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CARDIOGENIC SHOCK CHF JANUARY/FEBRUARY 2003 35

Cardiogenic Shock: A Summarv of the


Randomized SHOCK Trial
Cardwgenic shck is the most c o m m cause of deathfor pa- Cardiogenic shock (CS) is the most common cause of
tients h s p l i z e d with acute myocardial infarction. The death for patients hospitalized with acute myocardial
Should We Emergently Revasculariz Occluded Cmmulries infarction (MI).l?*Although the overall incidence re-
for Cardwgenic Shock (SHOCK) hialrandomly asszgned mains unchanged, mortality rates from this clinical
302patients with p e h i n a n t l.Jt ventricular failurefollow- entity appear to be declining.3.4 This favorable trend
ing an acute myocardial infarctiun to a strategy of emergency has been associated with increasing utilization of
rmascularhtim or initial m e d i d stabiliultion. Emergency reperfusion therapy, revascularization, and hemody-
rmascularhtim by either c o r m r y artery bypass graftzng or namic support with intra-aortic balloon pumping
angwphty was required within 6 hours of randomization. (IABP).The superior outcome among CS patients in
Patients assigned to initial medical stabdimtian could under- the United States over their non-American counter-
go delayed rmasculahtion at a minimum of 54 hours post- parts has also been attributed to this aggressive ap-
randomization. Thepwnury end point of the study was 30- proach.5 Despite this positive relationship, these ob-
day all-cause mortalq. Overall suruival at 30 days did not servations do not directly prove cause and effect.
d@er significantly between the emergency rmasculariiultion Revascularization in these reports was not protocol-
and initial medical stabilization groups (53%us. 44%; mandated, but driven by individual clinical judg-
p=0.109). Howmer, at the 6- and 12-monthfollow-up, there ment. Sophisticated post-hoc statistical adjustment
was a signajikant suruival benefit with early rmasculahtion cannot adjust for unmeasured variables and this sets
(50% us. 37%; p=0.027 and 47% us. 34%; p=0.025, re- up the possibility of selection bias.6
spectively). The benefit appeared to be greatat for t h s e less Designing a randomized, controlled trial in the set-
than 75years of age, with 20 lives saved at 6 months per 100 ting of CS complicating acute MI is limited by the
patients treated. According to the results of the SHOCK trial, need for expedient therapy, the rapid demise of criti-
the American College of CardiologylAmericanHeart Associa- cally ill patients, and physician bias. Prospective data
tion pia'elimsfor myocardial infarction now recommend in this area were, however, clearly warranted. The Na-
emergency revascularhtimfor patients younger than 75 tional Heart, Lung, and Blood Institute supported the
years with cardwgenic shock. (CHF. 2003;9:35-39,46) SHOCK (Should We Emergently Revascularize Oc-
W O O 3 CHF, Inc. cluded Coronaries for Cardiogenic Shock) trial7 and
@)MASH(Swiss) Multicenter Trial of Angioplasty for
Shock,E which were designed to fill this void. Both tri-
als examined the benefit of early revascularization in
Venu Menon, MD; Rupert Fincke, M D
the setting of CS. Regrettably, @)MASHwas terminat-
From the Division of Cardiology, St. LukekRoosevelt ed prematurely due to insuf€icient patient enrollment.
Hospital Center, Columbia University, New York, N Y
The SHOCK trial was successfully completed and en-
rollment was stopped in November, 1998. In this re-
Address for correspondence:
view, we briefly describe the SHOCK trial design and
Venu Menon, MD, Assistant Director of Cardiac Research,
highlight salient trial findings.
Division of Cardiology, St. Luke's-Roosmelt Hospital
Center, 1111Amsterdam Avenue, New York, NY 10025
E-mail: vmenon@slrhc.org Trial Design
Manuscript received December 21, 2000;
The hypothesis and design of the SHOCK trial have
accepted January 4, 2001
been previously published.9 Figure 1 outlines the trial
design. The trial aimed to test the superiority of a
strategy of early committed revascularization (ERV)
over that of initial medical stabilization (IMS). Pa-
tients assigned to the IMS arm could undergo delayed
revascularization at a minimum of 54 hours post-ran-
domization, as per the decision of the local site inves-
tigator. For patients to qualify, CS had to occur within
36 CARDIOGENIC SHOCK CHF JANUARY/FEBRUARY2003

formed consent. All participating sites had institu-


tional review board or ethics committee approval. Pa-
tients ineligible for the trial were enrolled in a
prospective SHOCK registry.
The primary end point of the study, 30-day all-cause
mortality, was monitored by the Data and Safety Moni-
Emergency Initial medical
toring Board. The final sample size of 302 patients had
revascularization stabilization 88%-89% power to detect an absolute 20% mortality
difference between the two treatment strategies.

Figure 1. Design of the Should We Emergently Revascular-


Timing of Shock
ize Occluded Coronaries for Cardiogenic Shock (SHOCK) CS may present as an early complication following ST
Trial and suggested treatment according to group assign- elevation and MI. In the SHOCK trial, the median
ment. Revascularization in the initial medical stabilization time from MI to shock onset was 5.0 hours (25th to
arm was at least 48 hours later than in the emergency re- 75th percentile, 2.2-12.0 hours) in the ERV group
vascularization arm. and 6.2 hours (2.4-15.5 hours) in the IMS group.
PTCA =percutaneous transluminal coronary angioplasty;
CABG=coronary artery bypass grafting; IABP=intra-aor- Similarly, in the SHOCK registry it was 7.0 hours
tic balloon pumping (1.8-2.2 hours). This is in contrast to the Global Uti-
lization of Streptokinase and Tissue Plasminogen Ac-
36 hours of the index MI, and randomization had to tivator for Occluded Coronary Arteries (GUSTO)-1
occur within 12 hours of shock diagnosis. The ERV thrombolytic megatrial, in which a majority of pa-
arm required angioplasty or bypass surgery as soon as tients developed CS later, after randomization.1 Al-
possible and within 6 hours of randomization. IABP though GUSTO-1 did not exclude patients with CS,
counterpulsation was strongly recommended for both this disparity in timing reflects the selective nature of
treatment arms. patients entering thrombolytic trials. Site investiga-
Standard clinical and hemodynamic criteria were tors in thrombolytic trials may not consider patients
applied for the definition of shock, as outlined in the who are moribund at admission or at high risk for
Table. Only patients with CS arising from predomi- early death. Consequently, the recorded timing of
nant left ventricular (LV) failure following MI with ST shock may be skewed in these studies.
elevation or new left bundle branch block were in-
cluded. Exclusion criteria included ventricular septal Etiology of Shock
rupture, cardiac tamponade, severe valvular disease,
isolated right ventricular CS, known dilated car- The etiology of shock was aggressively pursued in the
diomyopathy, shock from other causes (e.g., sepsis, SHOCK trial and registry. While the trial enrolled
hypovolemia), prior severe systemic illness, rehsal by patients with predominant LV failure, other causes of
the patient’s physician, and failure to provide in- CS were included in the registry10 (predominant LV
failure, 74.3%; acute, severe mitral regurgitation,
8.3%; ventricular septal rupture, 4.6%; “isolated”
_ - right ventricular shock, 3.4%; tamponade rupture,
Table. Definition of Shock Clinical and Hemody-
namic Criteria 1.7%; other, 8%).Contrary to classical teaching, me-
chanical complications occurred early post-MI and
Cardiogenic shock: clinical criteria the median time from MI to interventricular septal
Systolic blood pressure <90 mm Hg for 30 min-
rupture (VSR) in this setting was 16 hours.’’ Reasons
utes before inotropes/vasopressors, or vasopres-
sors or IABP are required to maintain systolic for this discrepancy deserve mention. Classical teach-
blood pressure 190 mm Hg ing was largely based on surgical series that reported
Evidence of decreased organ perfusion mainly on rupture patients surviving to the operating
Heart rate 260 beats per minute (including room.12113 Further, the mean time to VSR was fre-
paced rhythms) quently used. As VSR can occur both early and late
Cardiogenic shock: hemodynamic criteria post-MI, the true timing may have been misrepre-
PCWP 215 mm Hg sented in these skewed observations. Overall outcome
Cardiac index 22.2 Ijmin/mz for patients with diagnosed VSR in the setting of CS
was dismal: of the 55 patients registered, only seven
IABP= intra-aorticballoon pumping; PCWP= pul-
monary capillary wedge pressure
survived. Thirty-one patients underwent ventricular
septal repair, but only six survived. Consequently, all
CARDIOGENIC SHOCK CHF JANUARY/FEBRUARY 2003 37

patients with VSR complicating acute MI should be cess with unprotected left main stenting as well as mul-
immediately referred for surgery. The onset of hemo- tivessel angioplasty in this critical setting. Limited ex-
dynamic instability in this population is unpre- pertise also limits the performance of multivessel angio-
dictable and associated with a poor prognosis. plasty under percutaneous bypass.16 A strategy of per-
cutaneous transluminal coronary angioplasty (PTCA)of
Location of MI. By virtue of infarct size, CS is more the infarct related artery followed by coronary artery
common after anterior MI (60% in SHOCK).7 How- bypass grafting (CABG) may be useful in certain
ever, a sizable minority of subjects enrolled in the anatomic subsets but remains formally untested.
SHOCK trial had an index inferior wall MI. In the
SHOCK registry, more than one third of patients
with inferior MI had either a prior MI or a mechani- Salient Findings
cal cause of shock.10 Patients with inferior MI and CS Emergency Revascularization vs. Initial Medical
need to be carefully evaluated. An early screening Stabilization. The superiority of an ERV over an IMS
echocardiogram in this group appears to be of great strategy did not reach statistical significance at 30 days
clinical utility. The echo image quantifies the area of in the SHOCK trial (Figure 2). This was because the
LV infarction and the compensatory response of the 9% absolute difference in 30-day survival seen with
remote myocardium. It confirms the integrity of car- ERV was less than the expected 20% benefit predicted
diac anatomy by screening for ventricular or free wall at the time of the trial design. However, the potential
rupture, tamponade, and papillary muscle rupture, for nine absolute lives saved per 100 treated appears to
all of which necessitate emergent surgery. Finally, the support this approach. A larger sample size would be
functional status of the right ventricle can be evaluat- required to formally prove this, and future conduct of
ed. In the setting of severe right-sided dysfunction, ia- randomized trials appears unlikely. This ERV strategy
trogenic fluid overload may cause a significant septa1 is further supported by long-term follow-up survival
shift, impair LV filling, and cause right-to-left shunt- data. ERV was clearly superior to IMS at 6 months,
ing via a patent foramen ovale. with 13 lives saved per 100 patients treated. This bene-
ficial effect was stable at 1 year of follow-up (Figure 2).
Coronary Anatomy. Subjects presenting with CS have The increasing survival benefit with ERV between 1
left main (20% in SHOCK) or triple-vessel disease and 6 months is in contradistinction to the parallel
(64%) and severely reduced LV function on cardiac lines beyond 30 days for thrombolysis over placebo17
catheterization (mean ejection fraction, 31%).7This is in and the decreasing benefit of primary PTCA over
contrast to the preserved LV function (mean ejection thrombolysis at 6 months in patients with acute MI and
fraction, 58%+ 15% on 90-minute ventriculograph in no shock.18JgIt is similar to the divergence in the long-

,
GUSTO-1)14 and single-vesseldisease (52%in GUSTO- term survival curves for patients with normal coronary
1) seen with the universe of ST elevation MI.15 Conse- flow (TIMI 111) and those with abnormal flow (TIMI
quently, any revascularization strategy in the setting of 0-11) in the GUSTO trial.20
CS must include provisions for emergent coronary
artery bypass surgery. An isolated percutaneous inter- Who Benefits? Only 15% of hospitals in the United
vention approach will be hampered by the limited suc- States have the capability to perform PTCA.21 Conse-
quently, adopting a universal strategy of ERV in the
setting of CS is difficult. Our experience in the
:1 p=.109 p= .027 p= .025
Bo 1 53
80 peo.01 p<o.o1
70 1
60
E 50
40 438 , 358 ,
8! 30
20 Treatment x Age group
10 Interaction p-valuer:
30-Day 6-Month 12Month 30-day: 0.012
0
6-month: 0.003
(302) (302) (301) 30-Day 6-Month
(N=246) (N=244)
Figure 2. Overall survival at 1, 6, and 12 months of fol-
low-up. Figure 3. Survival for patients less than 75 years of age.
ER V-emergency revascularization; IMS =initial med- ERV=emergency revascularization; IMS =initial med-
ical stabilization ical stabilization
38 CARDIOGENIC SHOCK CHF JANUARY/FEBRUARY 2003

SHOCK study indicates that benefit with an ERV neous intervention.9Thii-eight percent (n= 57/152) of
strategy is greatest for those less than 75 years of age, patients in the ERV group underwent this procedure.
with 20 lives saved at 6 months per 100 patients treat- Despite more extensive coronary disease, mortality
ed (Figure 3). On the basis of this evidence, we advo- with CABG was similar to that with percutaneous inter-
cate emergent transfer to tertiary facilities for this vention in both the SHOCK trial (41% vs. 40% for pa-
younger subset of patients. The recently updated tients assigned to ERV or IMS)7 and registry (28%vs.
American College of Cardiology/American Heart As- 46%).10 The ability to perform complete revasculariza-
sociation (ACC/AHA) guidelines adopt a similar tion and the myocardial protection offered by car-
stance, based on current evidence.22 When transfer is diopulmonary bypass may have contributed to this fa-
unfeasible and in those greater than 75 years of age, vorable outcome. CABG appears to be an excellent
an IMS approach similar to that in the SHOCK trial revascularization option in this scenario.
should be advocated. In the trial, the IMS strategy,
which included thrombolysis (63%), IABP support Role of Intra-Aortic Balloon Pumping. IABP
(86%),and physician-directed delayed revasculariza- support was strongly advocated in both arms of the
tion (25%),resulted in lower mortality rates than his- SHOCK trial and played an integral role in the med-
torical controls.3 This IMS strategy proved equivalent ical stabilization arm. The overall utilization of IABP
to an ERV strategy among the elderly and seems to be in this group was 86%,7considerably higher than the
an acceptable initial strategy. Alternatively, selective 24% and 25% balloon pump utilization rates seen
use of an ERV strategy in patients over 75 years of with shock in GUSTO-11 and GUSTO-III,31 respec-
age was associated with an excellent outcome in the tively. Although conclusions are speculative, IABP
SHOCK registry. may have been largely responsible for the favorable
historical outcome seen in this group.3 This is be-
Mode of Revascularization. The mode of revascu- cause there is experimental evidence suggesting en-
larization in the setting of CS is best guided by coro- hanced thrombolytic efficacy in this setting.32 This
nary anatomy, and both FTCA and CABG play pivotal positive experience is also supported by the large
roles. In the SHOCK trial, percutaneous intervention National Registry of Myocardial Infarction (NRMI)
was performed in 55% (n=83/152) of patients in the database33 and the randomized, multicenter Throm-
ERV group. The 77% procedural success with percuta- bolysis and Counterpulsation to Improve Cardio-
neous intervention in this setting is consistent with that genic Shock Survival (TACTICS) trial.34 TACTICS
of earlier reports 23 and lower than that reported with was terminated prematurely because of insufficient
primary angioplasty in the setting of all ST elevation patient recruitment, but the results suggest a 9% ab-
MIs.3,24,25This is presumably due to a combination of solute reduction of mortality at 6 months (p=0.23)
diffuse multivessel disease, large thrombus burden, with the combination of thrombolysis and IABP. Ac-
and coronary hypoperfision. Furthermore, the no re- cording to these findings, IABP should be used in
flow phenomenon may occur more often in CS.26 Suc- the management of CS. Unfortunately, IABP use is
cessful percutaneous intervention in this setting is uncommon in community hospitals. Reasons for this
clearly associated with a superior outcome and proce- may include lack of physician expertise and cost.
dural failure is associated with increased 30-day mor- Physician education and regional expertise are po-
tality (38% ~ ~ 7 9 p=0.003).
%; Overall mortality with tential solutions. Results of the SHOCK and TAC-
percutaneous intervention in this randomized trial was TICS trials may help to rectify this problem.
40% (n= 105).7 This is similar to the 44% cumulative
mortality (n= 1167) reported in 24 previous trials.23
The use of coronary stents and platelet glycoprotein Conclusion
IIb/IIIa receptor antagonists has revolutionized percu- Although there was no benefit at 30 days, among
taneous intervention in the past 5 years. A number of patients in CS due to LV dysfunction associated
single-center experiences in the setting of shock have with an ST elevation MI, a strategy of ERV was su-
been reported.27-30 In SHOCK, stent and IIb/IIIa re- perior to IMS at 6 and 12 months of follow-up. Pa-
ceptor antagonist use increased from 0% in 1993-1994 tients younger than 75 years of age benefited most,
to 74% and 59% in 1997 and 1998, respectively. No in- with 20 lives saved at 6 months per 100 patients
creased survival benefit was apparent in these small treated. According to the results of the SHOCK
subsets of patients.7 trial, ERV is now a class I indication for this patient
The feasibility of CABG in the setting of CS has been population in the ACC/AHA myocardical infarction
previously reported.23 In the SHOCK trial, CABG was guidelines.22 Mortality with CABG was similar to
recommended for severe triple-vessel coronary artery that with percutaneous intervention in this high-
disease, left main artery disease, and failed percuta- risk population.
CARDIOGENIC SHOCK CHF JANUARY/FEBRUARY 2003 39

13 Hutchins GM. Rupture of the interventricular septum compli-


Outlook cating myocardial infarction.A m Heart J. 1979;97:165-173.
The risk of developing CS increases with age.1,3>35,36 14 The effects of tissue plasminogen activator, streptokinase, or
both on coronary-artery patency, ventricular function, and
Age is also a potent predictor of mortality following survival after acute myocardial infarction. The GUSTO An-
acute MI.37,38 Consequently, although the age-ad- giographic Investigators. N Engl J Med. 1993;329:1615-1622.
justed case fatality rate following acute MI has fall- 15 Batchelor WB, Peterson ED, Mark DB, et al. A comparison of
US and Canadian cardiac catheterization practices in detecting
en dramatically over the past three decades, the in- severe coronary artery disease after myocardial infarction: efi-
cidence of MI, incidence of CS, and the unadjusted ciency, yield and long-term implications. J A m Coll Cardiol.
mortality rate following MI have remained relative- 1999;34:12-19.
16 Shawl FA, Domanski MJ, Hernandez TJ, et al. Emergency
ly constant. Present demographics will ensure an percutaneous cardiopulmonary bypass support in cardio-
increasing baseline risk in future MI populations. genic shock from acute myocardial infarction. A m J Cardiol.
The economic and health care demands arising 1989;64:967-970.
17 Franzosi MG, Santoro E, De Vita C, et al., on behalf of the
from this are staggering. Despite the advances in GISSI Investigators. Ten-year follow-up of the first megatrial
primary prevention, research in CS should remain testing thrombolytic therapy in patients with acute myocar-
a high priority. Novel modalities to preserve is- dial infarction. Circulation. 1998;98:2659-2665.
18 The Global Use of Strategies to Open Occluded Coronary Ar-
chemic myocardium need to be studied. One ap- teries in Acute Coronary Syndromes (GUSTOIIb) Angioplasty
proach that may warrant investigation in CS is the Substudy Investigators.A clinical trial comparing primary coro-
use of glucose-insulin-potassiuminfusions.39 In the nary angioplasty with tissue plasminogen activator for acute my-
ocardial infarction. N EnglJ Med. 1997;336:1621-1628.
interim, our clinical experiences in the SHOCK 19 Michels KB, Yusuf S. Does PTCA in acute myocardial infarc-
trial will help guide present available therapy. tion affect mortality and reinfarction rates? A quantitative
overview (meta-analysis)of the randomized clinical trials. Czr-
culation. 1995;91:476-485.
REFERENCES ~~ 20 Ross AM, Coyne KS, Moreyra E, et al. Extended mortality
1 Holmes DR, Bates ER, Kleiman NS, et al. Contemporary benefit of early postinfarction reperfusion. Circulation.
reperfusion therapy for cardiogenic shock: the GUSTO-I 1998;97:1549-1556.
trial experience. J Am Coll Cardiol. 1995;26:668-674. 21 American Hospital Association. Hospital Statistics. Chicago,
2 Becker RC, Gore JM, Lambrew C, et al. A composite view of IL: American Hospital Association; 1992:20&209.
cardiac rupture in the United States National Registry of My- 22 Ryan TJ, Antman EM, Brooks NH, et al. ACC/AHA guidelines
ocardial Infarction.J A m Coll Cardiol. 1996;27:1321-1326. for the management of patients with acute myocardial infarc-
3 Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends tion: a report of the American College of Cardiology/American
in cardiogenic shock complicating acute myocardial infarc- Heart Association Task Force on Practice Guidelines (Commit-
tion. N EnglJ Med. 1999;340:1162-1 168. tee on Management of Acute Myocardial Infarction).J A m Coll
4 Carnendran L, Abboud R,Gurunathan R,et al. Trends in cardio- Cardiol. 1999;34:890-911.
genic shock: report from the SHOCK study. Eur Heart J . 23 Hochman JS, Gersh BJ. Acute myocardial infarction: compli-
2001;22(6):472-478. cations. In: Topol EJ, ed. Textbook of Cardiovascular Medicine.
5 Holmes DR, Califf RM, Van de Werf F, et al. Difference in Philadelphia, P A Lippincott-Raven; 1998:437-480.
countries’ use of resources and clinical outcome for patients 24 Grines CL, Browne KF, Marco J, et al. A comparison of im-
with cardiogenic shock after myocardial infarction: results mediate angioplasty with thrombolytic therapy for acute my-
from the GUSTO trial. Lancet. 1997;349:75-78. ocardial infarction. N Engl J Med. 1993;328:673-679.
6 Hochman JS, Boland J, Sleeper LA, et al. Current spectrum 25 Zijlstra F, de Boer MJ, Hoorntje JCA, et al. A comparison of
of cardiogenic shock and effect of early revascularization on immediate coronary angioplasty with intravenous streptoki-
mortality: results of an international registry. Circulation. nase in acute myocardial infarction. N Engl J Med. 1993;
1995;91:873-881. 328:680-684.
7 Hochman JS, Sleeper LA, Webb JG, et al. Early revasculariza- 26 Webb J, Hochman J. Pathophysiology and management of
tion in acute myocardial infarction complicated by cardio- cardiogenic shock due to primary pump failure. In: Gersh
genic shock. N EnglJ Med. 1999;341:625-634. BJ, Rahimtoola SH, eds. Acute Myocardial Infarction. New
8 Urban P, StauRerJ-C, Bleed D, et al. A randomized evaluation of York, NY: Chapman and Hall; 1997:308-337.
early revascularization to treat shock complicating acute myocar- 27 Neumann FJ, Walter H, Richardt G, et al. Coronary Palmaz-
dial infarction: the (Swiss) Multicenter trial of Angioplasty for Schatz stent implantation in acute myocardial infarction.
Shock- @)MASH.Eur HeartJ. 1999,201030-1038. Heart. 1996;75:121-126
9 Hochman JS, Sleeper LA, Godfrey E, et al. Should we emer- 28 Webb JG, Carere RG, Hilton JD, et al. Usefulness of coronary
gently revascularize occluded coronaries for cardiogenic stenting for cardiogenic shock. A m J Cardiol. 1997;79:81-84.
shock: a n international randomized trial of emergency 29 Antoniucci D, Valenti R, Santoro GM, et al. Systematic direct
PTCNCABG-trial design. The SHOCK Trial Study Group. angioplasty and stent-supported direct angioplasty therapy
A m Heart J. 1999;137:313-32 1. for cardiogenic shock complicating acute myocardial infarc-
10 Hochman JS, Buller CE, Sleeper LA,et al. Cardiogenic shock tion: in-hospital and long-term survival. J A m Coll Cardiol.
complicating acute myocardial infarction-etiologies, man- 1998;31:294-300.
agement and outcome: a report from the SHOCK Trial Reg- 30 Schultz RD, Heuser RR, Hatler C, et al. Use of c7E3 Fab in
istry.J A m Coll Cardiol. 2000;36:1063-1070. conjunction with primary coronary stenting for acute myocar-
11 Menon V, Webb JG, Hillis LD, et al. Outcome and profile of dial infarctions complicated by cardiogenic shock. Cathet Car-
ventricular septa1 rupture with cardiogenic shock after my- diovasc Diagn. 1996;39:143-148.
ocardial infarction: a report from the SHOCK Trial Registry. 31 Hasdai D, Holmes DR Jr, Topol EJ, et al. Frequency and clini-
/ A m Coll Cardiol. 2000;36:1110-1116. cal outcome of cardiogenic shock during acute myocardial in-
12 Sanders RJ, Kern WH, Blount SG. Perforation of the inter- farction among patients receiving reteplase or alteplase: results
ventricular septum complicating myocardial infarction. A m from GUSTO-111. Eur HeartJ. 1999;20:128-135.
Heart J. 1956;51:736-748. 32 E’rewitt RM, Gu S, Schick U, et at. Intra-aortic balloon counter-

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