(Chest. 2001;120:1417-1420.)
© 2001
American College of Chest Physicians
Rescue Percutaneous Coronary Intervention Immediately Following Coronary Artery Bypass Grafting*
Robert N. Piana, MD;
Mark R. Adams, MBBS, PhD;
James L. Orford, MBChB;
Jeffrey J. Popma, MD;
David H. Adams, MD and
Samuel Z. Goldhaber, MD, FCCP
*
From the Cardiovascular Division (Dr. Piana), Vanderbilt University Medical Center, Nashville, TN; and the Cardiovascular and Cardiac Surgical Divisions (Drs. M. Adams, Orford, Popma, D. Adams, and Goldhaber), Brigham and Womens Hospital, Harvard Medical School, Boston, MA.
Correspondence to: Robert N. Piana, MD, Director, Cardiac Catheterization Laboratories, Vanderbilt University Medical Center, 2311 Pierce Ave, Nashville, TN 37232-8802; e-mail: Robert.Piana{at}mcmail.vanderbilt.edu
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Abstract
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Perioperative graft failure after coronary artery bypass graft
(CABG) can result in acute myocardial infarction with dire clinical
consequences. We report a case of rescue percutaneous coronary
intervention immediately after unsuccessful CABG. This approach
salvaged the patient from cardiogenic shock and should be recognized as
a viable alternative to immediate reoperation for certain
patients.
Key Words: angioplasty catheterization coronary artery bypass graft stent
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Introduction
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Immediate
cardiac surgical "backup" for coronary angioplasty has historically
been considered mandatory because procedural complications have
necessitated emergency "rescue" coronary artery bypass graft (CABG)
surgery in as many as 3% of cases. Here, we describe the reverse
circumstance of a patient who suffered an acute anterior myocardial
infarction immediately after CABG. In this case, rescue percutaneous
coronary intervention (PCI) was required for a complication of CABG.
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Case Report
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A 78-year-old woman had several episodes of chest pain at rest
and after eating. Results of a modified Bruce protocol exercise
treadmill test proved markedly positive, and coronary angiography
demonstrated a 70% ostial left main coronary artery stenosis and
three-vessel coronary artery disease. She was therefore referred
for urgent CABG. Preoperative echocardiography showed normal left
ventricular function. She received a left internal mammary artery
(LIMA) graft to the left anterior descending and reverse saphenous vein
grafts to the first marginal and to the posterior descending arteries.
Intraoperatively, the grafts had good flow and runoff. Concomitant left
carotid endarterectomy was performed because of an incidentally
discovered 85% left internal carotid artery stenosis. Cardiopulmonary
bypass time was 54 min, and aortic cross-clamp time was 43 min.
Postoperatively, 250 mg of protamine sulfate was administered and the
accelerated clotting time was 121 s on arrival in the ICU.
At the time of transfer to the ICU, her systemic arterial pressure fell
from 156/63 to 91/48 mm Hg. Initial ECG showed extensive ST-segment
elevation consistent with acute anterior and lateral infarction. Thirty
minutes later, a follow-up ECG showed loss of R waves and new Q waves
in the anterior precordial leads (Fig 1
), indicating evolution of myocardial infarction.

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Figure 1.. Top panel (on arrival in the ICU):
marked ST-segment elevation, especially prominent in leads
V2 through V6, consistent with an early
and massive anterior myocardial infarction. Middle panel
(30 min later): anterior and inferior Q waves have evolved, suggesting
a completed myocardial infarction. Bottom panel (after
PCI): R waves have reappeared in inferior and anterior leads,
suggesting persistent viability of myocardium. POD = postoperative
day; S/P = status post; POSTOP = postoperative.
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Emergent coronary angiography showed a 70% stenosis in the LIMA graft
at its anastomosis to the left anterior descending artery. Flow in the
LIMA graft was delayed and pulsatile, with no effective filling of the
left anterior descending artery. There was also a 90% stenosis in the
native left anterior descending coronary artery directly underlying the
LIMA graft anastomosis. The two vein grafts were widely patent.
Heparin, 3,000 IU, was administered, and an accelerated clotting time
of 292 s was documented prior to percutaneous coronary
intervention. The patient also received aspirin, 325 mg, and
clopidogrel, 150 mg, by nasogastric tube. Rescue balloon angioplasty of
the LIMA graft lesion resulted in a 30% residual stenosis with a small
linear dissection and improved antegrade flow, but without resolution
of the ST-segment elevation or hypotension. The stenosis in the native
left anterior descending artery was therefore dilated with a
3.0 x 18-mm Duet stent (Guidant Corporation; Temecula, CA),
delivered through the left main and positioned spanning the LIMA graft
anastomosis. The dissection site in the left internal mammary was then
corrected with a 2.5 x 16-mm Nir stent (Boston Scientific Scimed;
Maple Grove, MA). Finally, the left main coronary artery stenosis was
treated with a 3.0 x 8-mm GFX stent (Medtronic AVE; Santa Rosa, CA)
[Fig 2
].

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Figure 2.. Left: native left coronary
injection. There is both "tenting" and a severe stenosis (white
arrow) of the left anterior descending artery at the site of the LIMA
anastomosis. There is retrograde filling of the LIMA, which also has a
severe stenosis (black arrow) just proximal to its anastomosis on the
left anterior descending artery. Right: native left
coronary injection. After stenting both the left anterior descending
artery stenosis (spanning the site of the LIMA anastomosis; white
arrow) and the stenosis in the internal mammary (just proximal to
its anastomosis; black arrow), there is no residual angiographic
stenosis at either site. The tenting of the left anterior descending
artery is also straightened.
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After stenting, anterior ST-segment elevation resolved and R waves
reappeared across the precordium (Fig 1)
. Peak creatine kinase level
after the procedure was 1,367 U/L (normal range, 27 to 218 U/L), with a
quantitative creatine kinase-MB fraction of 189 ng/mL (normal range, 0
to 5.0 ng/mL). Follow-up echocardiography showed new akinesis of the
left ventricular apex, mild left ventricular dilation, and a calculated
ejection fraction of 0.55, which was a significant improvement when
compared with the preoperative ejection fraction of 0.40. The patient
was discharged to a rehabilitation facility 9 days after CABG and PCI.
Discharge medications included aspirin, 325 mg qd, and clopidogrel, 75
mg qd. No bleeding complications were encountered.
The patients subsequent medical history includes multiple hospital
admissions with recurrent chest discomfort within the first 9 months
following CABG and PCI (Table 1
). Thereafter, she has experienced no further episodes of angina
pectoris requiring hospitalization or additional cardiac testing. She
is active and independent 24 months after the index hospital admission
and surgical revascularization.
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Discussion
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Myocardial infarction may occur in 5 to 10% of patients following
CABG and can account for 60 to 70% of postoperative in-hospital
deaths.1
2
When perioperative myocardial infarction
is manifested by acute ST-segment elevation, rather than by
asymptomatic elevation of the cardiac enzymes, sudden graft occlusion
is frequently responsible. Early graft failure may also be heralded by
hemodynamic instability or sustained ventricular tachycardia.
LIMA grafts achieve improved long-term patency compared to saphenous
vein grafts, which have a 10% incidence of closure within 60 days of
CABG.3
However, LIMA graft failure can still occur due to
injury during harvesting, technical problems with the anastomosis, poor
distal runoff in the grafted native vessel, extreme mechanical
"kinking" of the graft, or undetected subclavian artery
stenosis.2
4
The relative contributions of the
aforementioned clinical entities are unclear, but thrombotic stenosis
or occlusion of the LIMA graft may be responsible for the acute
ischemic complications of CABG in at least a third of all
cases.2
The technical challenges for the surgeon may be
intensified when "minimally invasive" CABG is performed on a
beating heart.5
In our patient, graft failure resulted
from severe perianastomotic stenoses.
Rescue PCI for acute myocardial infarction following CABG yielded a
gratifying clinical and angiographic result in our patient. This
approach of urgent angiography allows immediate identification of the
source of ischemia and the development of an optimal treatment
strategy.
Rescue PCI for "early" graft failure has generally yielded
favorable results.6
7
8
9
10
11
12
In a case series6
of
45 patients, early postoperative balloon coronary angioplasty (without
stenting) to relieve anginal symptoms was reported at an average of 49
days after CABG; angioplasty was successful in 95% of native artery
lesions (n = 41), 89% of vein graft stenoses (n = 46), and 100%
of LIMA graft lesions (n = 11). Other groups7
8
9
have
routinely used PCI to manage ischemia or infarction within a month
after surgery but have only reported their results in preliminary
abstracts. Importantly, patent grafts were observed in 25 to 34% of
patients in these three series.7
8
9
This finding suggests
that angiographic confirmation should be sought whenever graft
occlusion is suspected rather than performing a "blind" reoperation
CABG. Our patient differs from the previously reported cases because
she underwent rescue PCI within hours of completion of CABG.
Rescue PCI is only one of several possible approaches to acute ischemia
following CABG. Compared to emergent reoperation, rescue PCI is less
invasive and more expeditious, while still offering the potential for
complete revascularization. Thrombolytic therapy risks intractable
hemorrhage in the postoperative patient and would not reverse the type
of mechanical anastomotic obstruction seen in our
patient.13
Conservative medical management would
undoubtedly fail to prevent the development of severe pump failure or
progression to fatal cardiogenic shock in a patient such as ours
presenting with a large territory of infarction, evolution of Q waves,
and persistent hypotension. Among the available options, rescue PCI may
therefore be the preferred treatment strategy in many patients with
acute perioperative graft failure.10
As illustrated by
this patients subsequent medical course, the immediate success of
this life-saving therapeutic intervention does not eliminate the need
for close clinical follow-up and treatment of the underlying
atherosclerotic process.
Rescue PCI for ischemic complications following CABG requires an
integrated approach that involves the general cardiologist, cardiac
surgeon, and interventional cardiologist. Patient outcomes may be
significantly improved as a result of this close collaboration and this
may lead to a new paradigm in which the cardiac catheterization
laboratory is routinely available to assist the surgeon when early
postoperative ischemia is identified.
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Footnotes
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Abbreviations: CABG = coronary artery bypass graft;
LIMA = left internal mammary artery; PCI = percutaneous coronary
intervention
Received for publication March 7, 2000.
Accepted for publication March 8, 2001.
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References
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Schieman, G, Cohen, BM, Buchbinder, M (1990) Standby percutaneous coronary angioplasty for coronary artery bypass surgery. Cathet Cardiovasc Diagn 21,159-161[ISI][Medline]
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Khurana, S, ONeill, WW, Sakwa, M, et al (1997) Acute occlusion of a left internal mammary artery graft immediately after redo coronary artery bypass surgery: successful rescue PTCA. Cathet Cardiovasc Diagn 41,166-169[CrossRef][ISI][Medline]
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Dauerman, HL, Cutlip, DE, Sellke, FW (1996) Intracoronary thrombolysis in the treatment of graft closure immediately after CABG. Ann Thorac Surg 62,280-283[Abstract/Free Full Text]
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