Most recently accepted definition established by the
Academic Research Consortium classifies ST as: early
(occurring within 30 days), late (30 days to one year)
or very late (after one year)
1. A 30-day incidence of
ST of 0.9 % and most events occur within one week.
The incidence of ST is associated with a high
frequency of major adverse clinical consequences.
There may be multiple causes for early stent
thrombosis
2. Stent underexpansion, incomplete
apposition, dissection, thrombus, tissue protrusion
persistent slow flow, acute coronary syndrome, vessel
size/lesion length and left ventricular function are some
of the suggested causes in medical literature. The
Armed Forces Institute of Pathology has reported an
autopsy study declaring bifurcation lesion, radiation
therapy, treatment of diffuse instent re-stenosis with
another stent, disruption of vulnerable plaque near stent
and stent strut penetration of necrotic core as the risk
factors for thrombosis
3.
Although drug eluting stent thrombosis is more
often seen due to early discontinuation of clopidogrel
treatment especially in diabetic patients, late bare metal
stent thrombosis is almost exclusively associated with
intracoronary radiation therapy. Although some case
reports are available describing VLST without any
established causes 4, there is no randomised trial
declaring true incidence of VLST of bare metal stent in
literature. In a case report by Bertrand et al. 5, instent
re-stenosis after 5 years of initial stent implantation has
been linked to VLST. In their case report, Trabattoni
and Bartorelli proposed instent re-stenosis as the main
mechanism leading to abrupt thrombotic vessel closure
and acute myocardial infarction 6. Danenberg et al.
7 found that acute myocardial infarction could be the
late presentation of intracoronary stent implantation
and proposed strenuous exercise as a possible cause.
Celik et al. 8. suggested an association between ST
and exercise-induced hypercoagulable state.
In our case, we did not observe much thrombus
burden, distal embolization or no-reflow after balloon
angioplasty. This finding suggested us that in-stent
critical stenosis would have been the main mechanism.
Our patient presented with acute myocardial infarction.
In their article, Chen and et al. 9 discovered that more
than one third of bare metal instent re-stenosis episodes
present with myocardial infarction or unstable angina
requiring hospitalization. In their retrospective
analysis, Nayak et al. 10 concluded that myocardial
infarction could be the presentation of instent restenosis.
Although exercise was not an issue
hypercoagulable state was proved by
hyperhomocysteinemia in our patient. A large number
of studies supported the presence of an association
between elevated homocysteine levels and various
atherothrombotic disease including stoke, venous
thromboembolism and ischemic cardiac disease 11. Histopathologic hallmarks of
atherothrombosis related to elevated homocysteine
levels include intimal thickening, elastic lamina
disruption, smooth muscle hypertrophy, platelet
accumulation, and the formation of platelet-enriched
occlusive thrombi 12. Several studies have
demonstrated the involvement of homocysteine in the
process of in-stent restenosis 13. Our patient did not
have any illnesses affecting homocysteine metabolism
as gastritis, anemia, chronic kidney disease
hypothyroidism, alcoholism, psoriasis, current
smoking, known cancer or medication but only had
deficiency of vitamin B12 as the possible causes of
hyperhomocysteinemia. Several randomized clinical
trials are underway to address the effect of folate, vitamin
B6, and vitamin B12 supplementation on
cardiovascular disease. Until complete results of these
studies become available, screening for
hyperhomocystinemia in patients undergoing coronary
stenting is only recommended in the case of premature
atherosclerotic disease (patients <45 years of age)
when there is a paucity of more conventional risk
factors, and in patients with a history of unexplained
venous thrombosis.
Stent underexpansion, distal poor run-off, or stent
fracture may effect the long-term patency of stents.
Initial use of IVUS during stent deployment showed
that 80% of stents were underexpanded and led to the
hypothesis that ST might be decreased as a result of
optimal stent placement under IVUS guidance. We did
not perform IVUS or angioscopic study before
coronary angioplasty in this case, so we do not know
the exact mechanism of ST. When considering minimal
thrombus burden, absence of distal embolization and
absence of no-reflow, high degree instent re-stenotic
lesion seems logical as the main mechanism. When we
studied on previous angioplasty records, we found that
3-mm stent diameter was appropriate for the patient
and the stent expanded well without any residual
stenosis. Last angioplasty records also showed that
there was not any new atherosclerotic lesion in the
vessel stented and this finding makes the distal poor
run-off unlikely for cause of stent thrombosis. Also, we
do not think that 14-mm long stent may fracture easily
in the mid-portion of the circumflex artery.
In conclusion, high turbulent flow and shear stress
associated with possible instent re-stenotic lesion and
augmented procoagulant state associated with
hyperhomocysteinemia may be the causes of very late
bare metal stent thrombosis in our patient.
Optimization of stent deployment, anti-coagulation
therapy, and screening for hyperhomocystinemia in
young patients undergoing coronary stenting can help
in preventing late ST.
)
)
)
)
)