Peri-infarct pacing to prevent left reverse remodelling: an unvalidated concept?

This editorial refers to ‘Peri-infarct zone pacing to prevent adverse left ventricular remodelling in patients with large myocardial infarction’†, by G.W. Stone et al., on page 484. The management of acute ST-segment elevation myocardial infarction (STEMI) has evolved considerably in recent decades. Modern treatment includes STEMI network activation, antithrombotic drugs, and rapid early revascularization (mainly by mechanical reperfusion).1,2 Cardioprotective interventions aimed at reducing the extent of myocardial necrosis have been evaluated in basic and clinical research with negative or minimal effects.1,2 After myocardial injury, left ventricular (LV) remodelling of the infarct zone and the circumferential residual viable myocardium leads to thinning and dilatation of the affected myocardium and hypertrophy of the viable myocardium. This process of LV remodelling impairs LV function, enlarges the left ventricle, and has a major effect on the patient's outcome in terms of quality of life, heart failure, and survival. Therapies that may attenuate or reverse the process of LV remodelling might have a favourable effect on the prognosis of patients with STEMI. In this issue of the journal, Stone et al. report the results of a clinical trial that assessed a new concept for preventing or attenuating LV remodelling after a myocardial infarction, namely peri-infarct pacing.3 Chronic cardiac pacing is not only indicated for patients with bradycardia but, as in most patients implanted with a cardiac resynchronization device, also for haemodynamic purposes.