Apical hypertrophic cardiomyopathy (HCM) is an uncommon variant of hypertrophic cardiomyopathy which predominantly affects the left ventricular (LV) apex [[1]Sakamoto T. Apical hypertrophic cardiomyopathy (apical hypertrophy): an overview.J Cardiol. 2001; 37: 161-178PubMed Google Scholar]. We present the case of a patient with apical HCM and the incidental finding of coronary artery fistulae who presents with features of STEMI. A 69 year old Caucasian woman presented to a rural ED with 3 hours of central chest pain and dizziness. This occurred on a background of intermittent ischaemic pain on exertion for the preceding 6 months. An ECG showed anterior ST elevation with deep T wave inversion in V5 and V6, as well as inferior leads. However, a point of care troponin returned negative and was confirmed on serial formal testing. Thrombolysis was not administered and the patient was transferred to a tertiary centre. Coronary angiography revealed no obstructive disease, but the incidental finding of tortuous vessels and the presence of a fistula to the LV. Left ventriculography demonstrated a ‘spade-like’ configuration of the LV cavity. The diagnosis of apical HCM was confirmed on transthoracic echocardiography. Apical HCM is usually asymptomatic, although ischaemic symptoms may be present [[2]Eriksson M.J. Sonnenberg B. Woo A. Rakowski P. Parker T.G. Wigle E.D. Rakowski H. Long-term outcome in patients with apical hypertrophic cardiomyopathy.J Am Coll Cardiol. 2002; 39: 638Crossref PubMed Scopus (311) Google Scholar]. Coronary fistulae are predominantly due to variations in embryological development, although trauma and previous cardiac surgery can also contribute. Small fistulae are generally asymptomatic, however the co-existence of apical HCM in this case may have precipitated a ‘coronary steal’ syndrome that may explain symptoms. The patient declined further investigation and was managed conservatively, but was a reminder of the need to correlate clinical and biochemical findings to avoid management pitfalls.