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Patients with atrial fibrillation (AF) were largely excluded from the major clinical trials of cardiac resynchronization therapy (CRT), despite the presence of AF in up to 40% of patients receiving CRT in clinical practice. AF appears to attenuate the response to CRT, by the combination of a reduction in biventricular pacing and the loss of atrioventricular synchrony. In addition, remodeling secondary to CRT may influence the progression of AF. Management options for patients with AF and CRT include rate control, with drugs or atrioventricular node ablation, or rhythm control, with electrical cardioversion and antiarrhythmic therapy, or AF catheter ablation. The evidence for these therapies in patients with CRT is largely limited to observational studies or inferred from randomized studies in the general heart failure population. In this review, we explore the complex interaction between AF, heart failure, and CRT and discuss the evidence for the treatment options in this difficult patient cohort.

Background: Patients who improve following cardiac resynchronization therapy (CRT) have left ventricular (LV) remodeling and improved cardiac output (CO). Effects on the systemic circulation are unknown. Objective: To explore the effects of CRT on aortic and pulmonary blood flow and systemic afterload. Methods: At CRT implant patients underwent a noninvasive assessment of central hemodynamics, including wave intensity analysis (n = 28). This was repeated at 6 months after CRT. A subsample (n = 11) underwent an invasive electrophysiological and hemodynamic assessment immediately following CRT. CRT response was defined as reduction in LV end-systolic volume ≥15% at 6 months. Results: In CRT responders (75% of those in the noninvasive arm), there was a significant increase in CO (from 3 ± 2 L/min to 4 ± 2 L/min, P = .002) and LV dP/dtmax (from 846 ± 162 mm Hg/s to 958 ± 194 mm Hg/s, P = .001), immediately after CRT in those in the invasive arm. They demonstrated a significant increase in aortic forward compression wave (FCW) both acutely and at follow-up. The relative change in LV dP/dtmax strongly correlated with changes in the aortic FCW (Rs 0.733, P = .025). CRT responders displayed a significant reduction in afterload, and a decrease in systemic vascular resistance and pulse wave velocity acutely; there was a significant decrease in acute pulmonary afterload measured by the pulmonary FCW and forward expansion wave. Conclusion: Improved cardiac function following CRT is attributable to a combination of changes in the cardiac and cardiovascular system. The relative importance of these 2 mechanisms may then be important for optimizing CRT.