Imperial College London
Alternate

DrZacharyWhinnett

Faculty of Medicine, National Heart & Lung Institute

Reader in Cardiac Electrophysiology
 
 
 
//

Contact

 

z.whinnett

 
 
//

Location

 

South- NHLI Cardiovascular ScienceBlock B Hammersmith HospitalHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Jones:2016:europace/euw136,
author = {Jones, S and Lumens, J and Sohaib, SMA and Finegold, JA and Kanagaratnam, P and Tanner, M and Duncan, E and Moore, P and Leyva, F and Frenneaux, M and Mason, M and Hughes, AD and Francis, D and Whinnett, ZI and the, BRAVO Investigators and on, behalf of the BRAVO Investigators},
doi = {europace/euw136},
journal = {Europace},
pages = {1178--1186},
title = {Cardiac Resynchronisation Therapy: mechanisms of action and scope for further improvement in cardiac function},
url = {http://dx.doi.org/10.1093/europace/euw136},
volume = {19},
year = {2016}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BackgroundCardiac resynchronisation therapy(CRT) may exert its beneficial hemodynamic effect by improving ventricular synchrony and improving atrioventricular(AV) timing.Aims To establish the relative importance of the mechanisms through which CRT improves cardiac function and explore the potential for additional improvements with improved ventricular resynchronisation. Methods We performed simulations using the CircAdapt haemodynamic model and performed haemodynamic measurements while adjusting AV delay, at low and high heart rates, in 87 patients with CRT devices. We assessed QRS duration, presence of fusion and haemodynamic response.ResultsThe simulations suggest intrinsic PR interval and the magnitude of reduction in ventricular activation determine the relative importance of the mechanisms of benefit. For example, if PR interval is 201ms and LV activation time is reduced by 25ms (typical for current CRT methods) then AV delay optimisation is responsible for 69% of overall improvement. Reducing LV activation time by an additional 25ms produced an additional 2.6mmHg increase in BP (30% of effect size observed with current CRT).In the clinical population, ventricular fusion significantly shortened QRS duration (-27±23ms, P <0.001), and, improved SBP (mean 2.5 mmHg increase). Ventricular Fusion was present in 69% of patients, yet in 40% of patients with fusion, shortening AV delay (to a delay where fusion was not present) produced the optimal haemodynamic response.ConclusionsImproving LV preloading by shortening AV delay is an important mechanism through which cardiac function is improved with CRT. There is substantial scope for further improvement if methods for delivering more efficient ventricular resynchronisation can be developed.
AU  - Jones,S
AU  - Lumens,J
AU  - Sohaib,SMA
AU  - Finegold,JA
AU  - Kanagaratnam,P
AU  - Tanner,M
AU  - Duncan,E
AU  - Moore,P
AU  - Leyva,F
AU  - Frenneaux,M
AU  - Mason,M
AU  - Hughes,AD
AU  - Francis,D
AU  - Whinnett,ZI
AU  - the,BRAVO Investigators
AU  - on,behalf of the BRAVO Investigators
DO  - europace/euw136
EP  - 1186
PY  - 2016///
SN  - 1532-2092
SP  - 1178
TI  - Cardiac Resynchronisation Therapy: mechanisms of action and scope for further improvement in cardiac function
T2  - Europace
UR  - http://dx.doi.org/10.1093/europace/euw136
UR  - http://hdl.handle.net/10044/1/31554
VL  - 19
ER  -
Download