Subacute Coronary Stent Thrombosis as the Initial Presentation of Acute Myeloid Leukemia: A Case Report and Literature Review

Introduction

Stent thrombosis is an uncommon but potentially catastrophic complication of percutaneous coronary intervention (PCI), often associated with myocardial infarction, cardiogenic shock, and high mortality. It is classified by timing into acute (≤24 hours), subacute (1–30 days), late (31 days to 1 year), and very late (>1 year) after stent implantation. ¹ Subacute stent thrombosis typically occurs within the first month following PCI and is most frequently related to high thrombus burden, suboptimal stent deployment, premature cessation of dual antiplatelet therapy (DAPT), or underlying hypercoagulable states. ²

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy that can be complicated by clinically significant disturbances in hemostasis. While bleeding due to thrombocytopenia and coagulopathy is common, AML can also produce a prothrombotic milieu through leukemia-related inflammation, endothelial activation, and procoagulant activity associated with circulating blasts. ³ In particular, hyperleukocytosis (commonly defined as WBC >100,000/µL) can promote leukostasis, impair microvascular perfusion, and enhance platelet–leukocyte interactions, increasing the risk of arterial events including myocardial infarction. In the setting of coronary stent implantation, this biology may amplify thrombogenicity at the stent surface, predisposing to early occlusion even when standard antiplatelet therapy is administered. ⁴

We describe the case of a young adult male who developed subacute stent thrombosis ten days after myocardial infarction, which was subsequently found to be the initial manifestation of AML with profound hyperleukocytosis. This case underscores the importance of considering an occult hematologic malignancy in patients with unexplained thrombotic events after PCI, particularly when conventional risk factors for stent thrombosis are absent or when complete blood counts are abnormal. This case report has been prepared in line with the CARE (CAse REport) guidelines.

Case Presentation

A 33-year-old male presented to the emergency department with acute-onset, pressure-like retrosternal chest pain radiating to the left arm. The pain was constant, non-positional, and non-remitting, lasting for several hours. He denied nausea, vomiting, diaphoresis, or any previous similar episodes. His past medical history was notable for well-controlled type 2 diabetes mellitus, with a most recent glycated hemoglobin (HbA1c) of 6.5%. There was no family history of premature cardiovascular disease.

On presentation, his vital signs were stable, and physical examination was unremarkable. An electrocardiogram (ECG) revealed a new right bundle branch block (RBBB) and ST-segment elevations in the anterolateral leads (Figure 1). Laboratory investigations revealed elevated cardiac biomarkers, including a troponin level of 10,000 ng/L and creatine phosphokinase (CPK) of 1,600 U/L. Additional laboratory results showed a hemoglobin level of 11 g/dL, platelet count of 121,000/µL, white blood cell (WBC) count of 22,000/µL, and low-density lipoprotein (LDL) cholesterol of 102 mg/dL (Table 1). Transthoracic echocardiography demonstrated anterior wall hypokinesia with a left ventricular ejection fraction (LVEF) of 45%, without evidence of apical thrombus or valvular abnormalities.

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Figure 1.

ECG showing new RBBB and Anterolateral ST elevation

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Table 1.

Laboratory Results of the Patient Showing Leucocytosis

Name	Result	Unit	Normal range
WBCs	22.64	10^9 μL	4.5-11
RBCs	3.74	10^12 μL	4.3-5.7
Hemoglobin	11.2	g/dl	13.2-17.3
MCV	89.8	fL	80-100
Platelets	129	10^9 μL	150-400

Due to the unavailability of the cardiac catheterization laboratory within the designated time window the patient was treated with intravenous tissue plasminogen activator (tPA), which resulted in significant pain relief. On the second day of admission, coronary angiography revealed a large thrombus in the proximal left anterior descending (LAD) artery with Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow. A dominant left circumflex (LCX) artery was also noted (Figure 2A). The patient was treated with glycoprotein IIb/IIIa inhibitors, aspirin (once daily) and Ticagrelor (90 mg twice daily), atorvastatin (40 mg daily), bisoprolol, and an angiotensin-converting enzyme (ACE) inhibitor. Within 48 hours, he became asymptomatic, and repeat angiography showed restoration of TIMI grade 3 flow in the LAD.

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Figure 2.

(A) Angiography of the left coronary system (Right Anterior Oblique view) reveals large thrombus in the proximal LAD. (B) Angiographic view revealed in stent subacute stent thrombosis

Despite initial improvement, coronary angiography performed on day four revealed a persistent large thrombus burden in the proximal LAD. A drug-eluting stent (DES) measuring 4 × 26 mm was deployed. The patient was subsequently discharged three days later on dual antiplatelet therapy (DAPT), bisoprolol, ramipril, and spironolactone.

Ten days post-discharge, the patient returned to the emergency department with chest pain similar to his initial presentation. ECG findings were consistent with previous changes. Although the patient was compliant to DAPT, Repeat coronary angiography revealed stent thrombosis in the LAD [Figure 2B]. A BMW wire was advanced into the LAD and LCX, followed by thrombectomy and balloon pre-dilation with a non-compliant balloon, achieving TIMI grade 2 flow. Additional thrombi were identified in the distal left marginal (LM) artery and proximal LCX. Intracoronary tirofiban (Aggrastat) was administered, but residual thrombi persisted in the ostial LCX.

During the procedure, the patient experienced hemodynamic collapse. Two stents were placed—one in the ostial LAD and another at the LM–LCX bifurcation—followed by “kissing” balloon inflation with satisfactory angiographic outcome. Post-procedurally, the patient developed acute pulmonary edema and hypotension, requiring endotracheal intubation, minimal-dose norepinephrine infusion, and a 24-hour tirofiban infusion alongside ongoing DAPT.

Subsequent laboratory investigations showed a marked rise in WBC count to 54,000/µL, accompanied by bicytopenia, with a hemoglobin level of 10 g/dL and platelet count of 88,000/µL. Serial blood work revealed a progressive increase in WBCs: from 21,000 at initial presentation to 54,000, peaking at 108,000 within two weeks (Table 2). A peripheral blood smear demonstrated circulating blast cells (Figure 3), then Flow Cytometry and gating were performed, the results showed that 80% of the gated blast cells were positive with: CD33, CD117, and Anti-MPO. Immunophenotypic findings are consistent with the diagnosis of Acute Leukemia of Myeloid Lineage. Cytogenetic study for t(15,17) was performed on the current peripheral blood sample and revealed a negative result, however, molecular testing for cryptic translocation was recommended.

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Table 2.

Laboratory Results of the Patient Showing Hyperleukocytosis

Name	Result	Unit	Normal range
WBCs	108	10^9 μL	4.5-11
RBCs	2.72	10^12 μL	4.3-5.7
Hemoglobin	8.2	g/dl	13.2-17.3
MCV	86.4	fL	80-100
Platelets	114	10^9 μL	150-400

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Figure 3.

Blood film showing blast cells

The patient was initiated on cytoreductive therapy with hydroxyurea (1 g three times daily), dexamethasone (8 mg three times daily), all-trans retinoic acid (ATRA), and allopurinol. The following day, he developed tumor lysis syndrome (TLS) and acute kidney injury (AKI). He was treated with rasburicase and underwent dialysis as per nephrology recommendation. The patient’s clinical condition subsequently stabilized, and he was transferred to Al-Hussein Oncology Center for continued hematologic management. A summary of the case is provided in (Figure 4).

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Figure 4.

Summary of the case from initial presentation into his referral to the oncology center

Discussion

The description of thrombotic events in AML is not new. Wiernik PH et al in their work in 1969 described seven cases of pulmonary embolism in AML patients, further they discussed how even thrombocytopenic AML patients can develop thrombotic complications, and tried to understand the underlying mechanisms of such events. Lisker SA et al in 1967 described a case of myocardial infarction in an AML patient with moderate cytopenia (690000/mm3), although the biopsy did not confirm it. Y Cohen et al described a case of acute myocardial infarction as the first presentation of an AML patient with extreme hyperleukocytosis.^5,6

Our case illustrates the rare and diagnostically challenging presentation of Acute Myeloid Leukemia manifesting initially as recurrent coronary thrombosis following percutaneous coronary intervention. The patient, a young adult with minimal traditional cardiovascular risk factors, presented with ST-segment elevation myocardial infarction and was found to have a large thrombus burden in the proximal left anterior descending artery. Notably, abnormalities in the complete blood count, including leukocytosis, anemia, and thrombocytopenia, were already present at initial presentation but were not sufficiently pronounced to immediately suggest an underlying hematologic malignancy. The persistence of extensive intracoronary thrombus despite pharmacologic reperfusion and subsequent stent implantation represented an early indicator of a systemic prothrombotic state.

The development of subacute stent thrombosis ten days after discharge, despite reported adherence to dual antiplatelet therapy and the absence of clear mechanical or procedural factors, further supports the presence of a nontraditional driver of thrombosis. The subsequent identification of thrombotic involvement in multiple coronary territories, accompanied by hemodynamic deterioration, is atypical for isolated stent-related complications and is more consistent with an underlying malignancy-associated hypercoagulable condition. ⁷ During this period, the patient’s leukocyte count rose rapidly, ultimately exceeding 100,000/μL, while anemia and thrombocytopenia progressed, prompting hematologic evaluation and the diagnosis of acute myeloid leukemia.

Hyperleukocytosis likely played a central role in the pathogenesis of recurrent coronary thrombosis in this case. Elevated leukocyte counts increase blood viscosity and promote leukostasis, impairing microvascular flow and contributing to endothelial injury. ⁸ In addition, interactions between circulating blasts, platelets, and the vascular endothelium may have enhanced local thrombin generation and platelet activation at the stent surface. ⁹ The combination of systemic inflammation, leukemia-associated procoagulant activity, and endothelial disruption from stent implantation created a highly thrombogenic environment, predisposing to rapid stent occlusion despite standard antiplatelet therapy. ¹⁰

The coexistence of Acute Myeloid Leukemia and acute coronary syndrome (ACS) presents a therapeutic dilemma. As survival rates in leukemia improve, patients are more likely to undergo percutaneous coronary intervention (PCI). Consequently, awareness of the interplay between hematologic malignancies and cardiovascular complications is vital. A 2019 study demonstrated that leukemia patients undergoing PCI had higher in-hospital mortality, bleeding, and vascular complication rates, with a 40% increase in mortality risk compared to non-leukemic patients. ¹¹ So herein our case management was complicated by the competing risks of thrombosis and bleeding. Aggressive antiplatelet and antithrombotic therapy was required to restore and maintain coronary patency, while evolving thrombocytopenia and impending cytotoxic therapy increased hemorrhagic risk. ¹² The American Society of Hematology guidelines recommend stabilization with aspirin, beta-blockers, hydration, allopurinol for tumor lysis syndrome prophylaxis, and hydroxyurea for rapid leukoreduction. ¹³ To address hyperleukocytosis cytoreductive therapy was initiated, but this was followed by tumor lysis syndrome and acute kidney injury, underscoring the dynamic and high-risk nature of managing concurrent acute coronary syndrome and newly diagnosed AML. Stabilization of metabolic and hemodynamic derangements appropriately took precedence prior to definitive leukemia-directed therapy. ¹⁴

When PCI is indicated, bare-metal stents or balloon angioplasty are generally favored over drug-eluting stents to minimize the required duration of dual antiplatelet therapy (DAPT). Antiplatelet therapy should be titrated to platelet count. Aspirin is typically safe if platelets are above 10,000/μL, and clopidogrel may be added when counts exceed 30,000/μL. Potent P2Y₁₂ inhibitors and GP IIb/IIIa antagonists are generally avoided. ¹⁵

This case highlights the importance of maintaining a high index of suspicion for hematologic malignancy in patients with early or recurrent stent thrombosis, particularly when occurring in younger individuals or in the presence of unexplained abnormalities in blood counts. Early recognition of leukemia-associated hypercoagulability may influence revascularization strategy, intensity of antithrombotic therapy, and timing of hematologic intervention. Multidisciplinary collaboration between cardiology, hematology, and critical care teams is essential to optimize outcomes in this complex clinical scenario.

Conclusion

This case illustrates an exceptionally rare presentation of Acute Myeloid Leukemia (AML) manifesting as subacute stent thrombosis in a young adult, complicated by profound hyperleukocytosis. Early recognition of atypical laboratory findings such as leukocytosis, anemia, or thrombocytopenia in patients with acute coronary syndrome or early stent thrombosis should prompt urgent hematologic evaluation. Multidisciplinary collaboration between cardiology, hematology, and critical care teams is essential to balance the competing priorities of aggressive antithrombotic therapy and the high bleeding risk associated with AML. Awareness of this rare association may improve early diagnosis, guide optimal treatment strategies, and potentially reduce morbidity and mortality in similar cases.