(Chest. 2000;118:1769-1775.)
© 2000
American College of Chest Physicians
Clinical Conference on Management Dilemmas*
A Growing Vascular Mass in the Chest
Satyendra Gupta, MD;
Tauseef Khan, MD;
Larry W. Stephenson, MD;
Denton Cooley, MD, FCCP and
Jeff Schnader, MD, CM, FCCP
*
From the Department of Medicine (Drs. Gupta, Khan, and Schnader), Wright State University School of Medicine, and the Department of Medicine, Dayton VA Medical Center, Dayton, OH; the Department of Surgery (Dr. Stephenson), Wayne State University School of Medicine, Detroit, MI; and the Texas Heart Institute (Dr. Cooley), Texas Medical Center, Houston, TX.
Correspondence to: Jeff Schnader, MD, CM, FCCP, Chief, Division of Pulmonary and Critical Care Medicine, Wright State University School of Medicine, Dayton VA Medical Center (111), 4100 West Third St, Dayton, OH 45428; e-mail: jeff.schnader{at}med.va.gov
Key Words: coronary artery aneurysm • coronary artery
bypass grafting • coronary artery disease • internal mammary artery
graft • percutaneous transluminal coronary angioplasty • pseudoaneurysm • saphenous vein graft Abbreviations:
CPK = creatine phosphokinase • LAD = left anterior descending
artery • MRA = magnetic resonance angiography • PTCA = percutaneous
transluminal coronary angioplasty
 |
Introduction
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Clinicians
are often faced with management problems for which there are no answers
at hand, because there is no literature that definitely gives answers,
because there are conflicting data in the literature, or because the
circumstances surrounding the clinical cases are unusual enough to
prevent the application of existing scientific knowledge. When faced
with these problems, clinicians are forced to make decisions based on a
logical extension of their scientific knowledge into uncharted clinical
waters. They are forced to make judgments based on the conviction of
their speculations and on prior experiences.
This case conference addresses difficult management problems without
singularly correct decisions; its object is not necessarily
to seek consensus. Defining the exact issues, formulating rationales
for decision making, and committing to the decisions themselves are all
equally important in this presentation. This is a real case in which
the decisions were made by the "treating" physicians without input
from the other participants. The "responses of the experts" are
given only with the knowledge of the case presentation up to the moment
at which each expert gives his or her decision, and without the
knowledge of any of the other opinions rendered. The last
"commentary" opinions are given only with the knowledge of the
"case presentation" and the remarks of the treating physicians, but
without the knowledge of any of the other opinions rendered. Although
the commentary opinions are the last in the sequence of this
presentation, they are not necessarily offered as definitive solutions
to the problems posed in the case. The reader is the ultimate arbiter
in this presentation of decision-making alternatives.
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Case Presentation
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In 1984, a 52-year-old white man presented with symptoms of
severe retrosternal pressure associated with dyspnea, nausea, and
vomiting. Inferior wall myocardial infarction was diagnosed. Cardiac
catheterization revealed severe three-vessel coronary artery disease.
He underwent left internal mammary artery anastomosis to the mid left
anterior descending artery (LAD), and saphenous vein grafting to the
first diagonal, first obtuse marginal, and right coronary arteries.
He was physically active and employed in the construction business, but
he continued to smoke one pack of cigarettes per day. In July 1995, he
again had severe chest pain, and a second myocardial infarction was
diagnosed. A cardiac catheterization revealed that three of his four
grafts were severely diseased: there was complete occlusion of the
grafts to the right coronary and obtuse marginal arteries, subtotal
occlusion of the graft to the diagonal artery, and a patent left
internal mammary artery supplying the LAD.
Percutaneous transluminal coronary angioplasty (PTCA) successfully
revascularized the graft to the first diagonal artery. The patient quit
smoking, but he experienced chronic cough and exertional dyspnea after
walking two to three city blocks. A later examination in
primary-care clinic revealed expiratory wheezing without rales. There
was no jugular venous distention. Extremities did not show any
clubbing, cyanosis, or edema. Treatment was begun with albuterol and
ipratropium metered-dose inhalers for possible COPD. Pulmonary function
tests revealed an FEV1 of 1.59 L (56% of
predicted) and an FVC of 3.43 L (96%). There was a bronchodilator
response of 24% in the forced expiratory flow, midexpiratory
phase. The total lung capacity was 8.20 L (128%), the residual
volume was 4.67 L (210%), and the diffusing capacity of the lung for
carbon monoxide was 15.86 mL/min/mm Hg (56%). In May 1997, a cardiac
gated first pass (MUGA) scan revealed left and right ventricular
ejection fractions of 50% and 44%, respectively, with left
ventricular dilatation.
On September 10, 1998, the patient underwent a routine chest radiograph
that showed marked left hilar prominence (Fig 1
) that was not present on a radiograph from 10 months earlier. CT scan
of the chest revealed a smoothly marginated, sharply circumscribed 5-cm
spherical lesion lying to the left of the ascending aorta (Fig 2
). The patient’s internist noted that the patient had no complaints
except for his usual exertional angina, which was unchanged. There was
no fever, chills, or weight loss. Physical examination revealed a
moderately obese man with a BP of 145/78 mm Hg, heart rate of 78
beats/min, and respiratory rate of 18 breaths/min. He was afebrile.
There was no jugular venous distention. Findings from cardiac, lung,
abdominal, and extremities examinations were unremarkable.
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Figure 2.. Contrast-enhanced CT scan of the chest read by the
radiologist as a smoothly marginated, sharply circumscribed 5-cm
soft-tissue density mass with central contrast enhancement consistent
with a pseudoaneurysm. There is a soft tissue band extending to a
surgical clip at the ventral aortic root margin from this mass. A
second similar mass of 1.5- to 2-cm diameter, ventral to the first
mass, has a small area of centrally higher echodensity, likely blood,
and appears to have its own communicating soft-tissue band extending
toward a surgical clip at the aortic root. Top: image
21. Bottom: image 22.
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On October 6, 1998, the patient was seen by a pulmonologist for
exertional dyspnea that was believed to be due to COPD. He complained
of increasing frequency of chest pain that was no longer related solely
to exertion. Over the prior 2 weeks, he had had three episodes of chest
pain at rest, each lasting 5 to 10 min, each relieved by sublingual
nitroglycerin. During the pulmonary consultation, the patient
experienced another episode of severe left-sided chest pain radiating
to his left arm. He became short of breath and diaphoretic. He was
given two chewable baby aspirins and three sublingual nitroglycerin
tablets at 5-min intervals. This reduced the pain but did not eradicate
it.
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Response of the Cardiopulmonary Surgical Expert
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Larry W. Stephenson, MD; Detroit, MI
In my view at this point, the patient needs to be admitted to a
coronary-care unit to rule out myocardial infarction. Since his last
cardiac catheterization was 3 years previously, he will need to undergo
a repeat cardiac catheterization during this hospital admission. The
timing of the catheterization depends somewhat on the patient’s
symptoms and hospital course. The newly discovered mass on the chest
radiograph and by CT scan appears to be fluid filled and is most likely
some type of an aneurysm or false aneurysm of a coronary artery or one
of the bypass grafts.
This mass might be better delineated by MRI or coronary angiogram,
which the patient will need. My guess is that it is probably related to
the PTCA performed on his left diagonal vein graft 3 years before. The
balloon procedure might have caused an aneurysm in the area of
dilatation, but more likely caused a tear with subsequent extravasation
of blood into the surrounding tissue. The amount of blood extravasating
appears to have been more noticeable on recent chest radiographs, which
indicates that it may be slowly enlarging.
The patient’s old operative report from 1984 needs to be reviewed,
which should give us a better idea as to what the coronary vessels were
like back then and if any might warrant further bypass. This
information coupled with a repeat coronary angiogram would help
determine whether repeat coronary bypass surgery should be recommended.
If surgery is recommended, the aneurysm or false aneurysm can easily be
dealt with at that time. If, however, it is determined that surgical
revascularization is not the appropriate treatment, then one has to
decide about management of the aneurysm or false aneurysm. It is
unlikely that it would rupture into a free space, since there would be
a considerable amount of adhesions present, particularly in the area
where the internal mammary artery had been taken down. If the aneurysm
continues to enlarge over time, it will likely need to be dealt with
surgically. If it remains stable, and there are no other indications
for reperformed bypass grafting, then the aneurysm or contained rupture
can probably be followed.
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Comment by the Treating Pulmonologist
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Jeff Schnader, MD, CM, FCCP; Dayton, OH
When I saw this patient in the outpatient setting, I believed that
COPD could account for his dyspnea. But he also had a progressive chest
pain syndrome that could also have contributed to the dyspnea. The mass
seen on chest radiograph was of great concern: it was smooth and
resembled an enlarged vascular structure. And because of its location,
the pulmonary artery and coronary artery or saphenous
graft1
2
3
4
5
were the likely candidates for the
abnormalities. The CT scan, which had been performed previously, showed
that the mass was indeed a vascular structure with two components. In
the center, there was a 2-cm round area of contrast indicating a lumen.
This was surrounded by a doughnut-shaped or ring-like, sharply
marginated aneurysmal mass, 4 to 5 cm in total diameter, without
evidence of contrast. This "ring" may have been a vascular
dissection or pseudoaneurysm5
6
that had thrombosed within
its false lumen. On image 21, the mass appeared contiguous with the
aorta via a narrow vascular channel, close to the aortic root, just
cephalad to where the expected takeoffs of the coronary arteries would
be from their respective semilunar cusps of the aortic valve. On image
22, that narrow vascular channel appeared to have within it another,
smaller aneurysmal dilatation, just < 2 cm in diameter. My concern
was that the recent progressive nature of his symptoms could be from
worsening obstruction of his coronaries/grafts, due to clotting off or
expansion of one of the aneurysms, both of which may have arisen from
the old saphenous vein grafts. I considered the possibility of an
infected vascular structure,6
but the clinical
presentation initially did not make this the chief concern and
eventually did not support an infectious etiology. Postsurgical
vascular fistulization has even been reported,7
8
as has
embolization from clotted coronary aneurysms to the
myocardium.1
5
6
In this patient, the largest aneurysm
that appeared thrombosed seemed to be so rigid and thick walled that
the likelihood of rupture or expansion of this particular lesion seemed
less likely. However, the smaller aneurysm did not exhibit
these safer features. Because of his presentation, I hospitalized him
on the spot for further treatment.
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Hospital Course
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An ECG was performed (Fig 3
). He was admitted to the medical ICU for management and work-up, where
he appeared apprehensive with a BP of 155/80 mm Hg, heart rate of 102
beats/min, and respiratory rate of 22 breaths/min.
S1 and S2 were normal. The
cardiac point of maximal impulse was in the sixth intercostal space
just lateral to the midclavicular line. There was no jugular venous
distention, murmur, rub, gallop, thrill, or heave. The chest exhibited
normal air entry without wheeze, rub, rales, or rhonchi. Findings from
the abdomen and extremities examinations were unremarkable.
Treatment with IV heparin and nitroglycerin was begun. IV metoprolol, 5
mg, was administered. The vital signs remained stable, and the monitor
showed normal sinus rhythm. The chest pain was completely relieved
after 25 min. The first total creatine phosphokinase (CPK) was
88 U/L (normal, 35 to 374 U/L). MB and MB index were not calculated.
Troponin I obtained 6 h after onset of chest pain was 0.6 ng/mL
(normal, 0 to 0.6 ng/mL). The second total CPK was 106 U/L with MB of
5.6 ng/mL (normal, 0 to 5.8 ng/mL) and MB index of 5.3% (normal, 0 to
5.4%). The third total CPK was 101 U/L with MB 4.0 ng/mL and MB index
of 2.9%. Sodium was 139 mEq/L (136 to 145 mEq/L), potassium 4.4 mEq/L
(3.6 to 5.0 mEq/L), chloride 106 mEq/L (98 to 108 mEq/L), bicarbonate
23.3 mEq/L (22 to 31mEq/L), creatinine 1.1 mg/dL (0.5 to 1.4 mg/dL),
and urea nitrogen 12 mg/dL (6 to 20 mg/dL). The hemoglobin and
hematocrit were 14.2g/dL (14 to 18g/dL) and 45%, respectively. The WBC
count was 7.0 x 103/µL (4.8 to
10.8 x 103/µL) with a normal differential.
The patient was then treated for unstable angina and continued on a
regimen of heparin, switched to oral metoprolol, and given
lisinopril.
Magnetic resonance angiography (MRA) revealed a 5-cm middle mediastinal
mass, connected to the anterior aspect of the ascending aorta several
centimeters above the aortic valve (Fig 4
). The breath holding T2-weighted images showed high signal
intensity in the periphery of the mass, with a thin smooth rind of
intermediate signal intensity forming the border. There was another
similar mass just proximal to the first lesion connected to the
ascending aorta in the vicinity of a surgical clip.
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Figure 4.. MRA of the chest. Upper left,
upper right: A bypass vessel going from the aorta into
the larger of the two pseudoaneurysms. Bottom left,
bottom right: A bypass vessel going from the aorta into
the smaller of the two pseudoaneurysms. There is slow flow seen in both
pseudoaneurysms.
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The following day, a coronary angiogram was performed that confirmed
the diagnosis of venous graft aneurysms involving the grafts to the
obtuse marginal and the diagonal arteries. It further showed that left
ventricular chamber was not dilated and the inferior and posterior
segments of the wall were hypokinetic. The estimated ejection fraction
was 30%. The aortogram showed the aortic root to be dilated with 2+
aortic regurgitation. The left main coronary artery was totally
occluded proximally, and the left internal mammary artery graft to the
mid-LAD was patent. The distal LAD was patent. The saphenous vein
grafts to the diagonal and obtuse marginal grafts were totally
occluded. The right coronary artery was also totally occluded.
Collateral vessels were seen from the LAD to the posterior descending
artery and from the first diagonal to the obtuse marginal artery.
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Comments by the Treating Cardiologist
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Satyendra Gupta, MD; Dayton, OH
Our patient presented with a mediastinal mass found on routine
chest radiograph. A coronary angiogram was performed to assess the
reason for his chest pain, uncover the presence or absence of
aneurysms, and assess any progression of the patient’s garden-variety
coronary disease.3
We were particularly concerned with the
extent of atherosclerotic disease in the saphenous vein grafts to the
obtuse marginal branch of the circumflex. We believed that damage to
the saphenous vein graft wall with dissection during angioplasty was
the likely etiologic factor for the formation of aneurysm in this
patient. Along these lines, our major concern was that an aneurysm in a
venous structure would not behave in the same way as one in an artery.
We feared that a venous graft aneurysm might be more prone to rupture
than an arterial aneurysm, and the fact that a pseudoaneurysm might be
present made us fear a propensity to rupture could be greater than in
other patients.3
6
Both aneurysms also posed the threat of
embolization to the myocardium.1
5
6
We did not think the
patient needed another bypass or PTCA, and we were not afraid of
infection as the underlying cause of the vascular abnormalities in this
patient. Our own local experience with native coronary
artery aneurysms might amount to a half dozen cases over
many years, and all of these patients were followed with observation
and without surgical intervention. But we have never seen a coronary
venous graft aneurysm before, and this is the largest aneurysm of any
coronary-related structure we have ever seen. Although we believed that
the possibility of rupture was still low, we were also uncomfortable
with the patient’s chest pain, which we believed was not entirely
anginal in nature and could represent recent expansion of one or both
aneurysms, possibly a sentinel symptom for impending rupture. Although
other treatment approaches have been used,5
9
for the
foregoing reasons and the fact that the literature supports a surgical
approach in similar cases,1
2
3
4
6
we requested a surgical
opinion.
The occurrence of an aneurysm in a saphenous vein coronary artery
bypass graft is unusual.1
2
3
4
6
7
8
The natural history of
these lesions is not well known.2
6
Many of these graft
aneurysms are asymptomatic and detected only incidentally on a routine
chest radiograph. Saphenous vein bypass graft aneurysms appear as a new
parahilar or mediastinal mass on chest radiographs. Coronary angiogram
confirms the presence of graft dilatation and aneurysms, although CT
scan and MRI (MRA/MRI) are helpful.
The underlying pathologic mechanism and the subsequent development of
these saphenous vein graft aneurysms are not completely known.
Imperfect surgical techniques may play a role in some cases with false
aneurysms (pseudoaneurysms) that usually occur at the proximal or
distal anastomosis of the vein graft and occur relatively early in the
postoperative course. Occurrence of false aneurysms after coronary
angioplasty and stenting of the saphenous vein coronary artery bypass
graft to the coronary artery have also been described.6
True aneurysms are usually considered to be atherosclerotic in nature
and often occur > 5 years after the original coronary artery bypass
surgery. They are thought to occur more often in patients who continue
to have hyperlipidemia.10
Weakness in the vein graft wall
near valve sites has also been blamed.9
11
Here, the
muscular layer of the vein changes from circular to longitudinal, which
may predispose to the formation of an aneurysm. Other mechanisms of
development of these saphenous vein graft aneurysms are thought to
include trauma at the original operation and weakness of the veins
themselves.
Complications of these aneurysms include thrombosis with embolization,
rupture, and erosion into the cardiac chamber with resulting fistula
and hemothorax.12
With the increasing number of aging
patients undergoing primary coronary artery bypass grafts, graft
revisions, and angioplasties of the venous grafts, aneurysms of venous
grafts may occur with greater frequency in clinical practice. A high
index of suspicion and proper selection of imaging techniques can
provide an accurate anatomic assessment. Recommendations for treatment
of aneurysm of saphenous vein coronary bypass grafts are not well
established. Most large aneurysms with patent grafts should be treated
surgically because of the risk of embolization and rupture.
The risk of reintervention may be high. Thus, in patients who have the
distal anastomosis of the saphenous vein graft already occluded or who
are considered not to be operative candidates, nonsurgical coil
embolization of these aneurysms is an alternative way of
management.13
14
Coils must be placed well within the
grafts to prevent distal coil embolization.
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Follow-up
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The clinical data and coronary angiograms were reviewed by two
separate sets of surgical consultants. After review of the data, they
recommended conservative treatment with close follow-up. The reasons
behind this decision were as follows: (1) the aneurysm had thrombosed
and there was no effective flow occurring to the distal vessels; (2)
the left internal mammary artery graft to the LAD was widely patent,
and the LAD was supplying most of the myocardium via collaterals; (3)
the patient had moderately severe pulmonary disease; and 4) overall,
the patient was at high risk for reoperation.
Medical management was undertaken for the coronary artery disease. The
patient was discharged home on the fourth hospital day, with close
outpatient cardiology follow-up. A repeat CT scan of the chest with
contrast obtained on August 24, 1999 (11 months later) showed no change
in the sizes or configurations of the vascular dilatations.
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Commentary
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Denton A. Cooley, MD, FCCP; Houston, TX
I have reviewed the details of this case of myocardial ischemia,
which occurred in an obese 68-year-old man with complicating pulmonary
insufficiency. Fifteen years before, he had a triple-vessel coronary
artery bypass operation in which reversed saphenous vein grafts were
placed to the first diagonal, the first obtuse marginal, and the right
coronary arteries; and an internal thoracic artery graft was placed to
the LAD. All three of the vein grafts occluded; two resulted in venous
aneurysms.
Despite the risk of reoperating on an obese patient with pulmonary
disease, I believe the proper approach is surgical. During
cardiopulmonary bypass, the aneurysms should be opened and the contents
removed. New bypass grafts should then be placed in the distal
arteries, which may still be patent. Since the original saphenous vein
grafts deteriorated so severely, I would use only arterial grafts as
conduits: the right internal thoracic and gastroepiploic arteries as
pedicle grafts, or radial arteries as free grafts. I believe this
approach would be successful.
Several other options are also available, up to and including cardiac
transplantation. Interventional techniques, none of which seem
applicable in this case, include angioplasty with stents (including
covered stents) and insertion of coils, which are used mainly for
repair of pseudoaneurysms.
While the cause for the aneurysms described may be due in part to poor
basic structure of the saphenous veins, iatrogenic factors might also
be at fault.15
16
If varices were present at the time of
the bypass procedure, the surgeon may have selected a poor quality vein
and, thus, would have been responsible. Either traumatic manipulation
of the graft or excessive dilatation of the vein during preparation may
also have injured the graft. In this case, it is certainly possible
that the aneurysmal process was triggered by the angioplasty done in
1995, as this has been reported as a cause of vein graft
aneurysms.6
17
Since 1975, only 50 vein graft aneurysms (both true and pseudo) have
been reported.15
My experience includes perhaps five cases
of saphenous vein aneurysms in coronary bypass grafts, but many more in
vein grafts used peripherally—in the thighs and elsewhere. Usually
fibrosis and occlusion cause vein grafts to deteriorate, but in unusual
circumstances the vein wall is not capable of withstanding pulsatile
arterial stress.9
My approach to such problems is direct; in this patient, I would
operate. This particular case also illustrates the importance of
restoring circulation in the anterior descending artery with a pedicled
internal thoracic artery. If another operation is performed, the
surgeon must take great care not to damage the internal thoracic graft.
Without an operation, the patient is left with ischemia and angina, and
his life depends on the integrity of the existing graft to the anterior
descending artery.
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Long-term Follow-up
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The patient did well until February 2000, when he died
suddenly at home. No further details are available.
Received for publication April 27, 2000.
|
References
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-
Wyatt, DA, Gay, SB, Gimple, LW, et al (1993) Successful preoperative diagnosis and treatment of a saphenous vein coronary artery bypass graft aneurysm. Chest 104,283-284[Abstract/Free Full Text]
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Ferreira, A, Marchena, E, Awaad, M, et al (1997) Saphenous vein graft aneurysm presenting as a large mediastinal mass compressing the right atrium. Am J Cardiol 79,706-707[CrossRef][ISI][Medline]
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Wight, J, Salem, D, Vannan, M, et al (1997) Asymptomatic large coronary artery saphenous vein bypass graft aneurysm: a case report and review of the literature. Am Heart J 133,454-460[CrossRef][ISI][Medline]
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Wester, D, Martinez, H, Camp, A (1993) Aneurysm of a saphenous vein graft manifested as a mediastinal mass on chest radiographs. AJR Am J Roentgenol 161,951-952[Free Full Text]
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Doyle, M, Spizarny, D, Baker, D (1997) Saphenous vein graft aneurysm after coronary artery bypass surgery. AJR Am J Roentgenol 168,747-749[Abstract/Free Full Text]
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Le Breton, H, Pavin, D, Langanay, T, et al (1998) Aneurysms and pseudo-aneurysms of saphenous vein coronary artery bypass grafts. Heart 79,505-508[Abstract/Free Full Text]
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Jukema, J, van Dijkman, P, van der Wall, E (1992) Pseudoaneurysm of a saphenous vein coronary artery bypass graft with a fistula draining into the right atrium. Am Heart J 124,1397-1399[CrossRef][ISI][Medline]
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Zely, P, Delarche, N, Estrade, G, et al (1996) Double aneurysm of a venous aorto-coronary bypass graft. Arch Mal Coeur 89,1213-1216
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Benchimol, A, Harris, C, Desser, K, et al (1975) Aneurysms of an aorto-coronary artery saphenous vein bypass graft: a case report. J Vasc Surg 9,261-264
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Teja, K, Dillingham, R, Mentzer, R (1987) Saphenous vein aneurysms after aortocoronary bypass grafting: postoperative interval and hyperlipidemia as determining factors. Am Heart J 113,1527-1529[CrossRef][ISI][Medline]
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Vlodaver, Z, Edwards, J (1971) Pathologic changes in aortic-coronary arterial saphenous vein grafts. Circulation 44,719-728[Abstract/Free Full Text]
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Murphy, J, Jr, Shabb, B, Nishikawa, A, et al (1986) Rupture of an aortocoronary saphenous vein graft aneurysm. Am J Cardiol 58,555-557[CrossRef][ISI][Medline]
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Shapeero, L, Guthaner, D, Swerdlow, C, et al (1983) Rupture of a coronary bypass graft aneurysm: CT evaluation and coil occlusion therapy. AJR Am J Roentgenol 141,1060-1062[Free Full Text]
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Dimitri, W, Reid, A, Dunn, F (1992) Leaking false aneurysm of right coronary saphenous vein graft: successful treatment by percutaneous coil embolization. Br Heart J 68,619-620
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Kalimi, R, Palazzo, RS, Graver, LM (1999) Giant aneurysm of saphenous vein graft to coronary artery compressing the right atrium. Ann Thorac Surg 68,1433-1437[Abstract/Free Full Text]
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Trop, I, Samson, L, Cordeau, M-P, et al (1999) Anterior mediastinal mass in a patient with prior saphenous vein coronary artery bypass grafting. Chest 115,572-576[Free Full Text]
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Katsumata, T, Endo, M, Ihashi, K, et al (1995) Post-stenting enlarging false aneurysm of a saphenous vein graft. Ann Thorac Surg 60,1121-1123[Abstract/Free Full Text]
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Introduction
Case Presentation
