Carotid atherosclerosis has a high prevalence in adults with cardiovascular risk factors. Such carotid lesions have been shown to perturb baroreflex sensitivity as well as autonomic nervous system activity. Carotid atheroma induces locally structural changes that decrease the arterial distensibility with impairment of baroreflex sensitivity. The presence of carotid atheroma may also impair ventilatory flow characteristics through several pathways. The carotid plaque targets the carotid sinus, a structure known to be involved in the regulation of respiration. The baroreflex controls ventilation through changes in the frequency, tidal volume and breathing variability. Moreover, autonomic nervous system dysfunction occurs in the presence of a greater intima-media thickness of the carotid arteries and during carotid atherosclerosis. This sympatho-vagal imbalance could contribute to breathing control abnormalities as well. Consistent with our hypotheses, ventilatory chaos is SAR131675 VEGFR/PDGFR inhibitor impaired during carotid atherosclerosis. The main determinant of the flow dynamics alteration was the severity of the stenosis although other characteristics of the carotid plaque such as its localization and morphology also significantly decreased ventilatory chaos. Carotid endarterectomy reversed inspiratory flow chaos abnormalities, which reinforced the direct role played by the plaque in these alterations. Chaos impairment of inspiratory flow was strongly related to the severity of the carotid stenosis. In multiple regression analyses, the percentage of the carotid stenosis was the best in predicting the chaotic features of the inspiratory flow. However, other characteristics such as localization, surface features and morphology of the plaque also altered ventilatory chaos, independently of the degree of stenosis. The carotid plaques were classified depending on their echogenic features and surface morphology. The homogeneous echogenicity of the plaque is relied on histological characteristic such as collagen-rich, fibrous plaques, while heterogeneous echogenicity is found in lipid-rich or hemorrhagic plaques. Different local vascular consequences depending on the characteristics of the plaque may explain the differences evidenced in the largest Lyapunov exponent and the correlation dimension of the inspiratory flow. The structural changes of the vessel wall composition induce by the plaque directly impairs the baroreceptors and thus modifies the breathing pattern. In addition paracrine factors associated with atherosclerosis may potentiate the effects of structural modulation. Sympathovagal imbalance has also been described during carotid atheroma and this could contribute to ventilatory flow dynamics alterations. Indeed, baroreflex sensitivity has a significant effect in predicting the correlation dimension value and to a lesser extent the LLE of the inspiratory flow in multiple regression models.