See related article, pp. 903-911Location, like in real estate, is the most important question in electrophysiology as it determines the acute and long-term outcomes in patients undergoing ablation as well as placement of pacing or high voltage leads. Right ventricular (RV) apex is the most commonly selected location for placement of RV pacing leads. This preference reflects the ease, stability, and excellent pacing thresholds usually achieved at this location. However, human and experimental data have suggested potential deleterious effects of RV pacing on cardiac function, and thus, there has been an interest in alternate RV pacing sites. Singh et al in this issue of the journal present their study comparing right ventricular outflow tract (RVOT) and RV apical pacing using equilibrium radionuclide angiography (ERNA). To better understand and review the findings of their study or any trial of alternate site RV pacing, we must first answer the following questions.
WHY RV APICAL PACING IS DELETERIOUS TO CARDIAC FUNCTION?RV apical pacing leads to iatrogenic left bundle branch block (LBBB) resulting in altered left ventricular activation pattern. To appreciate why this is deleterious to left ventricle (LV) performance, we should contrast it with normal LV endocardial activation. In normal hearts with intact conduction system, LV endocardial activation occurs 0-15 ms after the onset of QRS almost simultaneously in two areas: the mid septum and the anterobasal wall. From here, it spreads briskly with total endocardial activation time of 30-50 ms, which results in synchronous mechanical contraction of all areas in the LV.1 In pacing-induced LBBB, the activation has to spread from right to left across the septum, which is slow, resulting in earliest LV endocardial activation around 50 ms after the onset of QRS and hence interventricular dyssynchrony. From here, the activation spreads across the rest of the LV with total endocardial activation time around 80-90 ms. This time can be exaggerated in patients with underlying cardiomyopathy or previous infarction as reflected by markedly longer paced QRS duration in these patients resulting in significant intraventricular dyssynchrony. The inter-and intraventricular dyssynchrony from RV pacing results in acute decrease in cardiac pump function as shown by a decrease in the maximum dp/dt, mean arterial pressure, stroke volume, and stroke work and an increase in isovolumetric contraction and relaxation times in both animal and human studies.2-4 The pressure volume relationship of the LV shifts rightward and it operates at a higher volume. Dyssynchrony in activation and subsequent contraction of the LV leads to heterogeneity of stretch and loading conditions in pacing-induced or native LBBB. This can cause regional changes in myocardial perfusion as seen by perfusion defects and wall motion abnormalities in many of these patients with angiographically normal coronary arteries. [5][6][7] These acute changes in LV performance when present over a long duration can lead to asymmetri...