Acute myocardial infarction in a young patient with diabetes and ulcerative colitis

This case report describes a young man in his early thirties with insulin-dependent diabetes mellitus and ulcerative colitis, who developed acute myocardial infarction (AMI) during an acute flare-up of ulcerative colitis. The case highlights the diagnostic and therapeutic challenges involved in managing AMI in patients with systemic inflammatory diseases and metabolic conditions. The patient was successfully treated with a combination of thrombectomy and a drug-eluting balloon procedure for coronary occlusion, along with pharmacotherapy consisting of intravenous steroids, intravenous glycoprotein IIb/IIIa inhibitor and the involvement of a multi-disciplinary team of cardiologists and gastroenterology specialists. This case underscores the need for an integrated care approach, aggressive cardiovascular risk management, and interdisciplinary collaboration to optimise outcomes in complex clinical scenarios where systemic inflammation intersects with cardiovascular events.

Introduction

Acute myocardial infarction (AMI) in young patients with systemic inflammatory diseases, such as ulcerative colitis and diabetes mellitus, presents a unique clinical challenge that deviates from traditional cardiovascular risk models. This case aims to highlight the complexities of managing AMI in the presence of systemic inflammation and metabolic disorders, emphasising the need for comprehensive care strategies and a multi-specialty approach for effective management in such cases. The report is relevant to current practice, as it stresses the importance of integrated and interdisciplinary care in managing cardiovascular risk in patients with inflammatory and metabolic conditions.

Case

A young man in his early thirties, with a significant medical history of insulin-dependent diabetes mellitus (diagnosed 23 years prior) and ulcerative colitis (diagnosed one year prior), was admitted due to an acute flare-up of ulcerative colitis, characterised by frequent bloody stools and abdominal pain. Despite the initiation of intravenous steroids by the gastroenterology team, he developed symptoms indicative of AMI five days later, confirmed by ST-elevation in the anterior electrocardiogram (ECG) leads (figure 1), and a significant rise in troponin levels, peaking at over 25,000 ng/L. Cardiac echocardiography revealed akinesia of apex, apical inferoseptal and mid-to-apical anteroseptal walls with mildly impaired left ventricular systolic function (figures 2 and 3). Noteworthy was the absence of obstructive atherosclerotic coronary disease in major epicardial vessels, apart from atherothrombotic occlusion in the left anterior descending (figure 4) and diagonal arteries (figure 5), which was addressed with thrombectomy via export catheter, a drug-eluting balloon and intravenous glycoprotein IIb/IIIa inhibitor.

Discussion

Inflammatory bowel disease (IBD) is a chronic inflammatory process of the gastrointestinal tract with extra-intestinal manifestations affecting liver, joints, eyes, and skin. Ulcerative colitis and Crohn’s disease are the main forms of the disease. Patients are usually diagnosed between ages 15 and 35 years, and present with abdominal pain/cramping, diarrhoea, rectal bleeding and weight loss.¹ IBD is associated with an increased risk of atherosclerotic cardiovascular diseases, cerebrovascular accidents, premature coronary artery disease, and atrial fibrillation. Theories for the mechanism underlying the association between IBD and atherosclerotic cardiovascular diseases include shared risk factors (obesity, diabetes, smoking, diet), gut microbiome dysfunction, or adverse effects from IBD itself or its treatment (chronic inflammation, dyslipidaemia, thrombocytosis, steroids).²

It has been well established that having diabetes increases an individual’s risk of cardiovascular complications. Patients with type 1 diabetes have an almost three-fold increased risk of mortality when compared with the general population,³ and cardiovascular disease is the main cause of this increased mortality.⁴ The anabolic effects of therapeutic insulin lead to weight gain, along with hypoglycaemia, which may further increase cardiovascular risk.⁵ Similarly, although steroids have an anti-inflammatory effect, several studies have demonstrated that during inflammatory states they may also inhibit fibrinolytic activity.⁶ Steroid use also causes glucose fluctuations and hyperglycaemia, which are triggers for inflammation and endothelial dysfunction, and subsequent atherogenesis.⁷

Venous thromboembolism is well documented in IBD, and studies suggest that it occurs due to several factors, including coagulation cascade, natural coagulation inhibitors, fibrinolytic system, endothelial dysfunction, immune system, and platelets.⁸ On the other hand, cases of arterial thromboses are not as common,⁹ but they do also occur in coronaries,¹⁰ left ventricle,¹¹ aorta, splanchnic and iliac arteries, or in the limb arteries¹² and cerebral circulation.¹³

The inflammatory process in IBD inhibits fibrinolysis, expresses procoagulants, suppresses anticoagulants, and promotes endothelial dysfunction, with a resultant altered gut microbiome and increased intestinal permeability. The increased permeability leads to a systemic inflammatory process and increased risk of arterial and venous thrombosis.¹⁴ The management of systemic thrombotic complications indeed presents a clinical challenge, particularly in the context of concurrent high bleeding risk, and the fact that both bleeding and thrombotic risks are highest during the active phases of the disease.¹⁵

Meta-analysis by D’Ascenzo et al. concluded that persons with IBD have approximately a 30% increased risk of myocardial infarction compared with the general population, despite a lower prevalence of the classic risk factors, such as hypertension, diabetes and dyslipidaemia.¹⁶

This case emphasises the importance of heightened cardiovascular risk awareness and an aggressive, multi-disciplinary approach to management. Balancing the significant bleeding risk, while addressing thrombotic complications, is crucial in patients with systemic inflammatory diseases. The successful interventions in this case suggest that early and targeted treatment can lead to favourable outcomes in patients with concurrent systemic inflammation and pre-existing comorbidities/therapeutic agents that increase, or have the potential to increase, the risk of cardiovascular disease. It was also necessary in this case to go beyond the acute interventions and initiate strategies to mitigate the increased cardiovascular risk. These strategies included initiation of statins and monoclonal antibody medication for their anti-inflammatory effects, antiplatelets for secondary prevention of cardiovascular disease, as well as ensuring adequate glycaemic control.

Limitations

One limitation of this case report is the single patient focus, which limits generalisability. Further studies involving larger patient populations are necessary to validate the findings and optimise management strategies for similar clinical scenarios.

Conflicts of interest

None declared.

Funding

None.

Patient consent

Informed consent was obtained from the patient for the publication of this case report and any accompanying images.

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