BACKGROUND: The influence of CRT on left ventricular wall thickness and left ventricular mass (LVM) is unknown. OBJECTIVES: To evaluate the effects of CRT on septal, posterior wall thickness (SWT, PWT) and LVM in patients with LBBB and non-LBBB as compared to ICD patients, and to assess the relationship between CRT-induced changes and cardiac events. METHODS: We investigated 843 with LBBB and 366 patients with non-LBBB, enrolled in MADIT-CRT to analyze changes in SWT, PWT and LVM at 12-month and subsequent outcome. The primary end point was heart failure (HF) or death; secondary end points included ventricular tachycardia (VT), ventricular fibrillation (VF) or death. RESULTS: In LBBB patients, reduction in SWT, PWT and LVM was more pronounced in CRT-D as compared to ICD (SWT: -6.7±4.4% vs. -1.0±1.9%; PWT:-6.4±4.3% vs. -0.8±1.9%, LVM -23.6±9.9% vs. -5.1±5.1%, p< 0.001 for all). In CRT-D patients with non-LBBB, LVM reduction was less pronounced, however the changes in SWT and PWT were comparable. Change in LVM correlated with changes in left ventricular end-diastolic volume. In CRT-D patients with LBBB, reduction in SWT, LVM was associated with reduction in HF/Death (SWT: HR=0.94, 95%CI: 0.89-0.99 per percent change, p=0.03) and VT/VF/Death (SWT: HR=0.95, 95%CI: 0.91-1.00, p= 0.04). CRT-D patients with non-LBBB did not show favorable reduction of clinical or arrhythmic end points related to changes in SWT, PWT or LVM. CONCLUSIONS: CRT-D was associated with significant reduction in SWT, PWT and LVM in patients with LBBB along with LV volume changes and associated favorable clinical and arrhythmic outcome.
[Show abstract][Hide abstract] ABSTRACT: Aims
Left-ventricular (LV) conduction disturbances are common in heart-failure patients and a left bundle-branch block (LBBB) electrocardiogram (ECG) type is often seen. The precise cause of this pattern is uncertain and is probably variable between patients, ranging from proximal interruption of the left bundle branch to diffuse distal conduction disease in the working myocardium. Using realistic numerical simulation methods and patient-tailored model anatomies, we investigated different hypotheses to explain the observed activation order on the LV endocardium, electrogram morphologies, and ECG features in two patients with heart failure and LBBB ECG.
Methods and results
Ventricular electrical activity was simulated using reaction–diffusion models with patient-specific anatomies. From the simulated action potentials, ECGs and cardiac electrograms were computed by solving the bidomain equation. Model parameters such as earliest activation sites, tissue conductivity, and densities of ionic currents were tuned to reproduce the measured signals. Electrocardiogram morphology and activation order could be matched simultaneously. Local electrograms matched well at some sites, but overall the measured waveforms had deeper S-waves than the simulated waveforms.
Tuning a reaction–diffusion model of the human heart to reproduce measured ECGs and electrograms is feasible and may provide insights in individual disease characteristics that cannot be obtained by other means.
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