Balancing Bleeding and Ischemic Risk: Dual Antiplatelet Therapy in a 90-Year-Old Man With Myocardial Infarction and Gastrointestinal Bleeding

Introduction

Managing acute myocardial infarction (MI) in the setting of active gastrointestinal (GI) bleeding poses a clinical challenge. Type 1 MI (T1MI) typically results from plaque rupture or erosion, whereas type 2 MI (T2MI) arises from an imbalance in myocardial oxygen supply and demand, often secondary to conditions such as anemia [1,2]. This distinction is critical because T1MI generally warrants aggressive antiplatelet therapy to prevent recurrent atherothrombotic events; T2MI management should focus on correction of the underlying supply–demand mismatch. In patients with concurrent coronary artery disease (CAD), it is difficult to distinguish between the 2 subtypes. Older patients with multimorbidity are particularly vulnerable to both ischemic and bleeding complications; thus, the coexistence of CAD, MI, and active GI bleeding warrants careful balance of competing risks and individualization of acute coronary syndrome (ACS) management. This report describes a 90-year-old patient with acute chest pain, severe anemia, and recurrent GI bleeding who required a highly individualized approach to antiplatelet therapy.

Case Report

A 90-year-old man presented to the emergency department from an independent living care center after 3 days of chest pain, dyspnea, indigestion, and black stools. His medical history included multiple hospitalizations over the preceding 4 years for lower GI bleeding secondary to colonic angiodysplasias, chronic iron deficiency anemia, hyperlipidemia, heart failure with preserved ejection fraction (54%), hypertension, obesity, and chronic kidney disease stage 3a. He also had a history of smoking (30 pack-years). He had no previous coronary balloon angioplasty or stenting.

On examination, the patient exhibited mild tachypnea, obesity (body mass index 38 kg/m2), and 2+ pitting edema in the bilateral lower extremities. He was hemodynamically stable; physical examination revealed slight wheezing and crackles in the lower lung fields. Laboratory tests showed hemoglobin 6.2 g/dL; high-sensitivity cardiac troponin T was 78 ng/L on arrival, 111 ng/L at 2 h, and 170 ng/L at 6 h (normal <15 ng/L). His 12-lead electrocardiogram demonstrated dynamic ST-segment depression in leads I and II, as well as the lateral precordial leads (Figure 1).

The patient was admitted with non-ST-segment elevation MI (NSTEMI), severe acute-on-chronic anemia (hemoglobin 7.8–9.8 g/dL 1 year prior), and acute-on-chronic heart failure. The presumed etiology of his myocardial injury was either T2MI (myocardial oxygen supply-demand mismatch) or T1MI (atherothrombotic plaque rupture). His chest pain substantially improved after transfusion with 2 units of packed red blood cells to a hemoglobin level of 8.2 g/dL. This response supported a diagnosis of T2MI; thus, initial management prioritized evaluation of his severe anemia. He was treated with aspirin, high-dose atorvastatin, metoprolol succinate, and gentle diuresis.

On hospital day 3, colonoscopy identified extensive angiodysplasias. Two actively bleeding lesions received treatment with argon beam coagulation and clipping. At this time, the patient’s troponin level increased to 353 ng/L, and his hemoglobin level was 8.6 g/dL. Transthoracic echocardiography demonstrated regional wall motion abnormalities corresponding to the left anterior descending artery (LAD) territory and an ejection fraction of 54%. He began a trial of dual antiplatelet therapy (DAPT) with clopidogrel and aspirin; no recurrent GI bleeding was evident after 2 days.

On hospital day 5, the patient underwent cardiac catheterization, which revealed severe CAD, including 70% obstruction in both the distal circumflex and mid-LAD, as well as 80% obstruction in the first diagonal artery. The LAD lesion was discrete with a focal aneurysmal region, corresponded to his regional wall abnormalities, and was suitable for stenting. Because stenting would require prolonged DAPT, a 2-week trial of DAPT was planned to monitor potential bleeding. He was discharged in stable condition after 6 days with a hemoglobin level of 10.1 g/dL and scheduled for outpatient percutaneous intervention (PCI).

Two weeks after discharge, the patient’s hemoglobin level dropped to 6.6 g/dL without overt signs of GI bleeding, suggesting that DAPT was contributing to indolent GI blood loss. After extensive shared decision making with the patient and his family, he expressed a goal to minimize hospital stays. He received 2 units of packed red blood cells as an outpatient, and PCI was canceled. Clopidogrel was discontinued while he continued aspirin monotherapy. His hemoglobin level increased to 9.1 g/dL after transfusion; 2 days later, it dropped to 8.4 g/dL. After further discussion with the patient and renewed emphasis on his goal to avoid hospitalization at age 90, aspirin was also discontinued.

After cessation of antiplatelet therapy, the patient’s hemoglobin level stabilized at 9.9 g/dL at the 2.5-month follow-up (ie, 2.5 months after discharge), and his symptoms responded to up-titration of antianginal medications. At the 3-month follow-up, he was hospitalized for active GI bleeding that required 3 units of packed red blood cells and hemostatic clipping of 5 actively bleeding angiodysplasias (Figure 2).

Discussion

This case highlights the challenges of managing acute MI in a patient with active GI bleeding. Although our patient most likely had T2MI, T1MI remained a consideration, and his coronary anatomy was unknown at the time of presentation. Coronary angiography can help determine the mechanism of MI; however, distinguishing T2MI from T1MI may be difficult and often requires integration of clinical and imaging findings, especially in patients with severe CAD [2]. Patients with T2MI are more often women and generally present with lower peak troponins, advanced age, and more comorbidities; they are less likely to demonstrate ischemic electrocardiogram changes or regional wall motion abnormalities [2]. Initial management of T2MI should address the underlying etiology – in this instance, anemia.

CAD is common in T2MI and can complicate treatment strategies. Approximately two-thirds of patients with T2MI also exhibit CAD; severe disease can limit myocardial blood flow reserve during stress or anemia, potentiating ischemic injury [3]. The benefit of revascularization in this population, however, remains unclear [4]. These patients are often older with multiple comorbidities, and their heterogeneous presentations limit the generation of robust clinical trial data. Importantly, DAPT is critical after PCI for at least 1 to 3 months to prevent stent thrombosis, a commitment that can carry substantial bleeding risk in frail older adults. For such patients, revascularization decisions must be highly individualized, balancing ischemic and bleeding risks while incorporating patient goals and preferences through shared decision making.

Even in the absence of revascularization, guideline-directed ACS management typically recommends 1 year of DAPT with aspirin plus a P2Y12 inhibitor (eg, clopidogrel, prasugrel, or ticagrelor) [5]. However, major bleeding on DAPT is associated with a 5-fold increase in mortality and a higher risk of recurrent ischemic events [6]. In practice, this means that strict adherence to ACS protocols may require adjustments in older patients with high bleeding risk. Alternative bleeding-risk reduction strategies, including proton pump inhibitors and endoscopic interventions as utilized in this case, may help but often fail to fully mitigate risk. Our patient had high bleeding risk according to standardized criteria; he experienced recurrent anemia on DAPT that warranted de-escalation to monotherapy [7,8]. Such stepwise adjustment underscores the need for pragmatic therapy adaptation in complex geriatric patients.

Although our patient’s treatment was de-escalated to aspirin monotherapy, clopidogrel monotherapy may have been a safer alternative. Historically, aspirin has been preferred over clopidogrel as monotherapy, primarily due to its greater availability and lower cost before clopidogrel became generic. The HOST-EXAM trial compared aspirin and clopidogrel monotherapy after drug-eluting stent placement; it demonstrated that clopidogrel was associated with lower incidences of all-cause death, MI, stroke, major bleeding, and readmission for ACS [9]. The PANTHER meta-analysis of patients with CAD showed similar findings, with a nonsignificant trend toward less major GI bleeding on P2Y12 inhibitor monotherapy [10]. Taken together, these data suggest that clopidogrel is a preferable option to aspirin monotherapy for patients with both atherothrombotic and GI bleeding risk. Nevertheless, aspirin remains commonly prescribed, as in the present case, highlighting a gap between current evidence and clinical practice [11]. Other P2Y12 inhibitors, such as ticagrelor or prasugrel, were avoided because they may increase bleeding risk in older patients with ACS [12].

The complexity of this case also underscores the importance of multidisciplinary care in older adults. Quality of life, life expectancy, and patient preferences should guide decision making when therapeutic trade-offs are unavoidable. Optimal management in this case required collaboration among cardiology, gastroenterology, and outpatient geriatrics to ensure that decisions aligned with both medical complexity and patient-centered goals.

Conclusions

Management of antiplatelet therapy in older patients with bleeding should be personalized, and flexibility should be exercised when applying standardized protocols. In the present case, control of severe GI bleeding and anemia was crucial to preventing further myocardial injury, given that DAPT paradoxically worsened both ischemic and bleeding risk. Should antiplatelet therapy be reconsidered for this patient in the future, clopidogrel monotherapy would be the most appropriate option. Our case emphasizes that the risks and benefits of DAPT for secondary prevention should be continually assessed in patients with high bleeding risk; T2MI management should prioritize correction of the underlying supply-demand mismatch. Furthermore, it reflects the growing challenge of caring for the expanding population of multimorbid older patients, highlights the importance of balancing competing risks and aligning therapy with patient goals, and underscores the need for further research and greater inclusion of geriatric patients in ongoing and future studies.