Abstract :
Carotid sinus hypersensitivity (CSH) is recognised in up to 45% of elderly patients with syncope, falls, and dizziness that may not be attributed to specific myocardial sinus node dysfunction, various diseases that affect pacemaker activity, cardiac output and blood supply to the brain. The pathophysiology of CSH is unclear but it is associated with ageing, hypertension, and ischaemic heart disease. CSH is potentially treatable with dual chamber pacing for prolonged sinus arrest (cardio-inhibitory CSH) but therapy for the more prevalent hypotension (vasodepressor CSH) is unsatisfactory. However, hypersensitivity of the carotid sinus is not consistent with the known blunting effects of senescence and hypertension on baroreflex sensitivity.
The present hypothesis proposes that CSH in elderly patients results from up-regulation of brainstem postsynaptic α-2 adrenoceptors. Reduced carotid sinus compliance in elderly arteriosclerotic hypertensive patients will reduce afferent impulse traffic in the baroreflex pathway. Such relative deafferentation may be expected to cause baroreflex postsynaptic hypersensitivity, mediated by up-regulation of the dominant postsynaptic receptor population in the baroreflex pathway, ie, α-2 adrenoceptors. Vigorous carotid sinus stimulation, eg, massage, could thus cause an overshoot baroreflex efferent response, resulting in profound hypotension and bradycardia. Hypotension and bradycardia are compounded by the effects of age, hypertension, ischaemic heart disease and arteriosclerosis on rapid cardiovascular compensation, resulting in cerebral hypoperfusion and syncope. Thus, CSH in elderly patients should be considered as a clinical marker of widespread arteriosclerotic disease, rather than as a distinct disease entity. If correct, this hypothesis has potentially important implications for the pharmacotherapy of hypotension-related symptoms in elderly arteriosclerotic patients.
