DISCUSSION
Ulcerative colitis is often associated with extra-intestinal
manifestations affecting the liver, skin, kidneys, eyes, and joints.
Several processes chronically stimulated in IBD patients have been
involved in the pathophysiology of ASCVD. These include local and
systemic inflammation, gut microbiome irregularities, endothelial
dysfunction, thrombosis, lipid dysfunction, and the negative effects of
IBD therapies, particularly corticosteroids.
Previous literature has suggested possible causative links between IBD
and coronary artery disease. [1,2]
A Finish epidemiological study first demonstrated an association between
IBD and IHD. Similarly, a meta-analysis of multiple cohort studies also
reported an increased incidence of ACS in IBD.(3)
A recent retrospective cross-sectional study showed that the incidence
of thromboembolic events in IBD patients was increasing over the past
decade, and more arterial thrombotic events were observed compared with
venous thrombotic events.[4], suggesting an increased risk of CAD.
Our patient had a flare of IBD-UC a month back, followed by ACS. This
can be explained by a systematic review which stated that the risk of
ACS increases significantly with acute active flares and
hospitalization, in addition to prolonged periods of active disease. On
the other hand, IBD patients in remission present with a lower risk for
ACS. (5)A cross-sectional observational study on the Egyptian population
also showed that the risk of ASCVD is higher in IBD patients,
particularly during active disease, with increased carotid intimal
thickness and wall stiffness. (6) The same was depicted in a recent
Danish nationwide cohort study showing that IBD flares are associated
with an increased risk of MI, stroke, and even cardiovascular death. (7)
It was found that traditional CVD risk factors were less prevalent in
IBD patients than in the general ACS population in a population-based
cohort study(8). Our patient was in a procoagulant state with elevated
inflammatory markers. Despite the absence of traditional ASCVD risk
factors, our patient also presented in ACS, presumably from a
non-atherosclerotic thrombus as confirmed by Coronary angiography. Case
reports of Hyon He and Yong Zhang also support the same. (9,10)
Corticosteroids may also have some prothrombotic effects. It remains
controversial whether corticosteroids may add risk to coronary artery
disease in IBD patients. Among systemic corticosteroid users, the risk
for AMI increased to 5-fold compared with the controls and 2.5-fold for
Heart failure (8). Our patient had a relapse treated with
corticosteroids a month back, followed by an ACS presentation indicating
that steroids may have some prothrombotic effects. But, further studies
are needed to confirm this association.
The risk-benefit ratio must be individualized for every patient before
stent placement. Stent thrombosis is not uncommon after angioplasty, and
its risk is increased in IBD patients owing to its hypercoagulable
state. Our patient with elevated inflammatory markers had a greater risk
of stent thrombosis; hence, a conservative approach was made.
Our patient with delayed presentation of MI, triple vessel blockade, and
active inflammatory state (suggested by elevated inflammatory markers –
thrombocytopenia, elevated hs-CRP, and RA factor) was in a procoagulant
state. And if angioplasty was planned, subsequent long-term dual
antiplatelet drugs pose an increased risk of bleeding with a high risk
of stent thrombosis. Our decision to manage patients with antiplatelet
infusions and avoid stent placement benefited the patient.
So, while managing such cases, a conservative approach can be made with
a close follow-up of the patient.