A New Paradigm for Physiologic Ventricular Pacing
Michael O. Sweeney, MD*,* and
Frits W. Prinzen, PhD
* Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands
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Figure 1 Effect of asynchronous ventricular activation on left ventricular (LV) pressure (upper tracing) and regional strain (lower tracings). During ventricular pacing, strain in different regions becomes asynchronous, as can be judged from the difference in onset of shortening (negative deflection of the curve). Asynchronous contraction causes reduction in ejection time and slows rates of increase and decrease of LV pressure and increases duration of isovolumic contraction (ic) and isovolumic relaxation (ir).
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Figure 2 Mechanisms of ventricular remodeling and progressive reduction in pump function during right ventricular apex pacing. For details, see text. P-V = pressure-volume.
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Figure 3 Paradigm for physiological pacing. For details, see text. BiV = biventricular pacing; LV = left ventricular; RV = right ventricular; RVA = right ventricular apex.
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Figure 4 Relationship between duration of mechanical asynchrony and heart failure development, as derived from various randomized clinical trials. This relationship indicates that attempts to avoid asynchronous activation may decrease the risk for developing heart failure most in patients requiring pacing for a longer time (children) and in patients with already-reduced pump function. A.U. = arbitrary units; RVA = right ventricular apex; Cum%VP = cumulative percent ventricular pacing.
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