Retrograde lysis of coronary artery thrombus by coronary

1262
JAM COLL CARDIOL
1983;1(5):1262-7
Retrograde Lysis of Coronary Artery Thrombus by Coronary Venous
Streptokinase Administration
SAMUEL MEERBAUM, PhD, FACC, TZU-WANG LANG, MD, FACC, MOYSEY POVZHITKOV, MD,
ROBERTO V. HAENDCHEN, MD, TAKAHISA UCHIYAMA, MD, FACC, JEFFREY BROFFMAN, BS,
ELIOT CORDAY, MD, FACC
Los Angeles, California
Thisstudy examinedwhether an occlusive thrombus within
a coronary artery can be lysed by streptokinase retroperfusion into the associated regional coronary vein. Experimental coronary artery thrombosis was induced in
15 closed chest dogs by placing a small copper coil at a
proximal site of the left anterior descending coronary
artery. Total thrombotic obstruction of this artery was
verified within 10 to 60 minutes (38.0 ± 15.8, mean ±
standard deviation) and streptokinase was administered
within 94.0 ± 17.4 minutes from coil insertion at an
average rate of 42 IU/kg per minute by one of three
modes: 1) intermittent 10 minute direct coronary venous
retroinfusion (fivedogs); 2) continuous infusion into the
pumping circuit of synchronized phased retroperfusion
of the great cardiac vein with arterial blood (five dogs);
and 3) for comparison, streptokinase administered intravenously (fivedogs). The intracoronary thrombus was
fullylysedand anterograde reperfusion established within
Evidence has accumulated that a substantive percent of myocardial infarcts result from intracoronary thrombosis (I).
Therefore, interest has recently been aroused about prompt
nonsurgical thrombolytic reperfusion of coronary arteries
for treatment of evolving acute myocardial infarction. In a
widely reported new technique currently undergoing extensive clinical evaluation (2-5), angiographic confirmation of
thrombotic coronary occlusion is followed by intracoronary
From the Department of Medicine, Division of Cardiology and the
Department of Pathology, Cedars-Sinai Medical Center and the Department
of Medicine, UCLA School of Medicine, Los Angeles, California. This
work was supported in part by Grants HL 14644-08 and HL 17651-06
from the National Heart, Lung, and Blood Institute, National Institutes of
Health, Bethesda, Maryland, the Ahmanson Foundation, the W. M. Keck
Foundation, the Lillian D. Truyens Foundation, the Feintech Family Foundation, Mrs. Anna Bing Arnold, Mr. and Mrs. E. E. Fogelson, Mr. and
Mrs. Ira Gershwin, Mr. and Mrs. Edward Mitchell and Mrs. Rita Schreiber,
Los Angeles, California.
Address for reprints; Samuel Meerbaum, PhD, Cedars-Sinal Medical
Center, Halper Research Building, 8700 Beverly Boulevard, Los Angeles,
California 90048.
© 1983 by the American College of Cardiology
51.0 ± 18.7 minutes by intermittent streptokinase retroinfusion, and in 50.0 ± 6.1 minutes by streptokinase
supplemented synchronized retroperfusion (50.5 ± 13.2
minutes for pooled retrograde coronary venous delivery). Lysis was also induced by systemic streptokinase,
but the time to lysis was significantly longer and more
variable (131.6 ± 60.6 minutes) than with retrograde
administration (p < 0.01).
The retroperfusion modality appears the preferable
technique because it provides early thrombolysis and,
at the same time, improves cardiac function and maintains myocardial viability of the jeopardized ischemic
zone pending achievement of full reflow. Thus, streptokinase retroperfusion, if promptly instituted, may be
a useful complemental nonsurgical treatment of evolving
acute myocardial infarction after thrombotic coronary
artery occiusion.
infusion of streptokinase to achieve thrombolysis and restore
essential perfusion to the jeopardized ischemic myocardium.
Results to date appear encouraging and suggest that the new
method can be effective, provided the treatment is instituted
early enough to ensure effective coronary reflow to the acutely
ischemic myocardium before it is irreversibly injured. Thus,
intracoronary streptokinase could lyse an occlusive thrombus within 15 to 60 minutes in patients in whom the thrombolytic intervention is instituted within 3 to 4 hours after
the initial event (3). Current protocols for this treatment of
acute myocardial infarction specify standby surgical coronary artery revascularization in the event that lysis cannot
be achieved or if complications result.
Selective coronary angiography has been safely performed in the setting of acute myocardial infarction (6) and
offers the obvious course for intracoronary infusion of
thrombolytic agents. Although the entire coronary artery
thrombus may be readily and promptly acted on by the
infusate, physical factors such as character, shape, size and
0735-1097/83/0501262-6$03.00
RETROGRADE LYSIS OF CORONARY ARTERY THROMB US
J AM COLL CARDIOL
1983.1(5) 1262- 7
surface of the thrombus could influence the initial site and
subsequent course of thrombolysi s. The particular location
of the intracoronary thrombus , its length, complexity of
configuration and relation to the underlying lesion are bound
to have a bearing on any delay or impedance to successful
coronary artery thromboly sis. An excessive delay between
acute thrombotic coronary occlusion and its lysis will result
in the development of irreversible damage to the jeopardized
cardiac tissue , regardless of eventual lytic reopening of the
coronary artery .
We have developed a coronary venous synchronized retroperfusion method (7) that provides prompt and safe retrograde delivery of treatment to acutely ischemic myocardium distal to an acutely obstructed coronary artery (Fig.
I) . The electrocardiogram-triggered pulsatile approach provides retroperfusion in diastole while facilitating coronary
venous drainage in systole. In experiments, arterial blood
retroperfu sion of the injured tissue was found to significantly
improve cardiac function and reduce infarct size by virtue
of enhanced myocardial perfusion (8) and may constitute
an effective temporary circulatory support in several physiologic settings . We recently extended the technique to allow
concomitant retrograde delivery of pharmacologic agents
and application of regionally administered moderate hypothermia (9-11). Extensive measurements indicated that
these new adaptations of the retroperfusion method further
improved cardiac mechanical function and strikingly extended viability of reversibly injured acutely ischemic myocardium (12). Observations during experimental investigations indicated not only significantly increased myocardial
perfusion (13), but suggested that some retrograde infusate
penetrated into the epicardial coronary artery distal to the
site of its occlusion (8).
Therefore, we decided to explore whether streptokinase
retroinfusion through the regional coronary vein could in
retrograde manner lyse a thrombotic obstruction in the corresponding coronary artery (14) . We also planned to compare this retrograde coronary artery thrombolysis with systemic streptokinase administration, a simple alternative
thrombolytic treatment that has recently received attention
(15) .
Methods
The study was performed in 15 closed chest dogs weighing 25 to 35 kg. The dogs were anesthetized with morphine
(1.2 mg/kg intramuscularly) and pentobarbital (30 rng/kg
intravenously) . Respiration was controlled with a Harvard
respirator pump. During initial instrumentation , catheters
were maintained with a saline solution drip. Selective coronary angiography defined the anatomy of the left anterior
descending coronary artery. By using a previously reported
method (16), a small copper coil (8 to 10 mm long and 2
1263
to 3 mm outer diameter) was inserted under fluoroscopic
control over a guidewire introduced into the left anterior
descending coronary artery through a 7F catheter passed
from the left carotid artery . The copper coil was positioned
at a relatively proximal site of the coronary artery and its
stable placement was verified by Renografin-76 injections .
After full thrombotic obstruction of the coronary artery ,
generally within 10 to 60 minutes , (38.0 ± 15.8 minutes,
mean ± standard deviation) , heparin (3 to 5,000 IV in an
intravenous bolus) was administered to the closed chest dogs
and instrumentation was completed. Repeated contrast injections served to establish that full coronary artery occlusion was maintained despite the Renografin and heparin
procedures.
Retrograde streptokinase administration. Retrograde
streptokinase treatment was carried out in 10 dogs. In five
dogs (series A), a double lumen balloon catheter was passed
from the jugular vein by way of the right atrium and through
the coronary sinus into the great cardiac vein. The catheter
balloon was positioned deep within the great cardiac vein
near the anterior interventricular vein bifurcation . Balloon
inflation facilitated unidirection al drug infusion through the
center lumen of the coronary venous catheter in the direction
of the ischemic region of the left ventricle subserved by the
left anterior descending coronary artery. Ninety minutes
after coil insertion into the coronary artery and on an average
of about 60 minutes after angiographically demonstrated
total and persistent thrombotic coronary obstruction (confirmed by ST segment elevations), streptokinase (12,500 IV
diluted in 50 cc of 5% dextrose in water) was administered
in water with a syringe during 10 minute periods. These
streptokinase retrograde infusions were repeated after 10
minute periods without retroinfusion, until the thrombus was
lysed and coronary artery flow was angiographically proved
to be reestablished and maintained. In five additional dogs
(series B), the coronary venous retroinfusion protocol was
modified to continuously infuse an average 42 IV/kg per
minute of streptokinase introduced (model 600-900 Harvard
infusion withdrawal pump) into the synchronized retroperfusion system. The latter admixed the streptokinase to the
shunted arterial blood at the extracorporeal synchronized
phased bladder pump , causing the mixture to be diastolicall y
retroinfu sed into the ischemic zone . The streptokinase-arterial blood mixture was delivered via the center lumen of
the special 7F retroperfusion autoinflatable balloon catheter
until effective left anterior descending coronary thrombo lysis was verified . The previously described experimental
preparation (Fig. 1) was used for the dogs in series B (9).
Systemic streptokinase administration. For comparative purposes, intravenous administration of streptokinase
after thrombotic left anterior descending artery occlusion
was performed in an otherwise equivalent protocol in five
identically prepared closed chest dogs (series C). The schedule of drug administration was equivalent to that in series
J AM COLL CARDIOL
1983;1(5):1262-7
1264
MEERBAUM ET AL
SYNCHRONIZED PUMP
,- BALLOON
CATHETER
LAD ARTERY
AORTIC
ARCH
A and the intravenous streptokinase dosage was 1,000 to
2,000 IV/min. Systemic streptokinase effects on the left
anterior descending thrombotic occlusion were checked periodically by coronary angiography.
Analysis of results. Dogs in series A and B (coronary
venous streptokinase) were statistically compared as individual series, or as a combined retrograde series versus
series C (systemic streptokinase) in relation to the time
elapsed from start of treatment (after verified total thrombotic coronary occlusion) until reperfusion supervened and
stable effective thrombolysis was angiographically demonstrated. The data on this period pending lysis are presented
as mean ± standard deviation.
Because of dog to dog differences in the time from thrombotic coronary occlusion until lytic reperfusion, stratification
of measurements and rigorous comparisons of thrombolytic
effects on ischemic cardiac function or myocardial salvage
would have required multiple subsets and a much larger
number of dogs than were studied. However, during coronary obstruction and subsequent reflow, observations were
made in individual dogs with regard to cardiac rhythm,
hemodynamic consequences and left ventricular function
(utilizing cineangiography and two-dimensional
echocardiography) .
Results
Figure 2 illustrates the observed sequence of events recorded in a dog treated with streptokinase-synchronized retroperfusion. Left anterior descending coronary artery flow
was unimpeded before placement of the intracoronary copper coil, and total thrombotic obstruction at the relatively
proximal coronary site was noted from 10 to 60 minutes
Figure 1. The experimental system of synchronizedpulsatile coronary venous retroperfusion shunts
arterial blood into the coronary sinus or great cardiac vein in diastole and facilitates coronary venous
drainage in systole. Thus, an acutely ischemic region distal to intracoronary balloon occlusion of
the left anterior descending (LAD) coronary artery
is perfused in retrograde manner by arterial blood.
An electrocardiographic-synchronized gas-actuated
bladder pump causes a highly pulsatile delivery of
the shunted blood in cardiac diastole, with flow
pumpedin retrogrademanner into the coronary vein
through a special retroperfusion catheter. The latter
has an "autoinflatable" balloon that provides unidirectionalretroinfusionand is activated by pressure
from within the catheter lumen. When forward flow
is rapidly reduced and stopped by the synchronized
pump in cardiac systole, the retroperfusion catheter
balloon promptly collapses because of the external
pressure in the coronary vein. The schematic figure
indicates pressure and flow measurements incorporated into the retroperfusion circuit. AI = anterior interventricular; EM = electromagnetic; SRP
= synchronized retroperfusion.
after coil insertion. Early electrocardiographic signs of
thrombolysis, observed after great cardiac vein streptokinase
retroinfusion, were recorded but not considered to be an
adequate index of reperfusion because of instances of reocelusion. Fully stable reestablishment of previously obstructed left anterior descending coronary flow was proved
with several coronary angiograms.
Incidence and rapidity of thrombolysis (Fig. 3 and 4).
Thrombolysis was achieved in all 15 dogs in series A, B
and C; however, the period of streptokinase infusion required to achieve full reperfusion had a narrower range and
its mean value was much shorter (27 to 75 minutes, mean
50.5 ± 13.2 standard deviation) with retrograde coronary
venous delivery (combined series A and B) as compared
with coronary artery thrombolysis by systemic streptokinase
administration, which required 65 to 200 minutes (mean
131.6 ± 60.6 standard deviation). The difference between
the times for systemic and coronary venous retrograde streptokinase thrombolysis was highly significant (p < 0.001).
Figure 3 shows the individual data from this limited study,
indicating small variability of the time to streptokinaseinduced lysis in the synchronized retroperfusion series (55,
50, 43, 57 and 45 minutes, mean 50.0 ± 6.1), larger variability with intermittent coronary venous retroinfusion (45,
27, 65, 44 and 75 minutes, mean 51. a ± 18.7) and major
variability with systemic streptokinase (200, 65, 75, 180
and 138 minutes, mean 131.6 ± 60.6). The earliest signs
of lysis were noted at 26.7 ± 9.2 minutes in combined
retrograde series A and B, compared with 75.0 ± 35.0
minutes for systemic series C.
Observations of effects of streptokinase administration. The effects observed in individual dogs during the
variable periods up to total thrombotic left anterior descend-
J AM COLL CARDIOL
1983.1(5).1262-7
RETROGRADE LYSIS OF CORONARY ARTERY THROMBUS
1265
Figure 2. Angiographic documentation
of an experimental sequence of coronary
artery events before and after streptokinase retroperfusion-induced thrombolysis
in one closed chest dog: (a) selective
coronary angiography in the control state,
showing the left anterior descending coronary artery and its branches; (b) total
thrombotic obstruction of the left anterior
descending artery (see arrow) beyond the
small copper coil placed at a relatively
proximal site; (c) initial left anterior
descending coronary reflow after streptokinase treatment by way of coronary
venous retroperfusion; and (d) fully reestablished coronary flow noted 50 minutes after start of the streptokinase retroperfusion via great cardiac vein (see
arrows). Similar coronary artery thrombolysis was achieved in all dogs treated
with retrograde coronary venous streptokinase infusion.
ing coronary occlusion and during subsequent total coronary
occlusion up to the start of streptokinase treatment extended
by differing times to thrombolytic reperfusion corresponded
to previous experience in similar closed chest dog preparations with time controlled intracoronary occlusion (9,12).
Thus, postocclusion heart rate was increased, left ventricular
end-diastolic pressures varied but remained elevated, cardiac output and left ventricular ejection fraction were depressed and other hemodynamic variables fluctuated nonsignificantly. Pending lysis, synchronized retroperfusion (with
Figure 3. Time from start of streptokinase administration to full
lysis of coronary artery thrombus. Individual data, as well as mean
± standard deviation, are shown for the three approaches of streptokinase administration: intermittent coronary venous retroinfusion, synchronized venous retroperfusion and intravenous method.
The dog preparation and dosage were equivalent. Note the apparent
repeatability and promptness of the retroperfusion modality, followed by equally short but somewhat more variable results with
intermittent retroinfusion, and substantial scatter and significantly
longer time to lysis when streptokinase was administered
intravenously.
•
160
•
~
E 120
~
40
0
200
* ••
••
19
RETROINFUSION
* I
••
INTRAVENOUS
*
c
E
::E
f=
120
80
40
0
RETROPERFUSION
.r,
160
w
w
80
Figure 4. Time from start of streptokinase administration to full
thrombolysis. Same data as in Figure 3, except that all retrograde
administration measurements were gathered to emphasize the relatively small variability and significantly shorter time to lysis as
compared with the intravenous method.
•
200
:!
supplemental streptokinase) resulted in improvement of
ischemic zone function (observed with two-dimensional
echocardiography). However, the magnitude of these benefits depended significantly on the total time of the coronary
occlusion. No arrhythmias were encountered during and
after thrombolytic reperfusion. After thrombolysis (which
occurred at different postocclusion times from dog to dog),
effects of reperfusion varied. Whereas relatively early reperfusion (after 57 minute total occlusion in one dog in
series A, was reflected by partial return of ischemic zone
cardiac function and a small infarction (analyzed with the
triphenyl tetrazolium chloride technique), delayed reper-
*
(I
RETROGRADE
INTRAVENOUS
MiSD
p<O.OOI
1266
J AM COLL CARDIOL
MEERBACM ET AL
1983,1(5): 1262-7
fusion (200 minutes after coronary occlusion in one dog in
series C) failed to provide early improvement of ischemic
zone function, and extensive necrosis was noted in left ventricular slabs. Postmortem examination in the dogs of this
study showed no intramural hemorrhages.
Discussion
This initial study indicates that retrograde coronary vein
streptokinase infusion into a regional coronary vein may
provide an alternate route for lysis of a thrombotic obstruction within the associated coronary artery. Thus, great cardiac vein streptokinase administration after verified total
thrombotic occlusion of the proximal left anterior descending coronary artery successfully lysed the coronary thrombus in all dogs (within a period of 50.5 ± 13.2 minutes).
Multiple coronary arteriography was performed before treatment to confirm fully established thrombotic obstruction of
the coronary artery and also at intervals during the treatment
to demonstrate lytic reopening of the artery after retrograde
streptokinase administration. Even though significantly delayed when compared with retrograde coronary venous
streptokinase infusion, thrombolysis was also achieved in
dogs receiving systemic streptokinase (65 to 200 versus 27
to 75 minutes).
The experimental simulation ofintracoronary thrombosis
merits discussion. Catheter insertion and placement of a
small copper coil at a specific coronary artery site was previously found to be a satisfactory method for inducing early
and total thrombotic obstruction in closed chest dogs (16).
The character of the resulting thrombotic process differs
from the clinical setting in which thrombosis may be initiated by intimal injury and propagates within a vascular
lesion toward the center of the coronary artery lumen. These
differences may have a bearing on the precise thrombus to
wall organization, even though pathologic examination indicated that the thrombosis in the dog exhibited features
similar to those encountered in human subjects (3).
Role of the coronary obstructive lesion in the lytic
process. In the human, there is an almost infinite number
of possible configurations of coronary lesions in which obstructive thrombosis can develop, resulting in acute myocardial ischemia. The underlying lesion may be of such
severity that lysis of the occluding thrombus would not
provide adequate myocardial perfusion and the coronary
artery may remain susceptible to thrombotic reocclusion. In
a coronary artery that is inherently restricted by as much as
80 to 90%, successful thrombolysis may well provide the
urgently needed perfusion, supplementing collateral circulation and assuring significant myocardial salvage. Lysis of
a thrombus obstructing a lesion with a large residual lumen
would, of course, be highly beneficial. Anterograde intracoronary infusion of lytic agents directly onto the thrombus
has now been demonstrated as an effective means of re-
establishing coronary blood flow. The potentials of modified
intravenous streptokinase administration are also being explored. Finally, in special instances, the configuration of
the coronary artery lesion, the nature of the thrombotic
occlusion and responsiveness to lytic agents may favor
thrombolytic treatment applied in a retrograde manner by
way of the coronary veins.
Therapeutic implications. On the basis of our prior
experience with retroperfusion and further current evaluation of retrograde administration of pharmacologic agents,
the streptokinase retroinfusion technique should present no
significant difficulties. Coronary venous catheterization was
found to be safe, and prompt application of either coronary
sinus or great cardiac vein catheterization was demonstrated
(17). The retrograde coronary venous infusions may be administered either by bolus or through continuous infusion.
In view of the relatively benign venous catheterization, retrograde thrombolytic treatment may prove to be a useful
intervention, alone or in combination with systematic or
anterograde coronary artery thrombolysis.
The primary rationale for the combined streptokinase
synchronized retroperfusion treatment is not only that it is
capable of inducing early thrombolytic reperfusion of acutely
ischemic tissue, but that it retrogradely supplies the acutely
ischemic zone, maintains cardiac function and extends viability of jeopardized myocardium during the critical period
awaiting thrombolysis and fully effective coronary artery
reflow. Our previous basic studies of coronary occlusion,
reperfusion and retroperfusion (7-9,12,18-21) indicate the
importance of applying treatment in the earliest phase of
evolving myocardial infarction. Even though arrhythmias
are frequent with sudden anterograde reperfusion, they were
not encountered during retrograde thrombolysis. Prompt
coronary venous retroperfusion with arterial blood coupled
with agents such as streptokinase should help overcome the
potential dangers of excessively delayed nonsurgical or surgical reperfusion procedures which would prove ineffective
when reflow is attempted in the presence of extensive myocardial necrosis.
We thank Myles Prevost and Rick Burchyett for their technical assistance
and Barbara Voigt and Jeanne Bloom for their help in preparing the
manuscript.
References
1. DeWood, Spores J, Notske R, et aI. Prevalence of total coronary
occlusion during the early hours of transmural myocardial infarction.
N Engl J Med 1980;303.897-902.
2. Rentrop KP, Blanke H, Karsch KR, et aI. Acute myocardial infarction:
intracoronary application of nitroglycerin and streptokinase. Clin Cardiol 1979;2:354-63.
3 Ganz W, Buchbinder N, Marcus H, et al. Intracoronary thrombolysis
in evolvmg myocardial infarction Am Heart J 198I; 101:4-13.
4. Mathey DG, Kuck KH, Tilsner V, Krebber HJ, Blelfeld W. Non-
RETROGRADE LYSIS OF CORONARY ARTERY THROMBUS
surgical coronary artery recanalization in acute transmural myocardial
infarction. Circulanon 1981;63:489-97.
5. Markis JE, Malagold MM, Parker JA, et al. Myocardial salvage after
intracoronary thrombolysis with streptokinase in acute myocardial 10farction. Assessment in intracoronary thallium-201. N Engl J Med
1981;305:777-82.
6. Rigaud M, Rocha P, Boschat J, Farcot JC, Bardet J, Bourdarias JP.
Regional left ventricular function assessed by contrast angiography in
acute myocardial infarction. Circulation 1979;60:130-9.
J AM COLL CARDIOL
1983:1(5):1262-7
1267
13. Berdeaux A, Farcot JC, Bourdarias JP, Barry M, Bardet J, Giudicelli
JF. Effects of diastolic synchromzed retroperfusion on regional coronary blood flow in expenmental myocardial Ischemia. Am J Cardiol
1981;47: 1022-40.
14 Meerbaum S, Povzhitov M, Haendchen R, Broffman J, Lang TW,
Corday E. Coronary artery thrombolysis by coronary venous streptokmase retroinfusion or systemic administration (abstr). Am J Cardiol
1982,49:1046.
7. Meerbaum S, Lang TW, Osher JV, et al. Diastolic retroperfusion of
acutely ischemic myocardium. Am J Cardiol 1976;37:588-98.
15. Schroder R, Biamino G, von Leitner ER. Intravenous short-time
thrombolysis 10 acute myocardial mfarction (abstr). Circulation
1981;64(suppl IV):IV-10.
8. Farcot JC, Meerbaum S, Lang TW, Kaplan L, Corday E. Synchronized retroperfusion of coronary vems: Circulatory support of Jeopardized ischemic myocardium. Am J Cardiol 1978;41:1191-201.
16. Kordenat RK, Kezdi P, Stanley EL. A new catheter technique for
producmg experimental coronary thrombosis and selective visualization. Am Heart J 1972;83:360-4.
9. Meerbaum S, Haendchen RV, Corday E, et al. Hypothermic coronary
venous phased retroperfusion: a closed chest treatment of acute regional myocardial ischemia. Circulation 1982;65:1435-45.
17. Chatterjee K, Magnusson P, Kaushik VS, Swan HJe. Selective cannulation of the anterior interventricular vein and coronary sinus: potential applications. Cathet Cardiovasc Diagn 1977;3:91-9.
10. Povzhitkov M, Haendchen RV, Meerbaum S, Fishbein M, Rit J,
Corday E. Protective effect of coronary venous prostaglandin E 1 retroperfusion during acute myocardial ischerruc (abstr). Am J Cardiol
1982;49: 1017.
18. Meerbaum S, Lang TW, Corday E, et al. Progressive alterations of
cardiac hemodynamics and regional metabolic function followmg acute
coronary occlusion. Am J Cardiol 1974;33:60-8.
II. Povzhitkov M, Haendchen RV, Meerbaum S, Fishbein MC, Y-Rit J,
Corday E. Mannitol coronary venous retroperfusion: improvement in
ischemic left ventricular function in acute coronary occlusion (abstr).
Clin Res 1982;30: 17A
12. Haendchen RV, Meerbaum S, Povzhitkov M, Rit J, Fishbein M,
Corday E. Hypothermic synchronized retroperfusion treatment of acute
myocardial ischemia dunng coronary occlusion and reperfusion: reduction in infarct size and improvement in cardiac function. J Am
Coll Cardiol (in press).
19. Lang TW, Corday E, Gold H, et al. Consequences of reperfusion
following coronary occlusion: effects on hemodynamic and regional
myocardial function. Am J Cardiol 1974;3:69-81.
20. Costantini C, Corday E, Lang TW, et al Revascularization after 3
hours of coronary artery occlusion: effects on regional cardiac metabolic function and mfarct size. Am J Cardiel 1975;36:368-84.
21. Corday E, Kaplan L, Meerbaum S, et al. Consequences of coronary
arterial occlusion on remote myocardium: effects of occlusion and
reperfusion. Am J Cardiol 1975;36:385-94.