Introduction
Aortocoronary dissection is an infrequent, yet potentially catastrophic complication
of coronary angiography (CAG) or percutaneous coronary intervention (PCI) that can
lead to emergency surgical aortic repair, coronary artery bypass graft surgery
(CABG) or death.
1,2
According to the extent of aortic root involvement, Dunning et
al.
3
proposed three classes
of aortocoronary dissection: Class I for focal dissection limited to the sinus of
Valsalva; Class II for dissection that propagated less than 40 mm to the ascending
aorta; and Class III for dissection extending 40 mm or more to the ascending aorta.
Management of this rare entity is still technically challenging and the optimal
treatment of aortocoronary dissection complicating CAG or PCI had not been clearly
established. In this article, we describe a case series of aortocoronary dissection
among consecutive diagnostic CAG and PCI procedures, which were successfully treated
by coronary ostial stenting.
Case 1
A 62-year-old woman with unstable angina pectoris was referred for diagnostic CAG
at a local hospital. The left coronary system appeared normal. During the
angiography of the right coronary artery (RCA), a coronary dissection
progressing retrogradely more than 40 mm (Dunning dissection class III) from the
proximal RCA into the Valsalva sinus and the ascending aorta occurred (Figure 1A and
1B). The patient suddenly complained of severe chest pain and
developed hypotension and bradycardia. She was transferred immediately to our
cath lab for the management of aortocoronary dissection. We decided to perform
ostial stenting to seal the entry site of dissection and to stop blood flow into
the false lumen. A Runthrough guidewire (Terumo, Japan) was rapidly advanced
into the distal RCA. After pre-dilation with a Maverick 2.0×20 mm balloon
(Boston Scientific, USA), a 3.0×24 mm stent (PROMUS Element, Boston
Scientific, USA) was immediately deployed at the RCA ostium to cover the
presumed entry-door of the dissection. Repeated angiography revealed no contrast
leakage into the ascending aorta false lumen (Figure 1C). A computed tomography angiography
(CTA) performed
immediately after the PCI demonstrated complete halt of the dissection without
progression. The patient had an uneventful hospital stay and repeated CTA
performed two weeks later showed complete resolution of the aortic hematoma.
Figure 1
(A) Angiogram demonstrating proximal right coronary artery
dissection, extending to sinus of Valsalva and ascending aorta. (B)
Persistent contrast staining was observed along the aortic wall of
the ascending aorta. (C) Stenting of the ostium of the right
coronary artery to coverage the entry point of the dissection and
final angiogram showed complete coverage of the aortocoronary
dissection. (D) Angiogram showing a dissection ostium of the right
coronary artery, extending retrogradely into the sinus of Valsalva
and ascending aorta. (E) Stent deployment aiming at full sealing of
the entry site of dissection and the RCA ostium. (F) Angiogram after
ostial stenting revealed the dissection limited to the sinus of
Valsalva
Case 2
A 60-year-old man with hypertension and diabetes was admitted with effort angina
for four months. CAG showed severe stenosis of the distal RCA. Transradial PCI
was performed using a 5F JR4.0 guiding catheter (Cordis, USA) and Rinato
guidewire (Terumo, Japan). The distal lesion was predilated using Maverick
2.0×15 mm balloon (Boston Scientific, USA). Immediately after removing
the balloon, the patient complained of anterior chest pain and back pain.
Angiography revealed a dissection at the RCA ostium, extending retrogradely into
the sinus of Valsalva and ascending aorta (Dunning dissection class II) (Figure 1D).
A 2.5×24 mm stent (EXCEL,
JW Medical System, China) was immediately implanted at the RCA ostium to cover
the entry point and RCA ostium, followed by post-dilatation (Figure 1E). After stenting,
angiogram
demonstrated no further extravasation of contrast medium (Figure 1F). An emergent
CTA scan showed a limited intramural
hematoma of ascending aorta. The clinical course was uneventful. At two-month
follow-up, control CTA showing total resolution of the intramural hematoma.
Case 3
A 63-year-old woman with hypertension was admitted for effort angina of 2 week
duration. CAG revealed proximal and mid-RCA diffused stenosis of approximately
90%. Transradial PCI was performed with a 6F JL 3.5 guiding catheter and a
Runthrough guidewire. After pre-dilation with a 2.0 mm balloon, a 3.0 mm
× 36 mm stent (Partner, Lepu Medical Technology, China) was successfully
implanted in the mid-RCA. To prepare for stenting of the proximal RCA, we used
the stent balloon of the mid-RCA to dilate the proximal portion at 14atm.
However, after pre-dilation of the proximal lesion, a proximal RCA dissection
occurred, which extended antegradely and also retrogradely into the Sinus of
Valsalva (Dunning dissection class I) (Figure
2A). A 3.5×29 mm stent (Partner, Lepu Medical Technology,
China) was immediately deployed at the proximal RCA, which was considered as the
entry point of the aortic dissection. The final angiogram showed the aortic
dissection was limited in the sinus of Valsalva (Figure 2B). A follow-up angiography
was performed one week later and
it revealed no residual contrast staining of the aortic wall (Figure 2C). The patient
remained asymptomatic
for one month without any clinical event.
Figure 2
(A) After pre-dilation, a dissection of the proximal right coronary
artery extending retrogradely into the sinus of Valsalva occurred.
(B) Repeated angiogram after stenting demonstrating the aortic
dissection was successfully sealed and limited in the sinus of
Valsalva. (C) Follow-up angiogram showing complete resolution of the
dissection. (D) After contrast injection, a dissection of the
proximal right coronary artery with propagation into the aortic
sinus and ascending aorta developed. (E) After right coronary artery
ostium stenting, angiogram showed no further contrast leakage from
the ostium entry point of the right coronary point to the false
lumen of the ascending aorta. (F) Persistent contrast dye present in
the wall of ascending aorta.
Case 4
A 52-year-old woman with hypertension and hyperlipidemia presented with chest
discomfort for one week. CAG demonstrated critical stenosis in the proximal and
mid-portion of the RCA. During PCI, the RCA ostium was engaged with a 6F
Amplatzer left1 (Cordis, USA) guiding catheter. Before attempting to advance the
guidewire, contrast medium was injected. Immediately after the injection, a
large proximal RCA dissection occurred, which quickly extended in a retrograde
fashion into the ascending aorta (Figure
2D). Despite obliteration of the RCA dissection with a PROMUS Element
3.0×38 mm stent, persistent dye staining of the ascending aorta was
present on final angiogram (Dunning dissection class III) (Figures 2E and 2F). A
computed tomography scan performed 12 hours later showed an intramural hematoma
ascending aorta without an intimal flap. The patient recovered well after
stenting and was discharged 7 days later. At the one-month follow-up, the
patient was asymptomatic and the CTA showing complete healing of the
dissection.
Discussion
Iatrogenic aortocoronary dissection complicating coronary interventions is extremely
rare and a few cases have been reported. The incidence of this complication was
approximately 0.02% for diagnostic coronary angiography and 0.02-0.83% for PCI
procedures.
2-5
The rapid propagation of aortocoronary dissection may become
immediately life threatening via several mechanisms, including hemorrhage into the
pericardium resulting in cardiac tamponade, occlusion of the contralateral coronary
ostium, or propagation of the dissection into the descending aorta.
6,7
Most reported iatrogenic
aortocoronary dissections have been related to procedures in the RCA, especially
during PCI for chronic total occlusions.
2
The RCA is more easily dissected retrogradely into the coronary
sinus than the left main coronary artery (LMCA). This may be because the periostial
wall and sinotubular junction of the LMCA are formed by more smooth muscle cells and
by a dense matrix of collagen type I fibers
8
.
Its mechanism involves disruption of the coronary intimal by mechanical trauma,
followed by vigorous contrast injection, which, in turn, contributes to subsequent
retrograde extension of the dissection. The entry port is usually created by direct
trauma from the catheter tip, forceful balloon inflation, the dilation of a
calcified plaque, from aggressive manipulation of rigid or hydrophilic guide wires,
or vigorous contrast injection with a wedged catheter.
1,9,10
In the present cases, the cause of dissection in case 1 and
case 4 was thought to be noncoaxial engagement of the catheter followed by
continuous vigorous contrast injection. In case 2, the trigger for the dissection
was thought to be direct trauma caused by the tip of the guiding catheter, whereas
in case 3, the dissection may have been caused by dilation of the balloon in the
proximal RCA, with its propagation into the ostium and the coronary sinus of
Valsalva.
To date, the optimal treatment of this rare entity has not been well established.
Several methods including emergent surgery, coronary artery stenting, or
conservative medical treatment have been proposed to manage aortocoronary
dissection.
11-13
Given that over 40% of the cases will spread rapidly to the
ascending aorta if the entry-door is not sealed rapidly, a “wait and see” approach
may be too risky for uncontrollable dissection and major complications.
9
Therefore, once aortocoronary
dissection occurred, every effort should be undertaken to prevent rapid progression
of the dissection. Dunning et al.
3
proposed that patients might be successfully managed by stenting of the entry point
of the coronary dissection if the dissection extends < 40 mm from the coronary
ostium and that surgical intervention might be required if the dissection extends
> 40 mm from the ostium. However, Park et al.
13
reported a case of iatrogenic coronary dissection with
extensive propagation into the entire ascending aorta complicating PCI for chronic
total occlusion of the RCA, which was successfully managed by stenting of the RCA
ostium with favorable outcome. Carstensen and Ward
9
reviewed 67 cases published in the literature and
suggested that even rapidly propagating dissections can be successfully managed
percutaneously and that attempting to halt propagation does not appear to compromise
the chances of surgical success if the initial approach fails. Additionally, the
surgical repair of catheter-related dissection may be more risky in the setting of
coronary ischemia and following PCI with full anticoagulation and antiplatelet
therapy. Boukhris et al.
2
recently
assessed the management strategy and outcomes of such a complication among 956 cases
of complicating PCI for chronic total occlusion, and found aortocoronary dissection
occurred in eight patients for an overall frequency of 0.83%. In all these cases,
rapid ostial stenting was performed and no emergency surgery was required. In
Shorrock et al
1
study, four of six
patients (67%) with aortocoronary dissection were treated with ostial stenting, one
underwent emergency CABG, and the remaining one was treated conservatively without
subsequent adverse clinical outcomes. Moreover, they performed a systematic
literature review of 107 published cases of aortocoronary dissection during PCI, and
showed that this complication were most commonly treated with stenting (49.5%) or
conservative management (21.5%) although approximately 29% required surgery. Hence,
Shorrock et al.
1
proposed that
emergency surgery for aortocoronary dissection is not needed in the vast majority
of
cases and should only be considered in cases of occlusion of the dissected vessel
with cessation of antegrade flow that cannot be restored percutaneously, and
extension of the dissection to the descending aorta.
In our case series, rapid ostial stenting was performed in all of them, and all
patients had uneventful recovery. Follow-up imaging with CTA or CAG showed complete
resolution of the dissection in all patients. So, the outcome of coronary stenting
for the management of aortocoronary dissection is relatively favorable.
It is worth noting that the best approach to management of aortocoronary dissection
is to prevent its occurrence. During catheterization, there should be a coaxial
alignment of the catheter with the coronary artery, and meticulous attention should
be paid to the pressure waveform. Once the pressure waveform is dampened, the
contrast should not be injected. Moreover, if aortocoronary dissection occurs,
stopping antegrade contrast injections is critical to avoid propagation and
enlargement of the dissection
12
.
In addition, a careful and gentle handling of wires and guiding catheter probably
would prevent some of the cases of this catastrophic complication.
Conclusion
Iatrogenic aortocoronary dissection is an infrequent but life-threatening
complication of diagnostic CAG and PCI, necessitating a prompt diagnosis and
appropriate treatment. Immediate coronary ostial stenting to seal off the entry
point of the dissection is a feasible and reasonable initial management for this
devastating complication.