Download Primary PCI for Myocardial Infarction with ST

The
n e w e ng l a n d j o u r na l
of
m e dic i n e
clinical therapeutics
Primary PCI for Myocardial Infarction
with ST-Segment Elevation
Ellen C. Keeley, M.D., and L. David Hillis, M.D.
This Journal feature begins with a case vignette that includes a therapeutic recommendation. A discussion
of the clinical problem and the mechanism of benefit of this form of therapy follows. Major clinical studies,
the clinical use of this therapy, and potential adverse effects are reviewed. Relevant formal guidelines,
if they exist, are presented. The article ends with the authors’ clinical recommendations.
A 58-year-old man has chest pain at 9:30 a.m.; 3 hours later, he calls for an ambulance. Paramedics arrive, provide standard treatment, and transport him to the nearest emergency department. On his arrival at a small hospital at 1 p.m., the findings
are diagnostic of a myocardial infarction with ST-segment elevation. The emergency
department physician recommends immediate transfer to a hospital 1 hour away for
primary percutaneous coronary intervention (PCI).
The Cl inic a l Probl e m
Coronary heart disease is the leading cause of death in the United States, with myocardial infarction a common manifestation of this disease. In 2006, approximately
1.2 million Americans sustained a myocardial infarction.1 Of these, one quarter to
one third had a myocardial infarction with ST-segment elevation.2,3
Of all patients having a myocardial infarction, 25 to 35% will die before receiving medical attention, most often from ventricular fibrillation.4 For those who reach
a medical facility, the prognosis is considerably better and has improved over the years:
in-hospital mortality rates fell from 11.2% in 1990 to 9.4% in 1999.2 Most of the decline is due to decreasing mortality rates among patients with myocardial infarction
with ST-segment elevation,3 as a consequence of improvements in initial therapy, including fibrinolysis and PCI. In an analysis by the National Registry of Myocardial
Infarction, the rate of in-hospital mortality was 5.7% among those receiving reperfusion therapy, as compared with 14.8% among those who were eligible for but did not
receive such therapy.5
From the Department of Internal Medicine (Cardiology Division), University of
Virginia School of Medicine, Charlottesville (E.C.K.); and the Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical
Center, Dallas (L.D.H.).
N Engl J Med 2007;356:47-54.
Copyright © 2007 Massachusetts Medical Society.
Pathoph ysiol o gy a nd Effec t of Ther a py
The pathogenesis of coronary atherosclerosis is multifactorial.6,7 Broadly, endothelial injury and dysfunction result in the adhesion and transmigration of leukocytes
from the circulation into the arterial intima as well as the migration of smooth-muscle
cells from the media into the intima, thus initiating the formation of an atheroma
or atherosclerotic plaque.7
Atherosclerotic plaques cause progressive narrowing of the coronary arteries and
eventually can cause a coronary occlusion. However, myocardial infarctions with
ST-segment elevation are more typically caused by the sudden thrombotic occlusion
of a coronary artery that previously was not severely narrowed. When such an occlusion occurs, the abrupt rupture, erosion, or fissuring of a previously minimally
n engl j med 356;1
www.nejm.org
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
47
The
n e w e ng l a n d j o u r na l
obstructive plaque creates a potent stimulus for
platelet aggregation and thrombus formation.6-8
If the stimulus for a thrombosis is robust, total
arterial occlusion can result (Fig. 1).
On occlusion of the infarct-related artery, all the
myocardium that is supplied by the artery becomes
ischemic, resulting in chest pain and electrocardiographic evidence of transmural (full-thickness)
ischemia (ST-segment elevation) in the leads reflective of that region of the heart. Subsequently,
necrosis begins within minutes and progresses
during several hours in a “wavefront” fashion from
A
Before myocardial infarction
No symptoms
B
During myocardial infarction
Acute onset of chest pain
C
of
m e dic i n e
the endocardial surface to the epicardial surface.
If ischemia persists for several hours, transmural
infarction results.9 In contrast, if blood flow is
restored during the period of progressive necrosis,
the ischemic myocardium is salvaged and the size
of the infarct is reduced. Since morbidity and mortality from a myocardial infarction correlate with
the size of the infarct, prompt restoration of blood
flow would also be expected to improve left ventricular function and survival.10
Primary PCI consists of urgent balloon angioplasty (with or without stenting), without the pre-
Primary balloon angioplasty
Chest pain resolving
D
Primary stent placement
Chest pain resolving
Elevation
of ST
segment
Resolving
ST-segment
elevation
Resolving
ST-segment
elevation
Normal electrocardiogram
Occlusive
thrombus
Deflated
balloon
Stent
Plaque
Plaque
Wire
Occlusive
thrombus
Non–flowlimiting plaque
Deflated
balloon
Ischemic
myocardium
Stent
Restoration
of blood flow
Restoration
of blood flow
Figure 1. Myocardial Infarction with ST-Segment Elevation before, during, and after PCI.
Symptomatic, electrocardiographic, morphologic, and anatomical findings in a patient with a myocardial infarction with ST-segment
elevation are shown before onset (Panel A) and during the infarction (Panel B), and after primary PCI with balloon angioplasty
(Panel C) or stent placement (Panel D).
48
n engl j med 356;1
www.nejm.org
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
clinical ther apeutics
vious administration of fibrinolytic therapy or
platelet glycoprotein IIb/IIIa inhibitors, to open the
infarct-related artery during an acute myocardial
infarction with ST-segment elevation. After the
identification on coronary angiography of the site
of recent thrombotic occlusion, a metal wire is
advanced past the thrombus over which a balloon
catheter (with or without a stent) is positioned at
the site of the occlusion and inflated, thereby mechanically restoring antegrade flow (Fig. 1). Primary PCI restores angiographically normal flow
in the previously occluded artery in more than
90% of patients,11,12 whereas fibrinolytic therapy
does so in only 50 to 60% of such patients.
Cl inic a l E v idence
In comparison with conservative management
(medical treatment without reperfusion therapy),
fibrinolytic therapy leads to improved left ventricular systolic function and survival in patients with
myocardial infarction associated with either STsegment elevation or left bundle-branch block. In
a pooled analysis of nine large trials, the rate of
death at 35 days was 9.6% among patients receiving fibrinolytic therapy, as compared with 11.5%
among control subjects.13
However, fibrinolytic therapy has several limitations. First, among those presenting with myocardial infarction with ST-segment elevation, some
patients (27% in one report)14 have a contraindication to fibrinolysis. Second, in approximately
15% of patients given fibrinolytic therapy, thrombolysis does not occur.15,16 Third, about a quarter of those receiving fibrinolytic therapy have
reocclusion of the infarct-related artery within
3 months after the myocardial infarction, with a
resultant reinfarction.17 These limitations are minimized with the use of primary PCI.
In a meta-analysis of 23 randomized, controlled
comparisons of primary PCI (involving 3872 patients) and fibrinolytic therapy (3867 patients), the
rate of death at 4 to 6 weeks after treatment was
significantly lower among those who underwent
primary PCI (7% vs. 9%).18 Rates of nonfatal reinfarction and stroke were also significantly reduced. Most of these trials were performed in
high-volume interventional centers by experienced
operators with minimal delay after the patient’s
arrival. If primary PCI is performed at low-volume
venues by less-experienced operators with longer
n engl j med 356;1
delays between arrival and treatment, such superior outcomes may not be seen.19
Cl inic a l Use
Reperfusion therapy (mechanical or pharmacologic) is indicated for patients with chest pain consistent with a myocardial infarction with a duration of 12 hours or less in association with
ST-segment elevation greater than 0.1 mV in two
or more contiguous electrocardiographic leads or
a new (or presumed new) left bundle-branch block.
Candidates for reperfusion therapy should be identified by an emergency department physician; the
process can be initiated by emergency-medicalservices personnel to minimize delay.
Primary PCI is preferred if a skilled interventional cardiologist and catheterization laboratory
with surgical backup are available and if the procedure can be performed within 90 minutes after initial medical contact with the patient.20 For
patients initially presenting to a hospital that does
not have interventional capabilities, rapid transfer to such a facility is recommended.
Primary PCI is preferable for certain patients
even if the interval between the first medical contact and the procedure (the “door-to-balloon” interval) exceeds 90 minutes. Such patients include
those with a contraindication to fibrinolytic therapy20; those with a high risk of bleeding with fibrinolytic therapy, including patients 75 years of age
or older (for whom the risk of intracranial hemorrhage with fibrinolytic therapy is increased)21;
those with clinical findings (i.e., tachycardia, hypotension, or pulmonary congestion) suggesting
a high risk of an infarct-related complicated medical course or death22; and those with cardiogenic
shock.23
Fibrinolytic therapy is preferred for patients
whose first medical contact occurs less than
3 hours after the onset of symptoms but for whom
PCI is not immediately available, those who seek
medical attention less than 1 hour after the onset of symptoms (in whom the therapy may abort
the infarction),24 and those with a history of anaphylaxis due to radiographic contrast material.
As compared with patients who undergo balloon angioplasty, among those who undergo baremetal stenting of the infarct-related artery, the
rates of restenosis and the frequencies of recurrent angina and repeated revascularization pro-
www.nejm.org
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
49
The
n e w e ng l a n d j o u r na l
cedures are lower.11,25 As a result, stenting of the
infarct-related artery is usually preferred. However, balloon angioplasty is preferred for patients in
whom clopidogrel (Plavix, Bristol-Myers Squibb)
is contraindicated (because of thrombocytopenia
or the presence of left main or extensive multivessel coronary artery disease, who may require
bypass surgery within days after successful primary PCI). Balloon angioplasty is also preferred
when the size of the infarct-related artery is insufficient for the placement of a stent.
As compared with bare-metal stents, drug-eluting stents appear to reduce further the rates of
restenosis within 12 months after primary PCI.26-28
If drug-eluting stents are used in this setting, it is
imperative that dual antiplatelet therapy (aspirin
and clopidogrel) be given for at least 12 months;
otherwise, subacute thrombosis may occur. There
are no good data on longer-term outcomes.
In addition to oral aspirin and intravenous unfractionated heparin, patients with a myocardial infarction with ST-segment elevation should
receive oral clopidogrel29-31 after it has been determined that emergency bypass surgery is not
required. Beta-adrenergic blockers32,33 and angiotensin-converting–enzyme inhibitors34 should be
initiated, provided that the patient has no contraindications and is stable hemodynamically.20 Platelet glycoprotein IIb/IIIa inhibitors or antibodies
often are given to patients undergoing primary
PCI.25 Treatment with a high dose of a 3-hydroxy3-methylglutaryl coenzyme A reductase inhibitor
(statin) is recommended for all patients with acute
myocardial infarction.35
The monetary costs of fibrinolytic therapy and
primary PCI are similar. Primary PCI is an expensive procedure, with professional fees ranging
from approximately $4,000 to $5,000 and hospital charges ranging from approximately $20,000
to $25,000 in the United States. However, patients
receiving fibrinolytic therapy have higher subsequent costs, because of higher rates of in-hospital morbidity and mortality and longer hospital
stays.36
In a report on 4366 primary PCIs performed at
40 sites in the United States between 1990 and
1994, the success rate (the proportion of patients
with a patent infarct-related artery at the end of
the procedure) was 91.5%.37 However, although
antegrade flow in the epicardial coronary artery
may appear normal after most of these procedures, perfusion of the tissue at the microvascu-
50
n engl j med 356;1
of
m e dic i n e
lar level is restored to normal in only a minority
of patients.38,39 In some patients, embolization of
microscopic debris with balloon inflation or stent
deployment compromises tissue perfusion. In such
patients, the magnitude of the ST-segment elevation does not diminish, even though antegrade
flow in the epicardial artery is restored. Among
these patients, survival is correspondingly reduced.40-43
In about 15% of patients undergoing primary
PCI, initial angiography shows a patent infarctrelated artery. In these patients, it is presumed that
spontaneous fibrinolysis occurred before angiography. In comparison with patients who have
diminished or no antegrade flow, these patients
are less likely to have hemodynamic instability or
left ventricular systolic dysfunction with congestive heart failure or to die as a result of myocardial infarction.
A dv er se Effec t s
Complications occasionally occur as a result of primary PCI. Local vascular complications include
bleeding, hematomas, pseudoaneurysms, and arteriovenous fistulae at the access site. These events
occur in 2 to 3% of patients, about two thirds of
whom require transfusion.44-46 Major bleeding (including bleeding at the access site) occurs in about
7% of patients undergoing the procedure.18 The
incidence of bleeding has declined, probably because lower doses of heparin and smaller catheters are used now than in the past, as well as
because of increasing experience among interventional cardiologists and ancillary personnel. The
incidence of intracranial hemorrhage is lower with
primary PCI than with fibrinolytic therapy (0.05%
vs. 1%, P<0.001).18
Severe nephropathy after PCI (caused, at least in
part, by radiographic contrast material) occurs in
up to 2% of patients.47 It occurs most often among
those with cardiogenic shock23 or underlying renal insufficiency48 and those of advanced age.49
Anaphylactic reactions to radiographic contrast
material are very rare.50
Ventricular tachycardia or fibrillation is reported in 4.3% of patients undergoing primary PCI.51
Although these patients remain in the hospital
longer than those who do not have ventricular
tachyarrhythmias, the long-term prognosis for
those with or without ventricular tachyarrhythmias
is similar.
www.nejm.org
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
clinical ther apeutics
In patients undergoing elective balloon angioplasty, the abrupt closing of the infarct-related artery (during or within hours after the procedure)
occurs in up to 3% of patients52; it may occur even
more frequently among those undergoing primary
balloon angioplasty. Stenting of the infarct-related artery decreases the incidence of abrupt closing to about 1%, thereby diminishing the need for
urgent bypass surgery53 and (in the opinion of
some investigators) obviating the need for on-site
surgical capability.54,55 Therefore, stenting is the
preferred primary intervention if the coronary
anatomy is suitable. As noted, stents also reduce the risk of restenosis, an effect shown to
be even more marked with the use of drug-eluting stents.26-28 In most trials of stenting, stent
thrombosis has occurred in less than 1.5% of patients receiving either a bare-metal stent or a drugeluting stent within the first year.28,56-58
Serious cardiovascular events occur in a small
percentage of patients undergoing primary PCI.
In the report of 4366 procedures described above,
the rates of emergency cardiac surgery and in-hospital death were 4.3% and 2.5%, respectively.37
Such events occur much more frequently among
patients in whom perfusion is not restored.
At centers where primary PCIs are performed,
there is a direct relationship between procedural
volume and outcomes. Among patients undergoing elective PCI at centers in which 200 or more
such procedures are performed each year, the incidence of urgent bypass surgery and death is lower
than among those whose procedure is performed
at a center where fewer than 200 PCIs per year are
performed.59
those receiving PCI alone.60 Despite this finding,
patients receiving facilitated intervention had increased rates of nonfatal reinfarction, urgent target-vessel revascularization, stroke, and death, as
compared with patients undergoing only PCI. The
increased rate of adverse events with facilitated
intervention was seen predominantly among patients receiving fibrinolytic therapy. At present, it
is unknown whether facilitated PCI with the use
of only platelet glycoprotein IIb/IIIa inhibitors is
superior to primary PCI alone.
Second, the choice between the use of fibrinolytic therapy and the transfer of the patient to
another facility for primary PCI depends on the
patient’s clinical characteristics and the rapidity
and efficiency of the transfer.59 Although several
randomized studies comparing on-site fibrinolytic
therapy with transfer for primary PCI showed better short-term outcomes in patients transferred
to another hospital for PCI, these studies were
conducted in highly efficient transfer networks.61
In the United States, such transfers often are inefficient, and unacceptable treatment delays occur.
Since most Americans live near a facility proficient in the performance of primary PCI, they
could receive this treatment if an organized and
efficient system of triage and transfer were available.62
Third, some patients with myocardial infarction with ST-segment elevation who undergo primary PCI are found to have severe multivessel
coronary artery disease. After the urgent restoration of antegrade flow in the infarct-related artery,
the management — medical, percutaneous, or
surgical — of the care of these patients, including
its timing, is uncertain.
A r e a s of Uncer ta in t y
Guidel ine s
Although the use of primary PCI is widespread,
some issues are unresolved. First, the administration of a fibrinolytic agent or platelet glycoprotein
IIb/IIIa inhibitor or both before PCI — called a
facilitated intervention — is based on the hypothesis that immediate pharmacologic therapy followed by prompt PCI will cause a faster and more
complete restoration of flow in the infarct-related
artery than PCI alone. A meta-analysis of trials
comparing these two procedures concluded that
patients with myocardial infarction with ST-segment elevation who received facilitated PCI were
more likely to have a patent infarct-related artery
at the time of initial coronary angiography than
n engl j med 356;1
According to the guidelines of the American College of Cardiology and American Heart Association, primary PCI is a class I indication in patients with myocardial infarction with ST-segment
elevation who can undergo the procedure within
12 hours after the onset of symptoms, provided
the procedure is performed in a timely manner
(balloon inflation or stent placement or both within 90 minutes after the first medical contact) by
experienced operators (those who perform more
than 75 interventional procedures per year) in a
facility in which more than 200 coronary interventional procedures are performed each year (at
www.nejm.org
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
51
The
n e w e ng l a n d j o u r na l
of
m e dic i n e
least 36 of them being primary in nature) and
which has a cardiac surgical capability, in case
such surgery is required.20 Similarly, the European
Society of Cardiology considers primary PCI the
preferred reperfusion strategy for patients with
myocardial infarction with ST-segment elevation
(as a class I indication).63
tion), we recommend his transfer for PCI, provided
that the procedure can be performed in a timely
fashion by an experienced operator in a high-volume catheterization laboratory. On the basis of the
data available on facilitated PCI, we do not recommend administration of a fibrinolytic agent or glycoprotein IIb/IIIa inhibitor before the transfer.
R ec om mendat ions
No potential conflict of interest relevant to this article was
reported.
The patient in the vignette has an anterior myocardial infarction with ST-segment elevation. He
was initially taken to a small community hospital
that lacked interventional capabilities. Since he has
no contraindication to fibrinolytic therapy, he could
receive this therapy there or, alternatively, he could
be transferred urgently for primary PCI. Because
his symptoms have been present for more than
3 hours and he has high-risk features (i.e., tachycardia, rales, and anterior location of the infarc-
A video animation showing balloon angioplasty
and stent placement is available
with the full text
of this article at
www.nejm.org.
References
1. American Heart Association. Car-
diovascular disease statistics, 2006. (Accessed December 7, 2006, at http://www.
americanheart.org.)
2. Rogers WJ, Canto JG, Lambrew CT, et
al. Temporal trends in the treatment of
over 1.5 million patients with myocardial
infarction in the U.S. from 1990 through
1999: the National Registry of Myocardial
Infarction 1, 2 and 3. J Am Coll Cardiol
2000;36:2056-63.
3. Furman MI, Dauerman HL, Goldberg
RJ, Yarzebski J, Lessard D, Gore JM. Twenty-two year (1975 to 1997) trends in the
incidence, in-hospital and long-term case
fatality rates from initial Q-wave and nonQ-wave myocardial infarction: a multi-hospital, community-wide perspective. J Am
Coll Cardiol 2001;37:1571-80.
4. Zheng ZJ, Croft JB, Giles WH, Mensah
GA. Sudden cardiac death in the United
States, 1989 to 1998. Circulation 2001;
104:2158-63.
5. Gibson CM. NRMI and current treatment patterns for ST-elevation myocardial infarction. Am Heart J 2004;148:
Suppl:S29-S33.
6. Libby P. Current concepts of the pathogenesis of the acute coronary syndromes.
Circulation 2001;104:365-72.
7. Libby P, Theroux P. Pathophysiology of
coronary artery disease. Circulation 2005;
111:3481-8.
8. Freedman JE. Molecular regulation of
platelet-dependent thrombosis. Circulation 2005;112:2725-34.
9. Reimer KA, Lowe JE, Rasmussen MM,
Jennings RB. The wavefront phenomenon
of ischemic cell death. 1. Myocardial in-
52
farct size vs duration of coronary occlusion in dogs. Circulation 1977;56:786-94.
10. Weir RA, McMurray JJ, Velazquez EJ.
Epidemiology of heart failure and left ventricular systolic dysfunction after acute
myocardial infarction: prevalence, clinical characteristics, and prognostic importance. Am J Cardiol 2006;97:Suppl 10A:
13F-25F.
11. Grines CL, Cox DA, Stone GW, et al.
Coronary angioplasty with or without stent
implantation for acute myocardial infarction. N Engl J Med 1999;341:1949-56.
12. Stone GW, Brodie BR, Griffin JJ, et al.
Prospective, multicenter study of the safety and feasibility of primary stenting in
acute myocardial infarction: in-hospital
and 30-day results of the PAMI stent pilot
trial. J Am Coll Cardiol 1998;31:23-30.
13. Fibrinolytic Therapy Trialists’ (FTT)
Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview
of early mortality and major morbidity results from all randomised trials of more
than 1000 patients. Lancet 1994;343:31122. [Erratum, Lancet 1994;343:742.]
14. Juliard J-M, Himbert D, Golmard J-L,
et al. Can we provide reperfusion therapy
to all unselected patients admitted with
acute myocardial infarction? J Am Coll
Cardiol 1997;30:157-64.
15. The GUSTO Angiographic Investigators. The effects of tissue plasminogen
activator, streptokinase, or both on coronary-artery patency, ventricular function,
and survival after acute myocardial infarction. N Engl J Med 1993;329:1615-22. [Erratum, N Engl J Med 1994;330:516.]
n engl j med 356;1
www.nejm.org
16. Anderson JL, Karagounis LA, Becker
LC, Sorensen SG, Menlove RL. TIMI perfusion grade 3 but not grade 2 results in
improved outcome after thrombolysis for
myocardial infarction: ventriculographic,
enzymatic, and electrocardiographic evidence from the TEAM-3 Study. Circulation 1993;87:1829-39.
17. Gibson CM, Karha J, Murphy SA, et al.
Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials.
J Am Coll Cardiol 2003;42:7-16.
18. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised
trials. Lancet 2003;361:13-20.
19. Nallamothu BK, Wang Y, Magid DJ, et
al. Relation between hospital specialization with primary percutaneous coronary
intervention and clinical outcomes in STsegment elevation myocardial infarction:
National Registry of Myocardial Infarction4 analysis. Circulation 2006;113:222-9.
20. Antman EM, Anbe DT, Armstrong PW,
et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction — executive summary:
a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for
the Management of Patients with Acute
Myocardial Infarction). Circulation 2004;
110:588-636. [Erratum, Circulation 2005;
111:2013.]
21. Ahmed S, Antman EM, Murphy SA, et
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
clinical ther apeutics
al. Poor outcomes after fibrinolytic therapy for ST-segment elevation myocardial
infarction: impact of age (a meta-analysis
of a decade of trials). J Thromb Thrombolysis 2006;21:119-29.
22. Thune JJ, Hoefsten DE, Lindholm MG,
et al. Simple risk stratification at admission to identify patients with reduced mortality from primary angioplasty. Circulation 2005;112:2017-21.
23. Hochman JS, Sleeper LA, Webb JG, et
al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med 1999;341:62534.
24. Taher T, Fu Y, Wagner GS, et al. Aborted myocardial infarction in patients with
ST-segment elevation: insights from the
Assessment of the Safety and Efficacy of a
New Thrombolytic Regimen-3 Trial Electrocardiographic Substudy. J Am Coll Cardiol 2004;44:38-43.
25. Stone GW, Grines CL, Cox DA, et al.
Comparison of angioplasty with stenting,
with or without abciximab, in acute myocardial infarction. N Engl J Med 2002;346:
957-66.
26. Valgimigli M, Percoco G, Malagutti P,
et al. Tirofiban and sirolimus-eluting stent
vs abciximab and bare-metal stent for
acute myocardial infarction: a randomized
trial. JAMA 2005;293:2109-17.
27. Spaulding C, Henry P, Teiger E, et al.
Sirolimus-eluting versus uncoated stents
in acute myocardial infarction. N Engl J
Med 2006;355:1093-104.
28. Laarman GJ, Suttorp MJ, Dirksen MT,
et al. Paclitaxel-eluting versus uncoated
stents in primary percutaneous coronary
intervention. N Engl J Med 2006;355:110513.
29. Sabatine MS, Cannon CP, Gibson CM,
et al. Effect of clopidogrel pretreatment
before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics:
the PCI-CLARITY study. JAMA 2005;294:
1224-32.
30. Sabatine MS, Cannon CP, Gibson CM,
et al. Addition of clopidogrel to aspirin and
fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl
J Med 2005;352:1179-89.
31. Chen ZM, Jiang LX, Chen YP, et al. Addition of clopidogrel to aspirin in 45,852
patients with acute myocardial infarction:
randomised placebo-controlled trial. Lancet 2005;366:1607-21.
32. Halkin A, Grines CL, Cox DA, et al.
Impact of intravenous beta-blockade before primary angioplasty on survival in
patients undergoing mechanical reperfusion therapy for acute myocardial infarction. J Am Coll Cardiol 2004;43:1780-7.
33. Kernis SJ, Harjai KJ, Stone GW, et al.
Does beta-blocker therapy improve clinical outcomes of acute myocardial infarction after successful primary angioplasty?
J Am Coll Cardiol 2004;43:1773-9.
34. ISIS-4 (Fourth International Study of
Infarct Survival) Collaborative Group. ISIS4: a randomised factorial trial assessing
early oral captopril, oral mononitrate, and
intravenous magnesium sulphate in 58,050
patients with suspected acute myocardial
infarction. Lancet 1995;345:669-85.
35. Cannon CP, Braunwald E, McCabe CH,
et al. Intensive versus moderate lipid lowering with statins after acute coronary
syndromes. N Engl J Med 2004;350:1495504. [Erratum, N Engl J Med 2006;354:
778.]
36. Stone GW, Grines CL, Rothbaum D, et
al. Analysis of the relative costs and effectiveness of primary angioplasty versus
tissue-type plasminogen activator: the Primary Angioplasty in Myocardial Infarction
(PAMI) trial. J Am Coll Cardiol 1997;29:
901-7.
37. Grassman ED, Johnson SA, Krone RJ.
Predictors of success and major complications for primary percutaneous transluminal coronary angioplasty in acute myocardial infarction: an analysis of the 1990
to 1994 Society for Cardiac Angiography
and Interventions registries. J Am Coll
Cardiol 1997;30:201-8.
38. Stone GW, Peterson MA, Lansky AJ,
Dangas G, Mehran R, Leon MB. Impact of
normalized myocardial perfusion after
successful angioplasty in acute myocardial
infarction. J Am Coll Cardiol 2002;39:
591-7.
39. De Luca G, van’t Hof AW, Ottervanger
JP, et al. Unsuccessful reperfusion in patients with ST-segment elevation myocardial infarction treated by primary angioplasty. Am Heart J 2005;150:557-62.
40. Prasad A, Stone GW, Stuckey TD, et
al. Impact of diabetes mellitus on myocardial perfusion after primary angioplasty in patients with acute myocardial
infarction. J Am Coll Cardiol 2005;45:50814.
41. Matetzky S, Novikov M, Gruberg L, et
al. The significance of persistent ST elevation versus early resolution of ST segment
elevation after primary PTCA. J Am Coll
Cardiol 1999;34:1932-8.
42. Tarantini G, Cacciavillani L, Corbetti
F, et al. Duration of ischemia is a major
determinant of transmurality and severe
microvascular obstruction after primary
angioplasty: a study performed with contrast-enhanced magnetic resonance. J Am
Coll Cardiol 2005;46:1229-35.
43. Kandzari DE, Tcheng JE, Gersh BJ, et
al. Relationship between infarct artery
location, epicardial flow, and myocardial
perfusion after primary percutaneous revascularization in acute myocardial infarction. Am Heart J 2006;151:1288-95.
44. Piper WD, Malenka DJ, Ryan TJ Jr, et
al. Predicting vascular complications in
percutaneous coronary interventions. Am
Heart J 2003;145:1022-9.
45. Grines CL, Browne KF, Marco J, et al.
A comparison of immediate angioplasty
n engl j med 356;1
www.nejm.org
with thrombolytic therapy for acute myocardial infarction. N Engl J Med 1993;
328:673-9.
46. Aversano T, Aversano LT, Passamani E,
et al. Thrombolytic therapy vs primary percutaneous coronary intervention for myocardial infarction in patients presenting
to hospitals without on-site cardiac surgery:
a randomized controlled trial. JAMA 2002;
287:1943-51. [Erratum, JAMA 2002;287:
3212.]
47. Bartholomew BA, Harjai KJ, Dukkipati S, et al. Impact of nephropathy after
percutaneous coronary intervention and a
method for risk stratification. Am J Cardiol 2004;93:1515-9.
48. Sadeghi HM, Stone GW, Grines CL, et
al. Impact of renal insufficiency in patients undergoing primary angioplasty for
acute myocardial infarction. Circulation
2003;108:2769-75.
49. DeGeare VS, Stone GW, Grines L, et
al. Angiographic and clinical characteristics associated with increased in-hospital
mortality in elderly patients with acute
myocardial infarction undergoing percutaneous intervention (a pooled analysis of
the primary angioplasty in myocardial infarction trials). Am J Cardiol 2000;86:30-4.
50. Goss JE, Chambers CE, Heupler FA Jr.
Systemic anaphylactoid reactions to iodinated contrast media during cardiac catheterization procedures: guidelines for prevention, diagnosis, and treatment. Cathet
Cardiovasc Diagn 1995;34:99-104.
51. Mehta RH, Harjai KJ, Grines L, et al.
Sustained ventricular tachycardia or fibrillation in the cardiac catheterization laboratory among patients receiving primary
percutaneous coronary intervention: incidence, predictors, and outcomes. J Am Coll
Cardiol 2004;43:1765-72.
52. Almeda FQ, Nathan S, Calvin JE, Parrillo JE, Klein LW. Frequency of abrupt
vessel closure and side branch occlusion
after percutaneous coronary intervention
in a 6.5-year period (1994 to 2000) at a
single medical center. Am J Cardiol 2002;
89:1151-5.
53. Yang EH, Gumina RJ, Lennon RJ,
Holmes DR Jr, Rihal CS, Singh M. Emergency coronary artery bypass surgery for
percutaneous coronary interventions:
changes in the incidence, clinical characteristics, and indications from 1979 to
2003. J Am Coll Cardiol 2005;46:2004-9.
54. Wharton TP Jr, Grines LL, Turco MA,
et al. Primary angioplasty in acute myocardial infarction at hospitals with no surgery
on-site (the PAMI-No SOS study) versus
transfer to surgical centers for primary angioplasty. J Am Coll Cardiol 2004;43:194350.
55. Wharton TP Jr. Should patients with
acute myocardial infarction be transferred
to a tertiary center for primary angioplasty
or receive it at qualified hospitals in community? The case for community hospital
angioplasty. Circulation 2005;112:3509-20.
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.
53
clinical ther apeutics
56. Bavry AA, Kumbhani DJ, Helton TJ,
Bhatt DL. What is the risk of stent thrombosis associated with the use of paclitaxeleluting stents for percutaneous coronary
intervention? A meta-analysis. J Am Coll
Cardiol 2005;45:941-6.
57. Moreno R, Fernandez C, Hernandez
R, et al. Drug-eluting stent thrombosis:
results from a pooled analysis including
10 randomized studies. J Am Coll Cardiol
2005;45:954-9.
58. Iakovou I, Schmidt T, Bonizzoni E, et
al. Incidence, predictors, and outcome of
thrombosis after successful implantation
of drug-eluting stents. JAMA 2005;293:
2126-30.
59. Keeley EC, Grines CL. Should patients
54
with acute myocardial infarction be transferred to a tertiary center for primary
angioplasty or receive it at qualified hospitals in the community? The case for emergency transfer for primary percutaneous
coronary intervention. Circulation 2005;
112:3520-32.
60. Keeley EC, Boura JA, Grines CL. Comparison of primary and facilitated percutaneous coronary interventions for ST-elevation myocardial infarction: quantitative
review of randomised trials. Lancet 2006;
367:579-88. [Erratum, Lancet 2006;367:
1656.]
61. Dalby M, Bouzamondo A, Lechat P,
Montalescot G. Transfer for primary angioplasty versus immediate thrombolysis
n engl j med 356;1
www.nejm.org
in acute myocardial infarction: a metaanalysis. Circulation 2003;108:1809-14.
62. Nallamothu BK, Bates ER, Wang Y,
Bradley EH, Krumholz HM. Driving times
and distances to hospitals with percutaneous coronary intervention in the United States: implications for prehospital
triage of patients with ST-elevation myocardial infarction. Circulation 2006;113:
1189-95.
63. Van de Werf F, Ardissino D, Betriu A,
et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2003;24:2866.
Copyright © 2007 Massachusetts Medical Society.
january 4, 2007
The New England Journal of Medicine
Downloaded from nejm.org by LUIS GALLUR on January 13, 2012. For personal use only. No other uses without permission.
Copyright © 2007 Massachusetts Medical Society. All rights reserved.