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.