle the response to
From the Cardiovascular Division, Department of Medicine,
Peter Bent Brigham Hospital and Harvard Medical School,
Boston, Massachusetts 02115.
This work was supported in part by U. S. Public Health
Service Grant HL 11306 and Training Grant HL 05890 from the
National Heart and Lung Institute.
Received May 13, 1974. Accepted for publication Januarv 3,
1975.
490
ventricular asynergy
isoproterenol
positive inotropic interventions may be attenuated
(5). Moreover, when coronary blood flow is limited,
sustained inotropic interventions may augment
oxygen requirements without enhancing the supply
and thus produce a secondary ischemic depression
of myocardial function (5).
Postextrasystolic potentiation (PESP) of cardiac
contractility was first demonstrated by Langendorff (6) and has subsequently been shown to be a
fundamental characteristic of both normal and
depressed mammalian myocardium (7). Continuous paired stimulation of normal myocardium
results in a substantial, sustained augmentation of
myocardial contractility (7) and represents a maximum inotropic drive to cardiac muscle (8). In the
ischemic myocardium, continuous paired stimulation induces an initial augmentation of contractility that cannot be sustained; this initial response is
followed by substantial depression (5). The initial
augmentation of contractility in the ischemic muscle, however, suggests that PESP following a single
paired extrasystole might serve to identify viable
but poorly perfused myocardium. Therefore, the
Circulation Research. Vol. 36. April 1975
INOTROPIC STIMULATION IN ACUTE ISCHEMIA
491
present study was done to compare the effects of
PESP and pharmacologic inotropic agents on
acutely ischemic muscle.
Representative data obtained from this preparation
are shown in Figure 2. During the control state, segmental shortening begins at point A, which is coincident with
the initial rise of left ventricular pressure (end-diastole),
and continues until ventricular pressure falls to its
diastolic nadir at point E (end-systole); segmental
lengthening occurs from end-systole to end-diastole of
the next beat (E to A). Figure 2 (top) shows a pressure-segment length loop obtained in these experiments.
Beginning at end-diastole (A), the loop is inscribed
counterclockwise (B to E). Five parameters were determined: (1) total shortening (length change from the
longest length to the shortest length [A to E]), (2)
shortening during ventricular ejection (B to D), (3) area
of the left ventricular pressure-segment length loop, (4)
segment length at peak systolic pressure (C), and (5)
time to peak shortening.
Methods
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Studies were performed on adult mongrel dogs (15-25
kg) anesthetized with sodium pentobarbital (25 mg/kg,
iv). Endotracheal ventilation was maintained with a
mixture of room air and oxygen. Following a left thoracotomy, the heart was supported in a pericardial cradle.
The left anterior descending coronary artery was cannulated with a 14- or 16-gauge metal cannula distal to
the first diagonal branch and perfused from a femoral
artery. The perfusion pressure was controlled using a
constant-flow pump (Sigmamotor). Ischemia could be
electively induced by reducing the flow in this circuit.
A caliper length gauge (9) was placed in the distribution of the cannulated artery and oriented so that it
measured the circumferential motion of the ventricular
wall. The gauge was coupled to the myocardium with
long pins attached to its feet and with epicardial sutures.
The calibration of the gauge was linear, i.e., lateral
motion of the legs of the gauge reflected a linear change
in distance between the feet. The initial length of the
gauge was set arbitrarily. A bipolar pacing electrode was
placed in the right ventricular outflow tract. The left
ventricular cavity was cannulated through a left atriotomy with a short steel cannula (Fig. 1).
Coronary perfusion pressure and left ventricular pressure (P) were recorded using Statham P23Db strain
gauges. Left ventricular dP/dt was obtained using a
resistance-capacitance differentiation circuit exhibiting
a constant phase shift of 90 ± 1 ° from 0 to 160 cps. Data
were recorded on a light-writing recorder (Honeywell
Visicorder) at 200 mm/sec and on a pen-writing recorder
(Brush) at 25 mm/sec. Photographs of the course of
segment length relative to left ventricular pressure were
obtained from a storage oscilloscope.
IEFT
VENTRICULAR
PRESSURE
A SINGLE PAIRED ELECTRICAL STIMULATION (PESP)
Single extrasystoles were produced by electrical stimulation (2 msec, 1-4 ma) from the right ventricular
pacing electrode.1 The interval between the QRS complex and the stimulus could be varied. In the present
experiment, maximum augmentation (100% increase)
occurred before the peak of the T wave (Fig. 3). Thus, a
single paired electrical stimulation was placed in the
cycle immediately after emergence from the refractory
period. The effects of this paired electrical stimulation
(PESP) were investigated during a control state and an
ischemic state characterized by a reduction in coronary
perfusion from control levels by an average of 64% (e.g.,
Fig. 4A-C). The duration of the ischemia usually was less
than 5 minutes, but in some dogs it was extended to as
long as 30 minutes.
PHARMACOLOGIC INOTROPIC STIMULATION
The effects of pharmacologic inotropic stimulation
were investigated during a control state and an ischemic
state like that used in the PESP study. Isoproterenol or
calcium was infused systemically (iv) or locally (ic) into
the cannulated segment. Doses were chosen so that the
augmentation of left ventricular dP/dt induced by either
drug given locally or systemically was approximately the
same (isoproterenol 2 mg/min, iv, and 0.2 mg/min, ic;
calcium 260 mg/min, iv, and 26 mg/min, ic).
Results
EFFECTS OF ACUTE REGIONAL ISCHEMIA
PERFUSION PUMP
FEMORAl MTEOT
FIGURE 1
Schematic diagram of the experimental model. Controlled
perfusion of the left anterior descending coronary artery was
provided from the femoral artery. Perfusion pressure and left
ventricular pressure were monitored. A caliper length gauge was
oriented circumferentially in the distribution of the left anterior
descending coronary artery. The gauge was attached using deep
penetrating pins and epicardial sutures (insert).
Circulation Research. Vol. 36. April 1975
Figure 4 shows the typical effects of acute
regional ischemia on segmental shortening; similar
results were obtained in 43 experiments on 12 dogs.
Reduction of coronary pressure caused a rapid
depression of segmental myocardial function in 15
seconds (Fig. 4A-C). The pattern of altered segmental shortening during ischemia was reproducible. Characteristically, early shortening was decreased, and frequently bulging of the segment
occurred in early systole. The shortening of the
segment that did occur was seen late in systole
during the period when left ventricular pressure
1
The stimulator was generously supplied by Mr. B. Berkovits, American Optical Co., Waltham, Mass.
492
DYKE. URSCHEL. SONNENBLICK. GORLIN. COHN
END SYSTOLE
4mm
z
END DIASTOLE1—y
0 mmHg
60
100 mmHg
END SYSTOLE 1=™-"
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O
Z
—
100 mmHg
END DIASTOLE I
0
increased. Figure 5B shows the effects of a single
paired electrical stimulation on segmental function
during acute severe ischemia. Following 30 minutes
of total occlusion, diastolic segment length was
increased, and the myocardial segment displayed a
total loss of shortening during systole. Shortening
beyond end-diastolic length occurred only late in
systole when left ventricular pressure had fallen to
diastolic levels. This late shortening was minimum
and probably passive. However, PESP of the
ischemic segment was still evident. During recovery (C), segmental function was restored to near
control values. Similar results were obtained in 14
experiments in six dogs. As shown in Table 1,
potentiation of segment function was noted consistently, although left ventricular dP/dt increased
100 ± 0.11% (P < 0.05). Early or late systolic
bulging ceased, and total shortening increased 49 ±
0.03% (P < 0.05), shortening during ejection rose
123 ± 0.08% (P < 0.05), and area of the pressurelength loop increased 144 ± 0.08% (P < 0.05).
EFFECTS OF PHARMACOLOGIC INOTROPIC STIMULATION
0 mmHg
FIGURE 2
Representative data. Top: Plot of segment length relative to left
ventricular pressure for the same data shown in the bottom of
the figure. Bottom: Simultaneous tracings of left ventricular
pressure and myocardial segment length. See text for additional
explanation.
The effects of intracoronary administration of
isoproterenol on the function of the ischemic myocardial segment (coronary perfusion pressure 45
mm Hg) are shown in Figure 6 (top). Intracoronary
administration of calcium produced similar
changes. Characteristically, these agents caused a
100
was falling toward diastolic levels. Reperfusion (D)
restored segment length and function to control
levels. Table 1 summarizes the data from the 12
dogs showing the effects of acute regional ischemia
on segmental function. With a decrease in coronary
pressure averaging 64%, total shortening fell 20 ±
0.02% (P < 0.05), shortening during ejection fell 58
± 0.07% (P < 0.05), and the area of the pressurelength loop fell 50 ± 0.04% (P < 0.05). Left
ventricular dP/dt declined only 4 ± 0.02% (P <
0.05).
% INCREASE IN
EJECTION
SHORTENING
BY PESP DURING ISCHEMIA
EFFECTS OF A SINGLE PAIRED ELECTRICAL STIMULATION (PESP)
The effects of a single paired electrical stimulation on segmental myocardial function are shown
in Figure 5. During the control period (A), the
extrasystole caused a slight mechanical contraction
followed by a compensatory pause. The subsequent
beat was markedly potentiated with augmentation
of segmental function (PESP). Starting from a
longer end-diastolic length, total segmental shortening, shortening of the segment during ejection,
and area of the pressure-segment length loop were
increased. In addition, left ventricular pressure was
ORS
I
100
msec
FIGURE 3
Effect of the QRS-stimulus interval on postextrasystolic potentiation (PESP) during ischemia. The time (msec) of the
stimulus from the onset of the QRS complex is shown on the
horizontal line. The percent increase in shortening during
ejection induced by PESP is shown on the vertical line.
Maximum augmentation (100% increase) occurred early on the
initial slope of the T wave, with a lesser amount of augmentation (less than a 50% increase) at and after the peak of the T
wave.
Circulation Research. Vol. 36. April 1975
493
INOTROPIC STIMULATION IN ACUTE ISCHEMIA
A
B
C
D
CP: 118
CP--S7
CP=43
CP> 118
iflMAM HWUUIM MMAM MlflAMM
E 100
"5
twww
21
IVWWW
I16.
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ZI8.5
3
z
21.
Si
16.
118.5
E 100
6
21.
FIGURE 4
Effect of acute reversible ischemia on segmental myocardial and left ventricular function. The top
three lines show the primary data of simultaneous left ventricular pressure (LVP), left ventricular
(LV) dP/dt, and myocardial segment length at several levels of coronary pressure (CP), and the
bottom two lines show segment length data like that described in Figure 2. A: Control state. B and
C: Progressive increments of acute ischemia. The two loops in C reflect the presence of pulsus
alternans. D: Reperfusion and return to control state.
marked increase in early segmental shortening.
The length at peak systolic pressure was shorter,
and the time to peak shortening was decreased 51
± 0.05% (P < 0.05).
Table 1 summarizes the data from 11 experi-
ments with isoproterenol in six dogs. There was no
consistent change in total shortening (9 ± 0.05%),
although it was slightly increased by intracoronary
administration of calcium (24 ± 0.07%, P < 0.05).
Segmental function was always worsened by local
TABLE 1
Percent Change in Segmental Myocardial Function and Left Ventricular dP/dt
Control— Ischemia
Ischemia— Ischemia plus
43
14
Total
shortening
(% change)
Ejection
shortening
(% change)
Area
(% change)
LV dP/dt
(% change)
- 2 0 ± 0.02*
49 ± 0.03*
- 5 8 ± 0.07*
123 ± 0.08*
- 5 0 ± 0.04*
144 ± 0.08*
- 4 ± 0.02*
100 ± 0.11*
9 ± 0.05
-180 ± 0.21*
-148 ± 0.18*
44 ±0.09*
0.0 ± 0.03
34 ± 0.13*
PESP
11
Ischemia— Ischemia plus
local inotropy
18
Ischemia— Ischemia plus
systemic inotropy
18 ± 0.10
Values are means ± SE. N = number of trials, and LV = left ventricular.
* P < 0.05.
Circulation Research. Vol. 36. April 1975
38 ± 0.04*
494
DYKE. URSCHEL. SONNENBLICK. GORLIN. COHN
B
C
TOTAL OCCLUSION/30 MINUTES
REPERFUSION
CP=8
CP=50
I 15.
x
5
Z-
20
z
UJ
0
100
LVP mmHg
E 100
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EfVUl/lAAJ
si
&2
0
100
LVP mmHg
lAAJWl/D
0
100
LVP mmHg
HAAJ
W
15
I
251
FIGURE S
Effect of a single paired electrical stimulation on segmental myocardial function. LVP = left
ventricular pressure, and CP = coronary pressure. A: Effect of PESP during the control state. B:
Effect of PESP during ischemia. C: Effect of PESP after reperfusion. In A and C, the outer loop is the
augmented beat {PESP), the middle loop the control beat, and the inner loop the extrasystole. In B,
the pressure-segmental length tracing during the ischemic period is the downsloping inner line, and
the extrasystole is the upgoing tail near the origin of the line. The outer loop in B shows PESP during
ischemia.
administration of inotropic stimulation. The area
of the pressure-length loop decreased 148 ± 0.18%
(P < 0.05), and due to late systolic bulging
shortening during ejection decreased 180 ± 0.21%
(P < 0.05). Often, net shortening during ejection
was negative with a longer length at end-ejection
relative to that at the beginning of ejection due to
early relaxation. In parallel with the early augmentation of shortening, peak left ventricular dP/dt
increased 44 ± 0.09% (P < 0.05).
The effects of systemically administered isoproterenol on segmental function during ischemia
(coronary perfusion pressure 45 mm Hg) are shown
in Figure 6 (bottom). A summary from 18 experiments in seven dogs is given in Table 1. Again,
calcium produced similar changes. Left ventricular
dP/dt increased 38 ± 0.04% (P < 0.05). Early
bulging was accentuated, and segment length at
peak systolic pressure was slightly longer. There
was no consistent change in total shortening (0.0 ±
0.03%), although shortening late in systole was
occasionally increased. On several occasions, these
agents induced pulsus alternans or increased the
alternans due to ischemia. The time to peak
shortening decreased 10 ± 0.02% (P < 0.05). There
was no significant change in the area of the
pressure-length loop (18 ± 0.01%); however, ejection shortening increased 34 ± 0.13% (P < 0.05).
A comparison of the effects of systemically
administered isoproterenol and a single paired
extrasystole (PESP) during the same state of
ischemia (coronary perfusion pressure 34 mm Hg)
is shown in Figure 7. In the experiment involving
PESP, two ischemic beats showing depressed function and slight alternans preceded the extrasystole.
In these beats, early systolic lengthening occurred
followed by late shortening as left ventricular
pressure was falling. The extrasystole produced
minor mechanical activity and was followed by a
compensatory pause. The subsequent beat was
markedly potentiated, and the early systolic
lengthening was abolished. Total shortening, ejection shortening, and the area of the pressure-segment length loop were increased, indicating subCircutation Research, Vol. 36. April 1975
495
INOTROPIC STIMULATION IN ACUTE ISCHEMIA
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stantial augmentation of segmental and left ventricular function with an increase in left ventricular
dP/dt. At comparable levels of ischemia, systemically administered isoproterenol increased left ventricular dP/dt but caused mechanical alternans of
the segment with increased early systolic bulging.
In the stronger beat of the alternans, the total
shortening and the shortening during ejection were
increased compared with those parameters during
ischemia alone (i.e., the first two beats of Fig. 7,
left). However, these changes were due to shortening from longer lengths as a result of the increased
early systolic bulging with subsequent shortening
in late systole. Even in the stronger beat, effective
segmental motion was increased only slightly,
whereas in the weaker beat it was less than that
during ischemia. In contrast, PESP was characterized by marked normalization of all parameters of
segmental function.
ISCHEMIA
ISCHEMIA PLUS
LOCAL ISOPROTERENOL
CP=45
CP = 45
o
ISCHEMIA
PLUS PESP
ISCHEMIA PLUS
SYSTEMIC ISOPROTERENOL
CP = 34
,_, J ^ u i_
1
<
u U
16.
Z18.5
21.'—
0
100
LVP mmHg
0
100
LVP mmHg
FIGURE 7
o
too
0
100
LVP mmHg
LVP mmHg
ISCHEMIA PLUS
ISCHEMIA
SYSTEMIC
ISOPROTERENOL
CP = 45
CP=45
100
LVP mmHg
LVP mmHg
FIGURE 6
Effect of pharmacologic inotropic agents on segmental function
illustrated by pressure-segment length loops. The top two loops
show the effect of locally administered isoproterenol, and the
bottom two show the effect of systemically administered isoproterenol. Segmental function during ischemia alone is shown
on the left, and the right sections show the alterations produced
by the pharmacologic inotropic agent during ischemia. LVP =
left ventricular pressure, and CP = coronary pressure.
Circulation Research. Vol. 36, April 1975
Comparison of the effects of systemically administered pharmacologic inotropic agents (right) and PESP (left) during the same
ischemic state. See legend to Figure 4 for explanation. LVP =
left ventricular pressure, and CP = coronary pressure.
Discussion
The detection of ischemic but viable muscle has
recently become clinically important, since restoration of flow to this muscle may improve segmental
and ventricular function under both acute and
chronic conditions. Chronic segmental dysfunction
can be reversible particularly following successful
revascularization of the ischemic heart (1, 2).
Observation of the response to inotropic stimulation has been proposed as a way of detecting
dysfunction in ischemic yet viable myocardium (3).
Systemically administered epinephrine induces
improvement in regions of ventricular akinesia or
hypokinesia in some patients with coronary artery
disease (3). Experimentally, it has been shown that
intracoronary administration of isoproterenol or
calcium can decrease or abolish early systolic
expansion in ischemic regions (4). Furthermore,
systemically administered isoproterenol can increase contractile force in an ischemic area (10),
although this increase cannot be sustained (5) and
depression may follow due to increased oxygen
496
Downloaded from http://circres.ahajournals.org/ by guest on June 16, 2017
requirements (11) in the absence of an augmented
coronary blood flow.
The results of the present study indicate that,
although pharmacologic inotropic stimulation with
isoproterenol or calcium may reveal residual function in acutely ischemic muscle, the response is
minimum and often inconsistent. On the other
hand, the introduction of a properly timed extrasystole results in consistent and significant improvement of segmental shortening during the subsequent beat. Moreover, the single-beat augmentation, although it may increase energy needs for a
single beat, does not produce prolonged secondary
myocardial depression due to augmented oxygen
needs.
Regional ischemia induces a characteristic, reversible pattern of early*systolic expansion followed
by shortening in late systole when left ventricular
pressure is falling to low levels (12). Intracoronary
administration of calcium or isoproterenol in the
presence of ischemia supplants this abnormal pattern of shortening with an equally abnormal but
different pattern, i.e., marked early systolic shortening followed by late systolic expansion. Segmental function appears to be worse during the pharmacologic stimulation than it is during ischemia
alone. Thus, a segment showing hypokinetic but
relatively normal shortening is converted to one
showing late paradoxical motion (dyskinesia) (Fig.
2). Intracoronary injections primarily affect the
segment perfused by the artery (13). Since both
calcium and isoproterenol increase the speed of
muscle contraction and shorten the duration of
contraction, they change the time course of contraction in the ischemic segment in relation to that
in the remaining normal muscle. Thus, the ischemic segment contracts maximally very early, and
the late bulging is probably caused by the later
contraction of the normal muscle in the remaining
parts of the left ventricle, interacting with the
more rapidly relaxing ischemic segment. Although
viability of the ischemic area is thus clearly identified by the replacement of early akinesia with
marked but abbreviated shortening, the practical
opportunity to perfuse only an akinetic area of
myocardium with an inotropic agent is quite limited.
Responses of the ischemic myocardium to the
systemic administration of pharmacologic inotropic stimulation are inconsistent. Unlike local
inotropic stimulation, this procedure never results
in a change in the basic pattern of shortening
during ischemia. However, systemic use of these
agents frequently increases the degree of early
DYKE. URSCHEL. SONNENBLICK. GORLIN. COHN
systolic expansion with some augmentation of late
shortening beginning about the time of peak pressure. Since this later shortening follows enhanced
early expansion, the net shortening during systole
is unchanged. Although enhancement of performance of the ischemic segment is sometimes seen
following systemic inotropic stimulation, the absence of such a response clearly cannot be used to
infer nonviability. Recent data indicate that the
effect of inotropic agents may be attenuated in
ischemic muscle (5). Thus, the effect of systemically administered agents may reflect differential
effects of the agents on normal and ischemic
muscle. Enhanced contractility in the normal muscle may cause early systolic expansion of the
ischemic muscle. In addition, these changes may
also reflect a differential ability to enhance oxygen
supply to meet the increased oxygen consumption
induced by the inotropic agent (11).
Other studies have suggested that pharmacologic
inotropic stimulation in the presence of regional
ischemia can have detrimental effects. Isoproterenol can extend the area of ischemia and
injury, presumably because of increased myocardial oxygen consumption (14).
In comparison to the pharmacologic agents,
PESP is consistent in demonstrating residual function and thus viability. Left ventricular dP/dt
increases (Table 1) and the segmental shortening
pattern is normalized. In addition, PESP can be
demonstrated for at least 30 minutes after total
coronary artery occlusion (Fig. 5) at a time when
the ischemic segment is doing no useful work.
The magnitude of PESP depends on the QRSstimulus interval preceding the augmented beat.
The more premature the extrasystole, the greater
the subsequent augmentation. In this study, maximum augmentation occurred when the premature
stimulus was introduced before the peak of the T
wave. Although this time dependence of PESP has
been noted previously (15, 16), it may account for
the lack of effect of extrasystoles noted during
ischemia in other studies (10) and of spontaneous
extrasystoles for which this interval is variable and
potentially long.
As demonstrated by the loops, in the present
experiments the filling pressures were normal and
the changes during ischemia were minor, since only
a segment of the myocardium was made ischemic.
The changes in motion of the loops were apparently
not significantly dependent on volume, and a small
increase in end-diastole volume did not restore the
inappropriate motion of the ischemic area.
Preliminary data indicate that PESP can also
Circulation Research, Vol. 36, April 1975
INOTROPIC STIMULATION IN ACUTE ISCHEMIA
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improve ventricular performance and enhance segmental function in patients with coronary artery
disease (17). Furthermore, the initial observations
in man have revealed that the extrasystole must be
introduced later in the electrical cycle (after the T
wave) to obtain depolarization and PESP (17).
Even though repetitive firing has occurred with
stimuli introduced at nearly all parts of the electrical cycle in the dog (18), the initiation of ventricular tachycardia or fibrillation was not encountered
in 15 patients with coronary artery disease (17).
Thus, although the vulnerable period is close to the
peak of the T wave and, in ischemic muscle,
becomes wider with the threshold for ventricular
tachycardia and fibrillation decreasing due to both
ischemia (19) and the extrasystole (20), this theoretical consideration does not appear to be a major
limiting factor in clinical use of this technique.
In summary, these experiments demonstrate
that a single extrasystole producing PESP can help
to identify viability in acutely ischemic muscle.
Investigators now have the capacity to repeatedly
determine inotropic contractile reserve, which may
not be evident during ambient conditions, without
augmenting oxygen needs, which may further
worsen the degree of ischemia. Pharmacologic
agents augment oxygen requirements and therefore
can have deleterious effects in ischemic muscle. It
is hoped that the preoperative use of PESP will
assist in detecting ischemic but viable muscle in
patients with coronary artery disease so that the
benefits of coronary bypass surgery can be optimized.
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S H Dyke, C W Urschel, E H Sonnenblick, R Gorlin and P F Cohn
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Circ Res. 1975;36:490-497
doi: 10.1161/01.RES.36.4.490
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