Permanent right ventricular pacing with left bundle branch block (LBBB) morphology is associated with pacing-induced cardiomyopathy, and it is reversible with pacing upgrade, with the left ventricle (LV) resynchronised. It can also cause angina in the absence of epicardial coronary artery disease (ANOCA) and LV systolic dysfunction (LVSD). A 55-year-old woman with ANOCA, obesity and a right ventricle apical pacemaker with 100% pacing rate in LBBB shows how LV dyssynchrony affects coronary flow. During atrial-synchronised RV pacing, raising the heart rate from 120 to 150 bpm drives her left anterior descending (LAD) artery flow ratios down from 1.58 to 1.13, while microvascular resistance rises proportionally from 0.38 to 0.84, compared with baseline coronary haemodynamics, using continuous thermodilution. When the LV is paced directly from the septum via the LAD pressure wire as a pacing lead with an external pulse generator at 120 bpm, the LAD flow climbs 15% over that of RV pacing at the same heart rate despite a lower blood pressure and expends less vasodilatory reserve. In simple terms, RV pacing is 25% less energy efficient in generating an equivalent level coronary flow in the LAD, and LBBB causes ischaemia due to failure of coronary flow to augment to meet demand, constrained by rising resistance. It is a global phenomenon than a localised ischaemia in the LV septum—the distinction between an inefficient heart generating less coronary flow generally versus a circumscribed dyssynchronous septal compression. The former is a more compelling mechanism for LBBB-induced LVSD, especially that painful LBBB is relatively rare.