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Transplantations of various stem cells or their progeny have repeatedly improved cardiac performance in animal models of myocardial injury; however, the benefits observed in clinical trials have been generally less consistent. Some of the recognized challenges are poor engraftment of implanted cells and, in the case of human cardiomyocytes, functional immaturity and lack of electrical integration, leading to limited contribution to the heart's contractile activity and increased arrhythmogenic risks. Advances in tissue and genetic engineering techniques are expected to improve the survival and integration of transplanted cells, and to support structural, functional, and bioenergetic recovery of the recipient hearts. Specifically, application of a prefabricated cardiac tissue patch to prevent dilation and to improve pumping efficiency of the infarcted heart offers a promising strategy for making stem cell therapy a clinical reality. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to compare the electrophysiologic substrate in ischemic cardiomyopathy (ICM) patients with and without sustained monomorphic ventricular tachycardia (SMVT). Background: Despite the universal presence of potentially arrhythmogenic left ventricular (LV) scarring, it is not clear why the majority of ICM patients never develop SMVT. Methods: Detailed electroanatomic mapping of the LV endocardium was performed in 17 stable control ICM patients (16 males) without clinical SMVT. They were compared with 17 ICM patients (15 males) with spontaneous SMVT. Standard definitions of low-voltage zones and fractionated, isolated, and very late potentials were used. Results: There were no significant baseline differences between the groups in terms of LV diameter, ejection fraction (27% vs. 28%), infarct territory, or time from infarction. However, control patients had smaller total low-voltage area ≤1.5 mv (30% of surface area vs. 55%, p < 0.001); smaller very low-voltage area <0.5 mv (7.3% vs. 29%, p < 0.001); higher mean voltage of low-voltage zones; fewer fractionated, isolated, and very late potentials with lower density of these scar-related electrograms per unit low-voltage area; and less SMVT inducibility. Potential conducting channels within dense scar and adjacent to the mitral annulus were more frequent in SMVT patients. Conclusions: Compared with ICM patients with SMVT, an otherwise similar control group demonstrated markedly smaller endocardial low-voltage zones, lower scar-related electrogram density, and fewer conducting channels with faster conduction velocity. These findings may explain why some ICM patients develop SMVT and others do not. [Copyright &y& Elsevier]

: ObjectivesWe sought to investigate to what extent intra-ventricular asynchrony (intraVA) and inter-ventricular asynchrony (interVA) determine left ventricular (LV) function in canine hearts with left bundle branch block (LBBB) during ventricular pacing.: BackgroundPacing therapy improves LV pump function in patients with heart failure and abnormal ventricular conduction supposedly due to resynchronization. However, the relationship between LV pump function and measures of asynchrony is not well established.: MethodsIn 15 experiments, LV (various sites) and biventricular (BiV) pacing was performed at atrioventricular (AV) delays of 20 to 140 ms. Measured were the maximum rate of increase (dP/dtmax) of LV pressure and LV stroke work (SW) (conductance catheter), interVA (time delay between the upslope of LV and RV pressures), and intraVA (from endocardial electrical activation maps).: ResultsInduction of LBBB increased interVA (−6.4 ± 8.6 to −28.4 ± 8.5 ms [RV earlier]) and intraVA (4.9 ± 2.4 to 18.0 ± 3.3 ms), whereas LV dP/dtmax and SW decreased (−13 ± 18% and −39 ± 24%, respectively). During LBBB, LV and BiV pacing increased LV dP/dtmax and SW (mean increases 14% to 21% and 11% to 15%, respectively) without changing diastolic function or preload. Optimal improvement in LV function was obtained consistently when intraVA returned to pre-LBBB values, while interVA remained elevated. Normalization of intraVA required AV delays shorter than the baseline PQ time during LV apex and BiV pacing, thus excluding endogenous LV activation, but AV delays virtually equal to the baseline PQ time (difference 4 ± 9 ms, p = NS) during pacing at (mid)lateral LV sites to obtain fusion between pacing-induced and endogenous activation.: ConclusionsIn LBBB hearts, optimal restoration of LV systolic function by pacing requires intra-ventricular resynchronization. The optimal AV delay to achieve this depends on both the site of pacing and baseline PQ time. [Copyright &y& Elsevier]