Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2016
Non-invasive, model-based measures of ventricular electrical dyssynchrony for predicting CRT outcomes.
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Villongco Christopher T, Krummen David E, Omens Jeffrey H, McCulloch Andrew D
Аннотация
AIMS: Left ventricular activation delay due to left bundle branch block (LBBB) is an important determinant of the severity of dyssynchronous heart failure (DHF). We investigated whether patient-specific computational models constructed from non-invasive measurements can provide measures of baseline dyssynchrony and its reduction after CRT that may explain the degree of long-term reverse ventricular remodelling.
METHODS AND RESULTS: LV end-systolic volume reduction (ΔESVLV) measured by 2D trans-thoracic echocardiography in eight patients following 6 months of CRT was significantly (P < 0.05) greater in responders (26 ± 20%, n = 4) than non-responders (11 ± 16%, n = 4). LV reverse remodelling did not correlate with baseline QRS duration or its change after biventricular pacing, but did correlate with baseline LV endocardial activation measured by electroanatomic mapping (R2 = 0.71, P < 0.01). Patient-specific models of LBBB ventricular activation with parameters obtained by matching model-computed vectorcardiograms (VCG) to those derived from standard patient ECGs yielded LV endocardial activation times that correlated well with those measured from endocardial maps (R2 = 0.90). Model-computed 3D LV activation times correlated strongly with the reduction in LVESV (R2 = 0.93, P < 0.001). Computed decreases due to simulated CRT in the time delay between LV septal and lateral activation correlated strongly with ΔESVLV (R2 = 0.92, P < 0.001). Models also suggested that optimizing VV delays may improve resynchronization by this measure of activation delay.
CONCLUSIONS: Patient-specific computational models constructed from non-invasive measurements can compute estimates of LV dyssynchrony and their changes after CRT that may be as good as or better than electroanatomic mapping for predicting long-term reverse remodelling.
METHODS AND RESULTS: LV end-systolic volume reduction (ΔESVLV) measured by 2D trans-thoracic echocardiography in eight patients following 6 months of CRT was significantly (P < 0.05) greater in responders (26 ± 20%, n = 4) than non-responders (11 ± 16%, n = 4). LV reverse remodelling did not correlate with baseline QRS duration or its change after biventricular pacing, but did correlate with baseline LV endocardial activation measured by electroanatomic mapping (R2 = 0.71, P < 0.01). Patient-specific models of LBBB ventricular activation with parameters obtained by matching model-computed vectorcardiograms (VCG) to those derived from standard patient ECGs yielded LV endocardial activation times that correlated well with those measured from endocardial maps (R2 = 0.90). Model-computed 3D LV activation times correlated strongly with the reduction in LVESV (R2 = 0.93, P < 0.001). Computed decreases due to simulated CRT in the time delay between LV septal and lateral activation correlated strongly with ΔESVLV (R2 = 0.92, P < 0.001). Models also suggested that optimizing VV delays may improve resynchronization by this measure of activation delay.
CONCLUSIONS: Patient-specific computational models constructed from non-invasive measurements can compute estimates of LV dyssynchrony and their changes after CRT that may be as good as or better than electroanatomic mapping for predicting long-term reverse remodelling.
Предметные рубрики MeSH
Action PotentialsAgedBundle-Branch BlockCardiac Resynchronization TherapyElectrocardiographyElectrophysiologic Techniques, CardiacHeart FailureHeart RateHumansMaleMiddle AgedModels, CardiovascularPatient-Specific ModelingPredictive Value of TestsRecovery of FunctionSignal Processing, Computer-AssistedStroke VolumeTime FactorsTreatment OutcomeVectorcardiographyVentricular Dysfunction, LeftVentricular Function, LeftVentricular Remodeling