Recently, McMullan et al. showed in rats that the variability of the inspiratory and expiratory time, as well as the complexity were altered during aortic baroreceptor activation, at low ventilatory drive. Indeed, baroreceptors afferents project to the nucleus tractus solitarius and the resulting baroreceptors-mediated effects on central respiratory neural activity and timing consist in changes in respiratory timing and volume. In patients with severe carotid stenosis, we found that carotid endarterectomy performed under regional anesthesia significantly increased inspiratory flow chaos. This finding pointed out the direct role of the carotid plaque in the ventilatory flow dynamics abnormalities, independently of possible confounding factors such as the age. Plaque removal completely reversed the increased coefficient of variation and autocorrelation coefficient. It also reversed the correlation dimension of the inspiratory flow whereas it partially reversed the LLE. Vascular alterations, including atherosclerosis and arterial stiffness have been associated with impaired pulmonary function. Reduced peak expiratory flow is linked to the development of carotid atherosclerosis whereas reduced FEV1 and FEV1/ FVC are associated with arterial stiffness. The mechanisms underlying these associations are still not entirely understood. Therefore we selected the subjects in our study based on their normal respiratory function to avoid the possible interaction with breathing control. Cardiac resynchronization therapy has evolved as an established treatment in patients with severe heart failure refractory to optimized neurohumoral therapy. Large clinical trials showed a significant benefit on mortality and on morbidity in patients with wide QRS complex in NYHA class III and severely impaired left ventricular ejection TH-302 fraction . There are many studies about electrophysiologic and mechanical mechanisms of CRT. Despite the fact that during CRT the right ventricular lead is placed endocardially and left ventricular pacing is performed using an epicardial lead placed within the coronary veins, little is known about endocardial and epicardial activation in these patients. Invasive catheter based mapping of ventricular activation reflects only right- and left ventricular endocardial sites. Information on epicardial activation is limited to a small area of the left ventricle accessible via mapping in the coronary sinus. Most of these data were obtained by conventional fluoroscopy guided electrophysiological mapping as well as by electromagnetic three-dimensional non-fluoroscopic electroanatomic contact mapping. This study was conducted to characterize biventricular endocardial and epicardial activation in heart failure patients undergoing CRT compared to a healthy control group using a novel noninvasive cardiac mapping tool –Noninvasive Imaging of Cardiac Electrophysiology. A bidomain model based boundary element formulation was applied to relate step-like local activation.