A 68-year-old female with no previous medical history or co-morbidities was admitted with a 1-week history of progressive dyspnoea in the context of CHB disclosed by 12-lead electrocardiogram (ECG). There were no clinical examination findings suggestive of pulmonary hypertension but there was evidence of LV failure. She was commenced on an intravenous infusion of isoprenaline for chronotropic support. A TTE was performed to exclude structural heart disease and confirmed normal biventricular size and systolic function. There was, however, moderate tricuspid regurgitation (TR) and her peak TR jet velocity (TR vel) was measured at 4.6 m/s resulting in an estimated RVSP of 99 mmHg [assuming a mean right atrial pressure (RAP) of 15 mmHg]. Interestingly, her RVOT velocity-time integral (VTI) was also incidentally noted to be significantly elevated at 23.9 cm (see ). An urgent computed tomography pulmonary angiogram reported no evidence of pulmonary embolism (PE) and, importantly, demonstrated no evidence of pulmonary arterial dilatation that is often associated with chronic pulmonary hypertension. She proceeded on to implantation of a permanent dual-chamber PPM with no complications. The patient returned for further invasive assessment of her possible pulmonary hypertension 4 weeks later. Her repeat TTE revealed reductions in TR severity to mild, TR vel to 2.9/s, with parallel decreases in her RAP to 3 mmHg and estimated RVSP to 37 mmHg. Her RVOT VTI was similarly measured lower at 14 cm. Right heart catheterization (RHC) confirmed relatively normal pulmonary haemodynamics with an invasive mean RAP of 4 mmHg, pulmonary arterial systolic/diastolic pressures of 20/6 mmHg, mean pulmonary arterial pressure of 12 mmHg, mean pulmonary capillary wedge pressure of 3 mmHg, cardiac output (by thermodilution) of 4.4 L/min, and calculated pulmonary vascular resistance (PVR) of 2.0 Wood units. We subsequently reviewed our echocardiographic database and identified 250 patients who had CHB and underwent pre-PPM implantation TTE studies. Two further patients from this cohort with both baseline and post-PPM TTEs demonstrated similar haemodynamic profiles of initial elevation in TR vel, RAP, RVSP, and RVOT VTI, which then significantly improved post-restoration of AV synchrony by permanent pacing (see ).