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Intraaortic Balloon Pumping for Ventricular Septal Defect
or Mitral Regurgitation
Complicating Acute Myocardial Infarction
By HERMAN K. GOLD, M.D., ROBERT C. LEINBACH, M.D., CHARLES
A. SANDERS, M.D.,
MORTIMER J. BUCKLEY, M.D., ELDRED D. MuNDTH, M.D.,
AND W. GERALD AuSTEN, M. D.
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SUMMARY
The intraaortic balloon pump (IABP) has been employed in the management of five patients
with ventricular septal rupture (VSD) and six patients with acute mitral regurgitation (AMR)
following myocardial infarction. All patients were in cardiogenic shock which responded poorly to
medical therapy including pressor and inotropic agents. IABP resulted in significant clinical and
hemodynamic improvement in all cases.
In patients with VSD, IABP produced a fall in wedge (PCW) pressure from 17 + 4 (SD) to
13 ±4 mm Hg (P < 0.01) while mean arterial pressure increased from 68 to 73 mm Hg. Systemic A-V 02 difference fell from 9.7 + 2.4 to 8.1 2.4 vol % (P < 0.05) while pulmonary A-V
02 difference was unchanged. Thus the pulmonic/systemic flow ratio (P/S) declined in all patients. In patients with AMR, PCW fell from 25 4 to 20 4 mm Hg (P < 0.02) with a significant diminution in "V"-wave amplitude. Cardiac output (CO) rose from 3.1 0.9 to 3.7 + 1.0
liters/min (P < 0.01). All patients underwent coronary angiography without complication in
preparation for emergency surgery.
IABP reduces AMR following acute myocardial infarction and reduces the P/S in VSD by a
selective augmentation of systemic CO. Such direct therapy acutely stabilizes these severely ill
patients. Detailed angiography may then be performed safely.
Additional Indexing Words:
Mechanical circulatory assistance
Left-to-right shunting
Afterload
the possible cost of increased myocardial ischemia.4
In contrast, counterpulsation can decrease ischemia
by raising coronary perfusion pressure and will
reduce afterload.5-12 This report summarizes our
experience in attempting to stabilize critically ill
patients with these mechanical complications utilizing the intraaortic balloon pump (IABP).
A CUTE MITRAL regurgitation or rupture of
the interventricular septum following myocardial infarction may lead to rapid clinical deterioration with pulmonary edema, hypotension, and a
high early mortality.'-3 Pressor agents which
increase afterload can aggravate mitral regurgitation and will increase left-to-right shunting. Inotropic agents can increase systemic output but at
Material and Methods
Hemodynamic studies were performed in 11 patients
admitted to the Myocardial Infarction Research Unit
Intensive Study Area. In all patients, acute myocardial
infarction was documented by a typical history,
diagnostic electrocardiographic changes, and serum
enzyme studies. Five patients had ventricular septal
defect (VSD) 1-9 days after acute infarction. In two
cases the infarction was anterior and in three inferior.
Six patients developed acute mitral regurgitation
(AMR) 1-14 days after infarction. In three patients the
infarction was anterior and in three inferior (table 1).
At the time of study all patients with VSD showed
vasoconstriction, systemic hypotension, and low central
venous oxygen saturation. Patients with AMR all
From the Medical and Surgical Services of the
Massachusetts General Hospital and the Departments of
Medicine and Surgery, Harvard Medical School, Boston,
Massachusetts.
Supported in part by U. S. Public Health Service Contract
No. 43-67-1443 (Myocardial Infarction Research Unit).
Presented before the 45th Scientific Sessions of the
American Heart Association on November 19, 1972, in
Dallas, Texas.
Address for reprints: Dr. Herman K. Gold, Cardiac
Catheterization Unit, Massachusetts General Hospital,
Boston, Massachusetts 02114.
Received December 28, 1972; revision accepted for
publication February 22, 1973.
Circulation, Volume XLVII, June 1973
Papillary mnuscle dysfunction
1191
1192
A
GOLG ET AL.
Table 1
Summary of Clinical Findings
Pt
C.B.
A.S.
R.L.
M.A.
W.J.
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H.A.
J.S.
A.J.
B.A.
J.G.
M.P.
Age
(yr)
Sex
Date of infarct
62
M
5/6
Inferior
5/11
54
M
8/31
Anterior
9/8
45
M
6/24
Inferior
6/26
39
F
3/5
Anterior
3/5
56
M
11/6
Inferior
11/9
62
65
63
68
54
63
M
M
M
M
F
F
10/6
4/5
6/30
9/15
Inferior
Inferior
10/8
4/10
7/3
9/26
Abbreviations: MR
Site of infa.rct
Anteroseptal
Inferior
Anterior
Anteroseptal
3/14
6/17
mitral repnurwitationn VSD
"
IIIALICAIA
v
1-1
demonstrated pulmonary edema, hypotension, and low
cardiac output. Both groups responded poorly to
medical therapy consisting of digitalis, diuretics, and
oxygen, and all but one were receiving catecholamine
infusion at the time of study.
Pulmonary artery and pulmonary capillary wedge
(PCW) pressures were monitored with the Swan-Ganz
flow-directed catheter and arterial pressures through an
indwelling radial artery cannula. Pulmonary-to-systemic
(P/S) flow ratio was determined by oxygen saturation.
Systemic venous samples were drawn from the superior
vena cava. In patients with AMR, cardiac output was
estimated by the dye-dilution technic with indocyanine
MEAN/
40 _ ARTERIAL
140
120[
120F
PRESSURE
100
DON IA8P
DOFF
IABP
az 80
//EARTJ
RATE
=
3/23
6/22
Diagnosis
MR; ruptuired posterior
papillary muscle
MR; infarction anterior and
posterior papillary muscle
MR; infarction posterior
papillary muscle
MR; infarction anterior and
posterior papillary muscle
MR; ruptured posterior
papillary muscle
VSD
VSI)
VSD
VSD
VSD
VSD
ventrinular-sental defect.
V Wi1 t)l s ty ususs-owIv t'vs wl wL U .
green injected into the pulmonary artery and sampled
from the radial artery.
In all patients an IABP "on-off" study was performed
daily. Systemic and pulmonary artery pressures, PCW
pressure, and electrocardiogram were recorded followed
by duplicate determinations of cardiac output and
oxygen saturation. IABP was then interrupted; 3-10 min
were allowed to elapse during which pressures were
monitored continuously. Before resuming IABP, cardiac
output and oxygen saturation determinations were
repeated. IABP was then resumed and after 5 min a
third set of measurements were taken.
In three patients (two VSD, one AMR) angiotensin
was then infused in low dose (1.25 p,g/min) during
continuous IABP to abolish the effect of IABP on
afterload. When systolic arterial pressure had been
matched to the level prior to the institution of pumping,
a fourth set of measurements was obtained.
100F
t 80
60[
Date murmur
appeared
Syslemic
60
40
40
201
20k
01
0
p/s
A-V 02
DOIFFERENCE
( V/s. % )
FL OW
RATIO
PUlmonrc
pc.0 05
NS
Figure 1
The hemodynamic response to IABP in five patients with
acute ventricular septal rupture. During IABP, the fall in
pulmonary wedge (PCW) pressure is accompanied by a small
but significant rise in mean arterial pressure. Vertical bars
represent 1 SD.
OFF
ON
OFF
ON
IABP
Figure 2
The maximal effect of IABP on systemic and pulmonary
A-V oxygen difference after ventricular septal rupture. During IABP the pulmonic/systemic (P/S) flow ratio fell from
5.2/1 to 4.1/1. Asterisks represent the mean.
Circulation, Volume XLVII, June 1973
1193
BALLOON PUMPING FOR VSD OR MR
1sec.
,/
/77-0/-40
MGH
ECG
ARTERIAL
PRESSURE
(mm h/g)
4+_J0
20
-t-F--q--
:-
-- b
I00LEELX 4
PCW
PRESSURE
+
----|
ON xX
IS
LABPi
OFIAB
|i1-r
Ill1 KIHI
E0AE
ANGIOTENSIN
(mm Hg)
02 SAT (%)
98
87
54
98
85
60
98
87
54
RAD
PA
SVC
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Figure 3
Reversal of IABP effect with angiotensin in a patient with
ventricular septal rupture. Initiation of IABP produces a
20-mnm reduction in systolic arterial pressure. When systolic
arterial pressure is returned to 80 mm Hg by angiotensin
infusion, oxygen saturation, PCW pressure, and P/S flow
ratio return to prepumping levels.
After
of 28 hours of IABP, selective
and left ventricular cineangiography was
performed by the Sones technic during uninterrupted
circulatory assistance in preparation for emergency
cardiac surgery.
an average
coronary
Results
In the patients with VSD, the mean PCW
pressure fell from 17 to 13 mm Hg (P < 0.01).
There was a small but significant rise in mean
arterial pressure without a significant change in
MAP
MEAN WEDGE
(mm
(bpmJ
Hfg)
CO
(L
/min)
PRESSURE
32~
(mm Hg)
80
pc0.02
IN S
I60
p<0.02
28~
70
140
24F
60
120
20
50
100
6
40
80
12
30
60
8
20
40
4
10
20
6~
p<
0005
5
T
1
4
3
2
01
0
IABP
OFF
ON
OL
Figure 4
The hemodynamic response to IABP in six patients with
acute mitral regurgi-tation. During IABP there is a significant fall in wedge pressure and small but significant rise
in cardiac output (CO). MAP = mean arterial pressure;
HR = heart rate.
a
Circulation, Volume XLVII, June 1973
heart rate (fig. 1). Systemic A-V 02 difference fell
from an average of 9.7 + 2.4 (SD) to 8.1 + 2.4 vol %
(P < 0.05) while pulmonary A-V 02 difference
remained low and unchanged. Thus the mean P/S
flow ration fell from 5.1/1 to 4.2/1 (P < 0.05)
secondary to a selective increase in systemic output
(fig. 2).
The effect on the intracardiac shunt was produced by a reduction in left ventricular afterload.
When angiotensin was infused during IABP and
systolic arterial pressure was matched to the level
present prior to the institution of balloon pumping,
the P/S flow ratio returned to prepumping levels in
spite of a marked increase in coronary perfusion
pressure (fig. 3).
In the patients with AMR, the mean PCW
pressure fell from 25 to 20 mm Hg (P < 0.02) with
initiation of IABP. Mean arterial pressure remained
unchanged while the heart rate fell from 99 to 95
beats/min (P <0.02). This was associated with an
average rise in cardiac output from 3.1 to 3.7
liters/min (P <0.01, fig. 4). Interruption of IABP
was accompanied by a rise in PCW pressure and an
increase in the amplitude of the systolic regurgitant
'Y' waves (fig. 5). Angiotensin was infused at 1.25
gg/min during IABP in one patient, and cardiac
output, PCW pressure, and regurgitant "V" waves
all returned to prepumping levels.
All patients in both groups improved hemodynamically and showed maximum stabilization by 24
hours. Nevertheless, at this point all continued to
show balloon dependence13 with inadequate circulatory dynamics during test interruption of IABP.
Two patients with VSD and three with AMP. were
continued on IABP for a longer period prior to
angiography. All showed hemodynamic deterioration despite continued circulatory assistance.
The angiograms revealed extensive coronary
disease in both groups. All patients with VSD
showed high-grade proximal left anterior descending coronary obstruction. Five of six showed highgrade proximal obstruction of the right coronary
artery, and two showed three-vessel disease. The
left ventriculograms in the right anterior oblique
position were partially obscured by the left-to-right
shunt and opacification of the right ventricle. When
segmental contraction could be appraised, abnormalities were found similar to those reported
elsewhere.13 All patients with AMR showed both
high-grade obstruction of the proximal left anterior
descending and right coronary arteries. Two
showed three-vessel disease. The angiographic
severity of mitral regurgitation was considered
GOLD ET AL.
1194
7L. MI 174 -50-80
..........
ECG
ARTERIAL
PRESSURE
(mm Hg)
POW
PRESSURE
( mm Hg )
*_
200
.,
100 F
TOO
P",t'
J ^.
"W4
i. Owomgw"~uki
40
20i
,
'
.
X
-
-
-
>
S
:
-
:S:
(
.
t
.:
.:. . ( .. - .... : g 5 . : :. S:.5
:. | ::X 1g5.E.PE:
t
ON
IABP
OFF
IABP
Figure
5
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The effect of IABP on acute mitral regurgitation. At the arrow the balloon pump is turned off. The increase
systolic arterial pressure is accompanied by a prompt rise in PCW pressure and an increase in the amplitude of systolic regurgitant "V" waves.
in
moderately severe in the four cases of papillary
dysfunction and severe in the two cases of papillary
rupture. Studies were performed even in the
presence of severe systolic hypotension (fig. 6) and
there were no significant complications.
Emergency
A
a
performed in four
VSD who received IABP within 24 hours of septal
with AMR secondary
Discussion
A
ECG
100
,h,
RAD/A L
was
rupture survived. One patient
to papillary muscle survived.
M. P MGH /78 -25-19
a
surgery
patients with VSD and five with AMR. Two
patients with anterior myocardial infarction and
50'
1
The onset of circulatory collapse associated with
abrupt appearance of a systolic murmer after acute
myocardial infarction presents a diagnostic and
therapeutic problem. In most cases the diagnosis
is mitral regurgitation secondary to papillary muscle
dysfunction or rupture or ventricular septal defect. 14 The diagnosis can be established at the
bedside with the passage of a Swan-Ganz flowdirected catheter.'5' Oxygen samples from the right
atrium, pulmonary artery, and radial artery will
identify the presence of a VSD and the inscription
of the PCW wave form will confirm mitral regurgitation.
Medical therapy for these complications often
produces only a limited effect. In VSD, infusion of
LV
0 L.
inotropic agent may increase systemic output.
this intervention is associated with
concomitant increase in left-to-right shunting without change in the P/S flow ratio, thereby resulting
in a marked increase in left ventricular work.
Agents which raise arterial pressure by increasing
afterload augment pulmonary flow, increase left-toright shunting, and may produce a critically lowoutput state. In AMR the degree of MR is
an
sec
Figure 6
Radial artery and left ventricular (LV) pressures prior to
angiography in a patient with ventricular septal rupture.
During IABP the peak LV pressure is 55 mm Hg while the
peak diastolic pressure is maintained at 75 mm Hg. The
patient is in sinus tachycardia. Electrocardiographic (ECG)
artifacts are timing indicators.
However,
Circulahion, Volume XLVII, June 1973
1195
BALLOON PUMPING FOR VSD OR MR
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aggravated by pressor agents. Inotropic agents
which may increase systemic output do so at the
expense of increased myocardial oxygen demand
and may further impair myocardial contraction in
ischemic areas."'
In both situations, the desired physiologic response possibly could be achieved by vasodilator
therapy. Reduction in systemic resistance in ventricular septal rupture would favor systemic flow and
decrease the left-to-right shunt. Moreover in
patients with papillary muscle dysfunction or
rupture, reduction in systemic resistance would
favor forward flow and reduce the degree of mitral
regurgitation. However, in these patients whose
clinical condition is characterized by cardiogenic
shock, any further reduction in systemic and
coronary perfusion pressure is hazardous.
IABP can selectively reduce systemic resistance
during left ventricular ejection thus producing the
beneficial effects of a vasodilator without a
reduction in mean arterial pressure. This is
accompanied by an increase in coronary perfusion
pressure which can reduced ischemic dysfunction.
This study confirms the effects of IABP in
patients in whom mechanical lesions have resulted
in cardiogenic shock. Although IABP produced
clinical and hemodynamic improvement in all
patients, a completely satisfactory correction of the
impaired circulatory dynamics could not be obtained. The peak improvement occurred within the
first 24 hours of pumping, and in no patient did
prolonged pumping produce further benefit. It was
not possible to maintain patients into a chronic
phase and thus avoid the high risk of emergency
surgery.17-20
IABP does produce a sufficient level of hemodynamic stability to permit both selective coronary
and left ventricular cineangiography in these
critically ill patients. The studies can be performed
with low risk. In addition to demonstrating the
mechanical abnormality, complete angiography also
uncovers multiple significant proximal coronary
artery obstructions amenable to surgical revascularization. The angiographic results in these patients
suggest that shock is the result of a mechanical
lesion superimposed upon an ischemic and infarcted ventricle. In this setting the greatest chance for a
therapeutic success lies in the early application of
circulatory assistance and the accurate identification
of both mechanical and coronary artery lesions
responsible.
Circulation, Volume XLVII, June 1973
Acknowledgment
We are indebted to Mr. John P. Hinckley, Jr., Mr. John F.
Drake, and Mr. Marc S. Newman for skilled technical
assistance, to the MIRU Nursing Staff, and to Mrs. J. A.
Kowalczyk-Beckworth and Mrs. B. Levin for their help in
the preparation of this manuscript.
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Circulation, Volume XLVII, June 1973
Intraaortic Balloon Pumping for Ventricular Septal Defect or Mitral Regurgitation
Complicating Acute Myocardial Infarction
HERMAN K. GOLD, ROBERT C. LEINBACH, CHARLES A. SANDERS, MORTIMER J.
BUCKLEY, ELDRED D. MUNDTH and W. GERALD AUSTEN
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Circulation. 1973;47:1191-1196
doi: 10.1161/01.CIR.47.6.1191
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