Bleeding poses a significant challenge in the management of cardiovascular disease, often necessitating the interruption or cessation of antithrombotic therapies and potentially triggering a prothrombotic systemic response [3]. In cases such as ours, where there is a progressive decline in hemoglobin levels following AMI, gastrointestinal bleeding should be considered as a primary concern. However, despite the presence of intermittent nasal bleeding without gastrointestinal symptoms, no active bleeding focus was identified during improved gastroscope and capsule endoscope examinations. Consequently, the decrease in hemoglobin attributed to nasal bleeding was disregarded, considering the patient's longstanding history of nasal bleeding and lack of attention to it, leading to severe anemia. Consistent with our case, the diagnosis of HHT was generally confirmed by genetic testing with epistaxis being the hallmark symptom [4]. Although hemorrhagic anemia secondary to epistaxis following acute myocardial infarction is rare, clinicians should remain vigilant regarding the possibility of HHT in such cases. To the recurrent bleeding. The expert panel recom-mends that clinicians consider the use of systemic anti-angiogenic agents for the management of epistaxis that has failed to respond to moisturizing topical therapies, ablative therapies, and/or tranexamic acid [5]. In this case, Although thalidomide has predominantly been associated with venous thrombotic events, arterial thrombotic events have also been reported, necessitating caution when prescribing this agent in HHT patients especially with Acute myocardial infarction.

Notably, antiplatelet treatment (AT) is generally well-tolerated in HHT patients, with a low rate of severe complications reported in the literature [6, 7]. However, our case demonstrated worsening epistaxis associated with dual antiplatelet therapy. While previous reports have highlighted cases of HHT patients presenting with myocardial infarction secondary to pulmonary arteriovenous malformations [8], our patient exhibited normal findings on pulmonary CTA examination, suggesting an alternative etiology for the myocardial infarction.

Hypercoagulable disorders contributing to coronary thrombosis encompass various conditions, including thrombotic thrombocytopenic purpura (TTP), antiphospholipid syndrome, heparin-induced thrombocytopenia (HIT), and myeloproliferative neoplasms. In our patient, relevant investigations revealed negative results for anti-nuclear antibody spectrum, anti-cardiolipin antibody, lupus anticoagulation factor monitoring, and anti-β2 glycoprotein antibody, with normal protein C and protein S activity [9]. Notably, the patient's risk factors, including hypertension and obesity, predispose him to coronary artery disease.

Given the lack of data on the management of ST-elevation myocardial infarction (STEMI) in HHT patients, treatment decisions should be individualized based on the patient's clinical presentation and underlying comorbidities [10]. Dospinescu et al. discuss the lack of data available in the treatment of STEMI in a patient with HHT. They state that the tPA contraindication in a patient with HHT led to the initiation of a heparin drip [11]. They demonstrates the importance of being aware of MI in HHT patients, especially in a younger patient population. They decided to place a bare-metal stent due to the decreased length of antiplatelet therapy that would be required. In addition, further studies are required to assess the efficacy of bare-metal stents as compared to drug-eluting stents in the HHT patient population who seem to carry both thrombotic and bleeding risks. Our case underscored the challenge of diagnosing HHT during emergency coronary angiography, necessitating the selection of drug-eluting stents over bare-metal stents. Further research is warranted to evaluate the comparative efficacy of these stents in HHT patients with concurrent thrombotic and bleeding risks. Our case underscored the challenge of diagnosing HHT during emergency coronary angiography, necessitating the selection of drug-eluting stents over bare-metal stents. Further research is warranted to evaluate the comparative efficacy of these stents in HHT patients with concurrent thrombotic and bleeding risks.

When considering AT in HHT patients, clinicians must carefully weigh the risks and benefits, while closely monitoring for bleeding complications and anemia. Additionally, systemic antiangiogenic agents may be considered for managing refractory epistaxis; however, patient and family preferences should be taken into account when discussing treatment options.