The incidence of iatrogenic aortocoronary dissection
during percutaneous coronary intervention (PCI) has
been reported close to 0.1%.[1] According to the
classification scheme developed by Eshtehardi et al.,[
3]
type 1 dissection is defined as a localized dissection
in left main coronary artery (LMCA) without
involvement of the LAD and Cx; type 2 dissection
refers to a dissection flap extending well into the
LAD and Cx; and type 3 dissection is defined as the
presence of a dissection involving the aortic root. In
the same study, type 1 dissections were associated with
excellent outcomes without hemodynamic instability
or in-hospital mortality, while type 3 dissections had
an in-hospital mortality rate of 100%.
Despite not fully understood, the etiology of
iatrogenic LMCA dissection during PCI reportedly
involves LMCA atherosclerosis (i.e., a type C,
calcified stenosis), an unusual LMCA anatomy
and location, operator experience, forceful manual
injection of contrast agent, catheter selection (size
and type differences; i.e., left Amplatz catheters are associated with a greater dissection risk), failure to
align guidewire and guiding catheter co-axially with
LMCA and subintimal canal (particularly with hard
and less maneuverable guidewires), deep catheter
intubation, and manipulations during seating the
guiding catheter to coronary ostium, as well as all
mechanical injuries to arterial wall during balloon
dilatation and stenting.[1,2,4-9]
It has also been reported that LMCA stenosis,
hypertension, Marfan syndrome, congenital uni- or
bicuspid aortic valve, and cystic medial necrosis may
increase the risk.[1] Fortunately, our case had no risk
factor other than hypertension.
We suggest that in our patient a Cx dissection
occurred due to the mechanical injury of arterial wall
during stenting (Integrity, Medtronic; Medtronic,
Inc., Santa Rosa, CA, USA) or intimal tear during predilatation
procedure, which retrogradely progressed to
LMCA due possibly to forceful dye injection or medial
degeneration.
Furthermore, LMCA dissection is a rare, albeit fatal
complication of coronary interventional procedures. To
date, several strategies have been proposed for the
management of LMCA dissection. A rapid, successful management requires a full cooperation between
cardiologists and cardiovascular surgeons. Emergent
stent implantation, emergent CABG or conservative
therapy are the available treatment options for an
iatrogenic LMCA dissection.
The presence of hemodynamic instability
constitutes the major incentive for coronary
intervention. Currently, percutaneous stenting of the
entry point of coronary dissection is the primary
treatment of choice in patients with limited aortic
involvement.[10] Surgical therapy is recommended,
when a dissection involves beyond coronary ostium or
40 mm into ascending aorta.[10] In patients with a distal
‘Thrombolysis In Myocardial Infarction: TIMI' III
flow and hemodynamic stability, conservative therapy
of iatrogenic non-occluding LMCA dissection has
been shown to be associated with quite favorable longterm
outcomes.[4]
In a large observational study including
38 patients with iatrogenic LMCA dissection,[3]
17 patients were treated with CABG and 14 patients
were treated with bailout stenting. The authors
reported no in-hospital mortality and the number of
stable patients with multivessel disease was higher
in the CABG group.
In conclusion, hemodynamic status, technical
feasibility, availability of therapy, and surgical
expertise are the major factors to be considered in
the management for LMCA and coronary artery
dissections. Based on our experiences, we suggest
that emergency aortocoronary bypass surgery before
hemodynamical status becomes worse is a life-saving
procedure in patients with coronary arterial dissection.
Declaration of conflicting interests
The authors declared no conflicts of interest with
respect to the authorship and/or publication of this
article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
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