WEDNESDAY MORNING, APRIL 16, 1975
8:30 A.M. Scientific
Session
Imperial Ballroom
MYOCARDIAL PRESERVATION
(Open Discussion)
Chairman - W. G. Bigelow
Metabolism (Abstract 23) David C. MacGregor
Biochemistry (Abstract 24) R.
W. Busuttil
Retrograde Coronary Perfusion (Abstract 25) Robert A. Poirier
Low Output Syndrome (Abstract 26) Gerald Buckberg
Subendocardial Flow (Abstract 27) Charles F.
Reuben
Local Deep Hypothermia (Abstract 28) Randall
B. Griepp
Intra-Aortic Balloon Pumping (Abstract 29) David Bregman
Intra-Aortic Balloon Pumping (By Invitation) Donald B. Effler
INTERMISSION - VISIT EXHIBITS (Albert Hall)
Coronary Perfusion (By Invitation) Dwight C.
McGoon
Anoxic Arrest (By Invitation) Denton A. Cooley
Ventricular Fibrillation (By Invitation) Ronald
J. Baird
Open Discussion (Seventy Minutes)
Summary and Perspective (By Invitation) James V. Maloney, Jr.
23. Ischemic Contracture of the Left Ventricle: Production and
Prevention
DAVID C. MacGREGOR*, GREGORY J. WILSON*, SHIGEO
TANAKA*,
DONALD E. HOLNESS*, WOLFGANG LIXFELD*,
MALCOLM D. SILVER* and LORRAINE J. RUBIS*,
Toronto, Ontario, Canada
Sponsored by W. G. Bigelow, Toronto, Canada
Ischemic contractive of the left ventricle ("stone
heart") is a recognized complication of prolonged periods of interruption of
the coronary circulation during open-heart surgery. We have examined the
effects of moderate hypothermia (28°C) and preoperative beta-adrenergic
blockade (propranolol, 0.5 mg/kg; 1.0 mg/kg) on contracture development during
ischemic arrest of the heart.
Four groups of 8 dogs each
were placed on total cardiopulmonary bypass and ischemic arrest of the heart
was produced by cross-clamping the ascending aorta and venting the left
ventricle. Intramyocardial carbon dioxide tension was continuously monitored by
mass spectrometry. When anaerobic energy production ceased, as indicated by a
final plateau in the intramyocardial carbon dioxide accumulation curve, the
ischemic arrest was terminated and the contractile state of the heart observed.
These results are tabulated below:
|
Group
|
Temperature
|
Propranolol
|
Termination of Arrest
|
Ischemic
Contracture
|
|
Time
|
PCO2
|
|
I
|
38°C
|
none
|
*54.4±4.2 mm
|
474±29 mm Hg
|
yes
|
|
II
|
38°C
|
0.5 mg/kg
|
79.6±5.1 min
|
527±38 mm Hg
|
yes
|
|
III
|
38°C
|
1.0 mg/kg
|
76.6±4.9 min
|
455±42 mm Hg
|
yes
|
|
IV
|
28°C
|
none
|
120.4±5.5 min
|
341±26mmHg
|
no
|
|
|
|
|
*Mean ± SEM; 8 dogs in each group
|
|
We conclude that beta-adrenergic blockade
delays, but does not prevent, the onset of ischemic contracture of the left
ventricle under normothermic conditions. Moderate hypothermia appears to
completely prevent this complication.
*By
invitation
24. Protective Effect of Methylprednisolone on the Heart During
Ischemic Arrest
R. W. BUSUTTIL*, W. J. GEORGE* and R. L.
HEWITT,
New Orleans, Louisiana
Although corticosteriods have been shown to
stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the
mechanism of membrane stabilization remains obscure, and the few reports
regarding use of steroids in myocardial ischemia have been conflicting. This
study was undertaken to determine if a pharmacological dose of the
glucocorticord, methylprednisolone, (MP) would protect the heart during
ischemic cardiac arrest.
A randomized double-blind
study was performed in 25 dogs. Biochemical and hemodynamic parameters were
assessed during and after cardiopulmonary bypass and 30 minutes of ischemic
cardiac arrest. Group I (11 animals) received MP 30 mg/Kg I.V. at 18 hours and
1 hour prior to surgery. Group If (13 animals) served as controls and received
MP vehicle at the same time periods. Blood pH, gases, and electrolytes were
measured; aortic, left aerial, and left ventricular pressures were monitored;
the first derivative of the left ventricular pressure (dp/dt max) was also
determined. Arterial and coronary sinus blood samples were assayed for iactate
levels and activity of the lysosomal enzyme, β-glucuronidase. Left
ventricular muscle was assayed for the nucleotides, cyclic AMP and cyclic GMP.
Following restoration of coronary flow, mean aortic
and left ventricular systolic pressures and left ventricular contractility as
determined by dp/dt max and dp/dt max/IP were depressed in both groups as
expected but were significantly higher in Group I than in Group II (p
<0.05). An increase in levels of both cyclic nucleotides occurred in each
group during ischemia, but this increase in cyclic GMP was significantly
greater in Group II (p <0.05). ^3-glucuronidase activity and myocardial
potassium loss as determined in coronary sinus blood were both significantly
greater in Group II than in Group I (p <.05).
Results of this study
demonstrate that pretreatment with a pharmacologic dose of MP significantly
enhances cardiac recovery after ischemia. Lysosomal membrane stability and
modulation of cyclic GMP levels may be critical determinants in the mechanism
of cardiac ischemia.
*By
invitation
25. Drip Retrograde Coronary Sinus Perfusion (RCSP) for Myocardial
Protection
ROBERT A. POIRIER*, ROBERT A. GUYTON*, and
CHARLES L. McINTOSH*, Bethesda, Maryland
Sponsored by A. G. Morrow, Bethesda, Maryland
Moderate hypothermia is frequently utilized as
a sole method of myocardial protection when the aortic root is cross-clamped
but not opened. This leaves the myocardium anoxic since at 27°C, oxygen
utilization has been shown to only be reduced 50%. A combination of low
pressure (15-20 mmHg), low flow (1cc/kg/ mm) RCSP with oxygenated blood and
moderate hypothermia (29°C) was demonstrated to yield significantly better
(P< 0.001) protection to LV function in dogs than moderate hypothermia
alone. The only apparatus was an ordinary intravenous bottle and tubing
periodically filled by the bypass pump, and perfusion was by gravity drip into
a balloon catheter inserted blindly into the coronary sinus through a stab
wound in the right atrial wall. Left ventricular function studies were recorded
prior to and following 1 hour of aortic cross-clamping at identical preloads
(LVEDP) and heart rates (atrial pacing). Aortic pressure (after-load) was
returned to a level as close to baseline as possible by constriction of the
descending thoracic aorta. Changes in ventricular function after one hr. of
aortic cross-clamping are noted below.
|
|
Cardiac Output
|
LV Stroke Work
|
Peak Dp/Dt
|
|
I RCSP at normothermia (8 dogs)
|
↓40%
|
↓42%
|
↓23%
|
|
II Moderate hypothermia (8 dogs)
|
↓62%
|
↓75%
|
↓44%
|
|
III RCSP and moderate hypothermia (8 dogs)
|
↓6%
|
↓9%
|
↓5%
|
Fifteen of sixteen hearts in Groups I and HI
continued to beat, and remained pink for the entire hour of cross-clamping (one
fibrillated at 20 minutes) while all those in Group II fibrillated (average of
17 min.). Following 1 hr. of aortic cross-clamping, the average aortic pressure
in Group III was returned to within 4% of baseline (1 with complete, 6 with
partial and 1 without aortic constriction), while Group II could only be
returned to a level which was 37% lower than baseline (despite complete aortic
constriction in all animals). The advantages of RCSP combined with moderate
hypothermia are (1) an additional mode of protection when the aortic root is
clamped but not opened, (2) a supply of oxygen to what is otherwise an anoxic
myocardium, (3) a technique and apparatus which are simple and require a
minimum of attention. With reference to possible intra-aortic surgery, this low
flow retrograde perfusion does not produce serious intra-aortic visual
obstruction. The above results, combined with the simplicity of the modality,
suggests that RCSP may be indicated when moderate hypothermia is otherwise
chosen to be the sole source of myocardial protection.
*By
invitation
26. Depressed Postoperative Myocardial Performance: A Preventable
Complication of Open Heart Surgery
GERALD BUCKBERG, GORDON OLINGER*, DONALD
MULDER,
JAMES V. MALONEY, JR., Los Angeles, California
Depressed postoperative
myocardial performance ("low output syndrome") requiring inotropic or
mechanical circulatory support is due to subendocardial necrosis and is the
major cause of death after open heart surgery (Taber, Najafi, Buckberg). Before
July 1972, we, as others, used ischemic arrest, profound topical hypothermia,
and ventricular fibrillation and needed inotropic drugs in approximately one-third
of patients undergoing aortic valve replacement or coronary revascularization
and in one-half of patients undergoing mitral valve replacement. Reported
mortalities (mitral valve replacement and high risk coronary
revascularizations) ranged from 10-40%. Our experimental studies show this
morbidity and mortality is caused by ischemic injury to the heart resulting
from inadequate myocardial protection during bypass.
Based on these experimental
studies, we have, since July 1972, employed the following principles
clinically: 1) maintain beating empty heart whenever possible, 2) avoid
ventricular fibrillation, 3) avoid prolonged profound topical hypothermic
arrest, 4) avoid severe hemodilution, 5) maintain adequate coronary perfusion
pressure (at least 80 mm Hg), 6) limit ischemic periods to less than 12
minutes, 7) prolong total bypass as necessary to repay myocardial oxygen
debt, 8) optimize DPTI/TTI (supply/demand ratio) pre and postoperatively.
In 189 consecutive operations
using these principles, postoperative inotropic support was required in a) one
(5%) of 22 mitral valve replacement patients (one death), b) one (2%) of 46
aortic valve replacements (two deaths), c) 10 (7%) of 121 coronary
revascularization patients (three deaths), including 56 high risk patients. Of
the 12 patients requiring inotropic support, the above principles were violated
in four and five others were high risk coronary revascularizations.
We conclude that postoperative
depressed myocardial performance requiring pharmacologic or mechanical
circulatory support can be virtually avoided by adhering to principles of
adequate cardiac protection during open heart surgery.
*By
invitation
27. Dynamics of Subendocardial Flow During Cardiopul-monary Bypass
CHARLES F. REUBEN*, HARJEET SINGH*, ALFRED J.
TECTOR*,
JOHN P. KAMPINE*, ROBERT J. FLEMMA and
DERWARD LEPLEY, Milwaukee, Wisconsin
Subendocardial flow was
measured as temperature differential between the epicardial and subendocardium
on cardiopulmonary bypass by a measured bolus of cold blood of known
temperature injected into the aortic root. The probes with 0.1 millisecond time
response were accurately placed in the subendocardium and epicardium,
equidistant from the nearest coronary vessel. The temperature of the myocardium
and blood in the aortic root were maintained constant by small variations from
the heat exchanger. Flow ratios were obtained from areas under the thermal
curves, integrating mean temperature change and time. D.C. operational
amplifier offset the basal temperature. Subendocardial and epicardial flow
ratios were recorded in 18 dogs: 1) at constant aortic root pressures during
sinus rhythm and ventricular fibrillation; 2) at varying aortic root pressures
during sinus rhythm; 3) at varying aortic root pressures during induced and
spontaneous ventricular fibrillation.
In the non-working heart, the
best flows to the subendocardium occurred consistently during sinus rhythm.
Fibrillating heart at low aortic root pressure was the most disadvantageous to
Subendocardial flow. High aortic root pressure during fibrillation improved
Subendocardial flow. The determinants of subendocardial flow under various
conditions of cardiopulmonary bypass help to explain the occurrence of
Subendocardial necrosis on ischemic basis.
*By
invitation
28. The Superiority of Aortic Crossclamping With Profound Local
Hypothermia For Myocardial Protection During Aortocoronary Bypass Surgery
RANDALL B. GRIEPP*, EDWARD B. STINSON* and
NORMAN E. SHUMWAY, Stanford, California
Two hundred fourteen patients undergoing
aortocoronary bypass grafting were allocated to two groups. In Group I (130
pts) distal anastomoses were carried out with the heart spontaneously
fibrillating and the left ventricle vented. In Group II (84 pts) distal
anastomoses were carried out with the aorta continuously crossclamped, and the
myocardium protected by profound local hypothermia (cold saline immersion). The
groups were equivalent with respect to age, sex, risk factors, and incidence of
preoperative ventricular dysfunction. Postoperative LDH and SCOT were assayed,
EKG's were reviewed for evidence of transmural myocardial infarction, and in a
subset of each group postoperative hemodynamics were measured. Results:
|
|
Group I
|
Group II
|
P Value
|
|
# Deaths
|
2
|
0
|
.3
|
|
# Transmural infarcts
|
18
|
5
|
.1
|
|
Post op day 1 SCOT
|
102
|
66
|
.001
|
|
excluding transmural
infarcts
|
90
|
62
|
.001
|
|
Post op day 1 LDH
|
359
|
298
|
.001
|
|
excluding transmural
infarcts
|
334
|
295
|
.01
|
|
Left atrial pressure (mmHg)
|
13.3
|
13
|
.8
|
|
Cardiac index (L/min/M2)
|
2.5
|
2.4
|
.8
|
|
Cardiopulmonary bypass time
(min/graft)
|
47
|
41
|
.001
|
These data indicate that in aortocoronary
bypass surgery the use of aortic crossclamping and local hypothermia during
performance of distal anastomoses: a) shortens operating time, b) reduces
myocardial injury as assessed by serum enzyme levels, c) does not alter
postoperative hemodynamics, d) possibly reduces the incidence of intraoperative
myocardial infarction.
*By
invitation
29. Intraoperative Unidirectional Intra-Aortic Balloon Pumping (IABP)
in the Management of Left Ventricular Power Failure
DAVID BREGMAN*, EDUARDO N. PARODI*, RICHARD N.
EDIE*,
FREDERICK O. BOWMAN, JR., KEITH REEMTSMA and
JAMES R. MALM,
New York, New York
Left ventricular power failure
and recurrent ventricular tachyarrhythmias following open heart surgery refractory
to catecholamine therapy are associated with a mortality in excess of 90%.
Unidirectional IABP was utilized in a group of intraoperative patients with the
following criteria: (1) cardiac index < 2L/ min/M2, (2) left
atrial pressure (LAP) ≥ 30 mmHg, (3) systolic BP ≤ 80 mmHg, (4) a
requirement for nigh dose inotropic support, and (5) recurrent ventricular
tachyarrhythmias.
Over a 24 month period, 25
patients were assisted following open heart surgery; 84% survived acutely and
64% were long-term survivors. All patients had a prompt fall in LAP (average
-18 mmHg) in conjunction with hemodynamic stability, fewer arrhythmias, and a
decreased requirement for pharmacologic support. Those patients who did not
respond to IABP had myocardial infarction and/or subendocardial ischemia of 80%
or more of the left ventricular myocardium.
Seven patients undergoing
coronary revascularization (including 3 with associated left ventricular
aneurysms) required intraoperative IABP, and 6 survived and were discharged.
Intraoperative coronary graft flows were measured and they increased an average
of 117% with IABP over baseline values. Coronary graft flows measured with and
without IABP support demonstrated an average increase of 80% (range 50-100%,
median 83%). An evaluation of simultaneous phasic coronary graft flow tracings,
measurements of subendocardial blood flow, and other hemodynamic parameters
have confirmed the beneficial clinical and experimental responses to
unidirectional IABP.
*By
invitation