Document Detail

Intra-ventricular resynchronization for optimal left ventricular function during pacing in experimental left bundle branch block.
MedLine Citation:
PMID:  12906989     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: We 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.
BACKGROUND: Pacing 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.
METHODS: In 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/dt(max)) 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).
RESULTS: Induction 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/dt(max) and SW decreased (-13 +/- 18% and -39 +/- 24%, respectively). During LBBB, LV and BiV pacing increased LV dP/dt(max) 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.
CONCLUSIONS: In 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.
Xander A A M Verbeek; Kevin Vernooy; Maaike Peschar; Richard N M Cornelussen; Frits W Prinzen
Related Documents :
2532959 - Effects of chronic sodium depletion on function of isolated normal and hypertensive hyp...
2956729 - Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic...
8856209 - Reduced left ventricular hypertrophy in type 1 diabetic patients with end-stage renal f...
16436889 - Predicted hemodynamic benefits of counterpulsation therapy using a superficial surgical...
1877659 - Collagen remodeling and changes in lv function during development and recovery from sup...
7837209 - Criteria for an informative trial of left ventricular hypertrophy regression.
22294959 - The accuracy of an automasking algorithm in plantar pressure measurements.
11751329 - The enzyme horseradish peroxidase is less compressible at higher pressures.
14752579 - Metabolic selectivity and growth of clostridium thermocellum in continuous culture unde...
Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  42     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-08-08     Completed Date:  2003-09-11     Revised Date:  2011-01-14    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  558-67     Citation Subset:  AIM; IM    
Department of Physiology, Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Bundle-Branch Block / complications,  therapy*
Cardiac Pacing, Artificial / methods*
Hemodynamics / physiology
Models, Animal
Models, Cardiovascular
Ventricular Dysfunction, Left / etiology,  therapy*
Ventricular Function, Left / physiology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Visualization of risk-area myocardium as a high-intensity, hyperenhanced "hot spot" by myocardial co...
Next Document:  Triphasic waveforms are superior to biphasic waveforms for transthoracic defibrillation: experimenta...