A 63-year-old woman was admitted to our hospital in June, 2008, with a 24-h history of central chest pain radiating to her neck. In the 7 days before admission, she had experienced intermittent chest tightness without any obvious precipitating cause. Her medical history was unremarkable. She did not smoke and was on no regular medication. There were no abnormalities on clinical examination. ECG showed inversion of T waves in leads III, V2, and V3. Serum troponin T concentration after 12 h was 1·22 μg/L (normal range [NR] 0–0·01 μg/L) indicating an inferior non-STelevation myocardial infarction. We started our patient on aspirin, clopidogrel, and dalteparin. Serum cholesterol was slightly high (5·3 mmol/L; normal up to 5 mmol/L) but no additional risk factors for coronary artery disease were evident. Blood tests showed haemoglobin 137 g/L (NR 120–160 g/L), leuco cytes 14·5×109/L (NR 4–11×109/L), neutrophils 12×109/L (NR 2·0–7·5×109/L), and platelets 614×109/L (NR 150–400×109/L), with normal eosinophil (0·08×109/L; NR 0–0·4×109/L) and basophil counts (0×109/L; NR 0–1×109/L). C-reactive protein concentration was 4 mg/L (normal up to 5 mg/L). After 24 h, leucocyte count had normalised, and the platelets decreased to 528×109/L. Coronary angiography showed normal left coronary arteries. The right coronary artery was dominant with a long layer of fresh thrombus in the proximal/mid vessel (fi gure A), clearly the cause of her symptoms. Because of the risk of distal embolisation, angioplasty was deferred and the patient was started on an infusion of the glycoprotein IIb/IIIa inhibitor, tirofi ban. Repeat angiography after 72 h of tirofi ban showed almost complete resolution of the thrombus (fi gure B) and we managed our patient conservatively thereafter, with the initiation of dual antiplatelet therapy. On closer scrutiny of the presenting blood count, despite normal haemoglobin and packed-cell volume, there was micro cytosis with reduced mean corpuscular volume (74·5 fL; NR 80–96 fL) and hypochromia (mean corpuscular haemoglobin 23 pg; NR 27–32 pg). The serum ferritin concentration (12 μg/L; NR 13–150 μg/L) confi rmed iron defi ciency. This conclusion was supported by the microscopic appearance of the blood, which showed anisopoikilocytosis with microcytic hypochromic cells, elliptocytes, and pencil cells (fi gure C). In addition, platelet anisocytosis and giant platelets were seen (fi gure D). Paradoxically, despite iron defi ciency, there was erythrocytosis (red cell count 5·96×1012/L; NR 3·8–4·8×1012/L) indicating loss of homoeostatic control of erythropoiesis. The suspicion of an iron-defi cient myelo proliferative disorder underlying the myocardial infarction was confi rmed by the presence of a heterozygous mutation (V617F) in the JAK2 gene, detected in 90–95% of patients with myeloproliferative polycythaemia. We started our patient on hydroxy carbamide, resulting in satisfactory control of the platelet count. When last seen in May, 2009, our patient was asymptomatic with no further angina. Myeloproliferative disorders are associated with thrombotic complications with predominance of arterial over venous events. The recognition of the somatic mutation JAK2V617F in most patients with myeloproliferative polycythaemia has improved the diagnostic accuracy and bone-marrow examination is not mandatory. Diagnosis of myeloproliferative polycyth ae mia is therefore straight forward in the setting of an elevated haemoglobin and packed-cell volume. Some patients may present with a normal haemoglobin and only subtle changes in red cell indices, as a result of iron-defi ciency; identifi cation of these patients is important because of the potential for life-threatening thrombosis through mechanisms independent of haemoglobin and packedcell volume. Despite iron defi ciency, these patients should not be given iron-replacement therapy unless closely supervised, because it could stimulate a rapid and potentially catastrophic increase in haemoglobin.