Left Ventricular Mechanics and Myocardial Blood Flow Following Restoration of Normal Activation Sequence in Paced Patients With Long-term Right Ventricular Apical Stimulation

Abstract

Asynchronous ventricular activation, as induced by ventricular pacing, is known to affect left ventricular (LV) systolic and diastolic function and myocardial blood flow. However, it is not clear whether the long-term disturbances it causes are reversible after the restoration of the normal ventricular activation sequence. In this study, we used the conductance catheter method and a Doppler guidewire to assess the changes in LV mechanics, and correspondingly in myocardial blood flow, after the restoration of the normal ventricular activation sequence in patients with long-term right ventricular apical pacing. Sixteen patients (mean [+/- SD] age, 61 +/- 11 years; 9 men) with right ventricular apical stimulation and complete ventricular pacing capture for a very long period were studied. In eight patients, we analyzed pressure-volume loops before and immediately after the restoration of the normal ventricular activation sequence, and in the remaining eight patients the myocardial blood flow and flow reserve were analyzed. End-systolic elastance (Ees) [5.503 +/- 0.6 vs 4.287 +/- 0.28 mm Hg/mL, respectively; p = 0.003] and its ratio to effective arterial elastance (1.63 +/- 0.51 vs 2.00 +/- 0.64, respectively; p = 0.009), which are indexes of systolic function and ventriculoarterial coupling, respectively, improved significantly after restoration of the normal ventricular activation sequence. Indexes of diastolic function and the predicted myocardial oxygen consumption (MO(2)) showed no clear change. Coronary flow in the dominant coronary artery increased significantly (46.55 +/- 14.12 vs 71.55 +/- 27.53 mL/min, respectively; p = 0.002), while the coronary flow reserve in the same artery decreased (3.5 +/- 1.0 vs 2.6 +/- 0.5, respectively; p = 0.008). The restoration of a normal activation sequence after long-term ventricular asynchrony enhances acutely contractile function without affecting MO(2). These changes in LV function do not appear to have causal relationships with myocardial blood flow changes.