from carotid baroreceptors and chemoreceptors ascend in anatomic proximity in the carotid sinus nerve, and therefore, the sequelae of baroreceptor and chemoreceptor denervation as a result of an iatrogenic injury typically arise in parallel.If the theory of Demirel et al were correct, patients who undergo bilateral e-CEA would represent a human model of carotid sinus denervation. In fact, we proved in our previous study 2 that this is not the case. Also, in patients treated with bilateral CEA not only were both baroreflexes and chemoreflexes preserved regardless the surgical technique, but unexpectedly, baroreflexes appeared better maintained in e-CEA than in patch CEA. Finally, we found that e-CEA, even when performed on both sides, did not increase long-term arterial pressure variability, and this suggests that perioperative hemodynamic derangements can be attributed to the temporary effects of surgical trauma.Finally, the remarks about our methods by Demirel et al 1 appear incorrect and inaccurate. In humans, the lack of carotid baroreceptors is not completely compensated by aortic and cardiopulmonary baroreceptors. 4 Furthermore, we did not perform only standard cardiovascular reflex tests but also spectral analysis of heart rate and blood pressure variability and concurrent peripheral chemoreflex function analysis that specifically accounts for the integrity of the carotid sinus nerve. Rather, the authors claim that in their study "unilateral carotid baroreflex function could be assessed in an invasive way, allowing a full pressure transmission to the carotid baroreceptors located in the carotid bulb." In fact, they more prosaically retrospectively reviewed patient records and compared perioperative routine records of two nonrandomized nor case-matched groups of patients.In conclusion, it should be apparent that the "carotid sinus denervation by e-CEA" theory is dead.