22 research outputs found
A rule-based method for predicting the electrical activation of the heart with cardiac resynchronization therapy from non-invasive clinical data
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Hydrodynamics of liquids of arbitrarily curved flux-lines and vortex loops
We derive a hydrodynamic model for a liquid of arbitrarily curved flux-lines
and vortex loops using the mapping of the vortex liquid onto a liquid of
relativistic charged quantum bosons in 2+1 dimensions recently suggested by
Tesanovic and by Sudbo and collaborators. The loops in the flux-line system
correspond to particle-antiparticle fluctuations in the bosons. We explicitly
incorporate the externally applied magnetic field which in the boson model
corresponds to a chemical potential associated with the conserved charge
density of the bosons. We propose this model as a convenient and physically
appealing starting point for studying the properties of the vortex liquid
Pathobiology of cardiac dyssynchrony and resynchronization therapy
Item does not contain fulltextSynchronous ventricular electrical activation is a prerequisite for adequate left ventricular (LV) systolic function. Conduction abnormalities such as left bundle branch block, and ventricular pacing lead to a dyssynchronous electrical activation sequence, which may have deleterious consequences. The present review attempts to connect the various processes involved in the development of 'dyssynchronopathy', and its correction by cardiac resynchronization therapy (CRT). Abnormal electrical impulse conduction leads to abnormal contraction, characterized by regional differences in timing as well as shortening patterns and amount of external work performed. Early activated regions may show 'wasted work', which leads to inefficient action of the entire left ventricle. Moreover, both the development of heart failure (HF) in general and the regional differences in mechanical load lead to structural, electrical, and contractile remodelling processes. These have been demonstrated at the level of the myocardium (asymmetric hypertrophy, fibrosis, prolongation of activation and reduction in repolarization forces, decrease in LV ejection fraction), cell (gap junctional remodelling, derangement of the T-tubular structure), and molecule (under or overexpression of ion channels and contractile proteins subtypes and abnormal calcium handling). The myocardial adaptations to dyssynchrony are 'maladaptive'. This also explains why CRT, unlike most pharmacological treatments, continues to increase its therapeutic effect over time. Finally, better understanding of all processes involved in dyssynchrony and CRT may also lead to new pharmacological agents for treating HF and to novel pacing strategies
Visualisation of coronary venous anatomy by computed tomography angiography prior to cardiac resynchronisation therapy implantation
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196192.pdf (publisher's version ) (Open Access
Response to cardiac resynchronization therapy is determined by intrinsic electrical substrate rather than by its modification
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Comparison between a count-based and geometrical approach for the assessment of left ventricular dyssynchrony using myocardial perfusion scintigraphy
Cardiovascular Aspects of Radiolog
Can We Use the Intrinsic Left Ventricular Delay (QLV) to Optimize the Pacing Configuration for Cardiac Resynchronization Therapy With a Quadripolar Left Ventricular Lead?
BACKGROUND: Previous studies indicated the importance of the intrinsic left ventricular (LV) electric delay (QLV) for optimal benefit to cardiac resynchronization therapy. We investigated the use of QLV for achieving optimal acute hemodynamic response to cardiac resynchronization therapy with a quadripolar LV lead. METHODS AND RESULTS: Forty-eight heart failure patients with a left bundle branch block were prospectively enrolled (31 men; age, 66+/-10 years; LV ejection fraction, 28+/-8%; QRS duration, 176+/-14 ms). Immediately after cardiac resynchronization therapy implantation, invasive LV pressure-volume loops were recorded during biventricular pacing with each separate electrode at 4 atrioventricular delays. Acute cardiac resynchronization therapy response, measured as change in stroke work (Delta%SW) compared with intrinsic conduction, was related to intrinsic interval between Q on the ECG and LV sensing delay (QLV), normalized for QRS duration (QLV/QRSd), and electrode position. QLV/QRSd was 84+/-9% and variation between the 4 electrodes 9+/-5%. Delta%SW was 89+/-64% and varied by 39+/-36% between the electrodes. In univariate analysis, an anterolateral or lateral electrode position and a high QLV/QRSd had a significant association with a large Delta%SW (all P <0.01). In a combined model, only QLV/QRSd remained significantly associated with Delta%SW (P<0.05). However, a direct relation between QLV/QRSd and Delta%SW was only seen in 24 patients, whereas 24 patients showed an inverse relation. CONCLUSIONS: The large variation in acute hemodynamic response indicates that the choice of the stimulated electrode on a quadripolar lead is important. Although QLV/QRSd was associated with acute hemodynamic response at group level, it cannot be used to select the optimal electrode in the individual patient