A 35-year-old male, presented with a 3-month history of skin petechiae and acute chest pain lasting 17 h. The patient had a history of psoriasis, fatty liver disease, and elevated transaminase levels. Laboratory tests revealed hyperuricemia (uric acid 548 μmol/L), mild dyslipidemia (triglycerides 1.75 mmol/L, LDL-C 2.13 mmol/L), and moderate hepatic steatosis on abdominal ultrasound, consistent with metabolic syndrome (2). He denied any history of connective tissue diseases, had a 15-year smoking history (10 cigarettes/day), and a family history of diabetes. Throughout the course of his psoriasis, he had not received systemic treatment, relying only on intermittent use of traditional Chinese medicine for symptomatic management.

Three months prior to admission, the patient had developed unprovoked petechiae on his limbs. Sixteen days before presentation, he visited an outpatient clinic due to oral blood blisters. Initial laboratory tests showed significant thrombocytopenia (2 × 10⁹/L), positive antinuclear antibodies (1:80), lupus anticoagulant (dRVVT-R: 1.34, normal 0.8–1.2), and anticardiolipin antibodies(31.5 U/mL, normal 0–10 U/mL). Following treatment with dexamethasone, intravenous immunoglobulin (IVIG), and intermittent platelet transfusions, his platelet count improved to 56 × 10⁹/L. Herombopag and prednisone were subsequently added to the treatment regimen. Seventeen hours prior to admission, he experienced persistent left-sided chest pain and tightness. Emergency evaluation revealed elevated high-sensitivity cardiac troponin I (hs-cTnI 1,011 pg/mL, normal <17.8 pg/mL), and ST-segment elevation in leads III and aVF on electrocardiogram. An initial diagnosis of acute inferior STEMI was made, and the patient was admitted to the cardiac care unit after receiving aspirin and clopidogrel as antiplatelet therapy. Atorvastatin 10 mg once daily at bedtime was initiated during hospitalization.

On admission, the patient's temperature was 36.5 °C, pulse rate was 84 beats/min, respiratory rate was 17 breaths/min, and blood pressure was 117/87 mmHg. He was 1.75 m tall and weighed 75 kg, yielding a body mass index (BMI) of 24.65 kg/m² (3). There were no rashes on his face, but scattered areas of depigmentation were noted on the right ear, neck, back, and limbs. Petechiae or ecchymoses were not observed. Cardiac, pulmonary, and abdominal examinations were unremarkable, and no joint swelling or tenderness was observed.

On admission, the platelet count was normal (182 × 10⁹/L), transaminase levels were elevated (ALT 96 U/L, normal 9–50 U/L;AST 41 U/L, normal 15–40 U/L), and uric acid levels were high (548 μmol/L, normal 208–428 μmol/L). Autoimmune profiling confirmed antiphospholipid syndrome, with persistent positivity for antinuclear antibodies, lupus anticoagulant, and IgG anticardiolipin antibodies (Supplementary Table S1). Hematologic assessment revealed no evidence of malignancy, showing grade III bone marrow hyperplasia, adequate nucleated cells, impaired megakaryocyte maturation, and reduced platelet production; immunophenotyping, cytogenetics, and molecular studies were unremarkable. Infection-related tests were positive for SARS-CoV-2 RNA, while other respiratory viruses, enteroviruses, blood cultures, and atypical pathogens were negative. Urinalysis revealed proteinuria (24-h urine protein: 140 mg). Acute inferior STEMI was confirmed by elevated troponin levels (hs-cTnI peak 11,673.4 pg/mL) (Figure 1) and ECG findings (pathological Q waves in leads III and aVF) (Figure 2A). Cardiac MRI with contrast enhancement showed delayed enhancement in the mid-to-distal inferoseptal and mid-inferior segments of the left ventricle (Figure 3). Coronary angiography showed no significant stenosis in the major epicardial vessels, and quantitative flow ratio (QFR) values were normal (LAD: 0.95; LCX: 0.97; RCA: 0.98), but angiographic microvascular resistance (AMR) was elevated in all three major vessels (LAD: 291; LCX: 319; RCA: 276; cutoff ≥266 mmHg s/m), indicating coronary microvascular dysfunction (4) (Figure 4).

Coronary angiography did not show significant epicardial vessel stenosis or thrombus formation; however, coronary microcirculatory dysfunction was evident (Figure 4). Based on ECG and cardiac injury marker dynamics as well as delayed enhancement features on cardiac MRI, the patient was diagnosed with acute inferior STEMI. Further laboratory tests ruled out connective tissue diseases, infectious diseases, and hematological malignancies. Antiphospholipid antibodies, including lupus anticoagulant and IgG anticardiolipin antibodies, were confirmed positive on two separate occasions more than 12 weeks apart (with aCL levels of 31.5 U/mL, 63.7 U/mL, and 54.9 U/mL in sequential tests), fulfilling the 2006 Sydney criteria for definite antiphospholipid syndrome (APS) (5, 6). Anti-β₂-glycoprotein I antibodies were negative. These findings led to a final diagnosis of PAPS.

Initial therapy included clopidogrel, low-molecular-weight heparin(LMWH), and hydroxychloroquine as antithrombotic and immunomodulatory therapies. The patient's condition improved, but his platelet count continued to decline (lowest 8 × 10⁹/L during hospitalization). Antithrombotic drugs were discontinued to prevent bleeding events and glucocorticoids and herombopag were resumed. However, the patient experienced recurrent chest pain and dynamic changes in cardiac injury markers and ECG findings (Figure 2B), suggesting another MI (the patient refused repeat coronary angiography). After multidisciplinary consultation involving cardiology, rheumatology, hematology, and pharmacy, the diagnosis of PAPS complicated by AMI was confirmed. Given an adjusted Global Antiphospholipid Syndrome Score (aGAPSS) of 11, indicating high thrombotic risk, a comprehensive risk-benefit analysis was performed (7).

Notably, herombopag, a thrombopoietin receptor agonist, has been associated with increased platelet activation and prothrombotic risk in autoimmune thrombocytopenia, particularly in patients with underlying antiphospholipid antibodies (8). Its potential contribution to recurrent thrombosis in this context warrants clinical caution. The treatment plan included methylprednisolone (40 mg daily) followed by prednisone (40 mg daily), rituximab (initial dose 200 mg, then 500 mg × 3 doses), enoxaparin followed by warfarin (4.5 mg daily), and clopidogrel (75 mg daily), along with hepatoprotective and infection prophylaxis. The patient's chest pain resolved and platelet count stabilized prior to discharge (Figure 1).

After discharge, the patient was regularly followed up by the cardiology and rheumatology departments. The patient did not experience recurrent chest pain, chest tightness, or bleeding from the skin, mucous membranes, or internal organs. Four months after discharge, his immune indicators improved, and he received a fourth dose of rituximab (500 mg). Prednisone and hydroxychloroquine were continued to treat the underlying diseases. Six months post-discharge, his immune indicators remained stable. One year after discharge, cardiac injury markers and antiphospholipid antibodies were negative, and echocardiography showed no significant blood flow abnormalities. He received another rituximab infusion (500 mg) and continued prednisone (5 mg/7.5 mg every other day) and hydroxychloroquine (200 mg twice daily). Antithrombotic therapy with clopidogrel (75 mg daily) and warfarin (4.5 mg daily) was maintained along with treatments for osteoporosis prevention and lipid stabilization (Figure 1).