A 64-year-old gentleman of mixed ancestry, with poorly controlled type 2 diabetes mellitus (HbA1C—12.7%/115 mmol/mol), hypertension, dyslipidaemia, and 30-pack-year smoking history with no previous history of ischaemic events or angina, presented to a non-PCI centre within our referral network with ischaemic chest pain. He reported intermittent episodes of short-lived (<10 min) pain which initially started 8 h prior to presentation, with subsequent development of non-remitting, central crushing chest pain which reached maximal intensity 2 h before presentation. Initial electrocardiogram (ECG), done within 10 min of presentation, showed evidence of an inferior STEMI () with V4R ST-elevation confirming right ventricular (RV) involvement. First-degree AV block was also noted, with no prior history of pre-syncope or syncope. On presentation, he had a blood pressure (BP) of 128/88 mmHg and pulse of 90 b.p.m. with SPO2 breathing ambient air of 97%. He had grade 1 hypertensive retinopathy and an otherwise normal clinical examination with no clinical evidence of heart failure. Patient was given 1.5 million units streptokinase as part of a pharmacoinvasive strategy (due to unavailability of an after-hours primary PCI service) for reperfusion which was infused over 30 min. In addition, he was given a loading dose of 300 mg aspirin, 300 mg clopidogrel, 30 mg intravenous enoxaparin (further 80 mg subcutaneously after 15 min), 50 mg atenolol, 40 mg simvastatin, and 10 mg enalapril. Cardiac biomarkers were initially not available. Echocardiography was suggestive of right coronary artery (RCA) occlusion with hypokinesia of the infero-postero left ventricular (LV) walls and reduced RV function. LV-systolic function was calculated at 39%. The hypokinetic regions were neither thin nor echobright, suggesting acute ischaemia as the cause for the myocardial dysfunction. The patient remained stable, but was deemed to have failed fibrinolytic therapy with <50% reduction in ST-elevation and ongoing chest pain at 60 min post-fibrinolysis (). He was transferred urgently to our PCI centre, where angiography confirmed critical, proximal RCA disease (Thrombolysis in Myocardial Infarction II flow) which was successfully stented with resolution of the patient’s chest pain and resolution of ST-elevation ( and Video 1). The other vessels showed mild disease without prognostic flow-limiting lesions (). A high-sensitivity Troponin T level, subsequent to the PCI was measured at 29 196 ng/L. An hour after angiography, the patient developed first-degree AV block progressing to Mobitz I and then to high-degree 2:1 AV block (). This was in the absence of new chest pain or ECG changes to suggest acute stent thrombosis. He remained haemodynamically stable throughout, albeit symptomatic with episodes of pre-syncope, with a minimum pulse rate of 34 b.p.m. and with no evidence to suggest re-infarction. In light of his symptomatic bradycardia, a temporary, transvenous pacing lead was inserted via the right femoral vein and left at a backup rate of 40 b.p.m. His beta-blockade was stopped and managed conservatively with the temporary pacing wire being replaced on Day 3 and Day 6. He regained sinus rhythm on Day 7 post-infarction with no evidence of AV block with successful reintroduction of beta-blockade prior to discharge.