Modulated dispersion of activation and repolarization by premature beats in @entity1 with XXXX at risk of sudden death.

@entity1 @entity296 @entity299 @entity943 @entity3457
Premature beats can trigger @entity943 in @entity299 , but the mechanisms are not well defined. We studied the effect of premature beats on activation and repolarization dispersion in seven @entity1 with @entity296 (57    10 yr, left ventricular ejection fraction 31    7%). @entity3457 ( @entity3457 ), activation-recovery interval (ARI), and total repolarization time (TRT) were measured from 26 unipolar electrograms during right ventricle (RV) endocardial (early) to left ventricle epicardial (late) activation in response to RV apical extrastimulation (S1S2). Early TRT dispersion increased significantly with shorter S1S2 (1.0    0.2 to 2.3    0.4 ms/mm, P < 0.0001), with minimal change in late TRT dispersion (0.8    0.1 to 1.0    0.3 ms, P = 0.02). This was associated with an increase in early @entity3457 dispersion (1.0    0.1 to 1.5    0.2 ms/mm, P = 0.05) but no change in late @entity3457 dispersion (0.6    0.1 to 0.7    0.2 ms/mm, P = 0.4). Early and late ARI dispersion did not change with shorter S1S2. @entity3457 restitution slopes were similar between early and late sites, as was slope heterogeneity. ARI restitution slope was greater in early vs. late sites (1.3    0.6 vs. 0.8    0.6, P = 0.03), but slope heterogeneity was similar. With shorter S1S2, @entity3457 -ARI slopes became less negative (flattened) at both early (-0.4    0.1 to +0.04    0.2) and late (-1.5    0.2 to +0.3    0.2) sites, implying less activation-repolarization coupling. There was no difference in @entity3457 -ARI slopes between early and late sites at short S1S2. In conclusion, high-risk @entity1 with @entity296 have greater TRT dispersion at tightly coupled S1S2 due to greater @entity3457 dispersion and activation-repolarization uncoupling. Modulated dispersion is more pronounced at early vs. late activated sites, which may predispose to reentrant @entity943 .
