Coronary artery anomalies are encountered in at least 5% of routine catheter-based diagnostic and CT coronary angiograms. These range from the coronary artery with an anomalous aortic origin, a complex fistula and a segment of an artery that tunnels under the myocardium. The last anomaly involving the left anterior descending (LAD) artery with a myocardial bridge (MB) appears to be the commonest—up to one third of the general population. In a patient with chest pain, it might be difficult to tease out if these coronary anomalies are contributory. Nevertheless, cardiac ischaemia is dictated by blood supply and fuel demand under stress; in the cardiac catheter laboratory, adenosine or dobutamine can be used and vasoreactivity tested with acetylcholine provocation. Further, these anomalies are usually an incidental finding in patients with competing comorbidities, including hypertension, left ventricular dysfunction, and a background of atherosclerotic coronary artery disease. The pressure-derived “surrogate” flow ratios are likely to be confounded. That was the reason for using the integrated diastolic fractional flow reserve (dFFR ≤ 0.76) with dobutamine for assessing MB. Although this was introduced over 20 years ago, it has not been adopted into daily clinical practice. Alternatively, now that actual volumetric coronary flow can be accurately measured in real time with continuous thermodilution, MB can be re-evaluated, with the potential that it might become the new gold standard. In the meantime, the clinical pathophysiology of MB is better understood. According to Francisco Torrent-Guasp’s helical myocardial ventricular band (HMVB) model where the heart can be origamically unfolded into a single strip of muscle, the “stray” muscle fibres running criss-cross from the right ventricle across the interventricular sulcus where the LAD is embedded to the left ventricle; when blunt-dissected with fingers the heart can be opened up like a lady’s purse. The MB is relatively immuned to the atherosclerotic process which renders it highly vasoreactive. On the other hand, the pre-MB LAD is a high stress area, making it liable to develop intimal thickening with plaque formation; when subjected to haemodynamic stress it can rupture, leading to coronary thrombosis and myocardial infarction. Finally, if the MB is stented inadvertently or when it is masked by a stunned myocardium, the reappearance of MB with myocardial recovery gives rise to repetitive radial strain on the stent, causing it to restenose or even fracture.