[Hypersensitivity of the carotid sinus in syncope and its diagnostic role: therapeutic implications and follow-up]. / Ipersensibilità del seno carotideo nella sincope e suo ruolo diagnostico: implicazioni terapeutiche e follow-up.

Our aim was to assess the incidence and clinical characteristics of carotid sinus hypersensitivity in a group of subjects suffering from syncope. The total number of patients was 118. Twenty-four of them (20%) were diagnosed as epileptics (first attack) and 38 (32%) as vasodepressors. 56 patients with unexplained syncope underwent carotid sinus massage during electrocardiographic registration and pressure monitoring. 41 patients were found to have carotid sinus hypersensitivity. 34 of these 41 patients received implantation of a pacemaker. Abnormal sinus node function was noted in 30, abnormal atrioventricular node function in 3 and combined abnormal sinus node and AV node function in 1. Furthermore three other patients who were negative to massage were implanted with a pacemaker because they had an organic heart disease and recurrent syncope. Different tests as 24-hour monitoring ecg and electrophysiologic study showed no better results in the diagnosis of syncope. Our data demonstrates the diagnostic importance of carotid sinus massage in the diagnosis of syncope. The validity of this method is confirmed by the 24 month follow-up.

Cerebral autoregulation in orthostatic hypotension. A transcranial Doppler study.

BACKGROUND AND PURPOSE: Transcranial Doppler measurements of blood flow velocity permit an assessment of variations in intracranial hemodynamics in response to acute arterial pressure variations. The purpose of this study was to scan healthy volunteers and patients with autonomic failure for differences in cerebral hemodynamic patterns under an acute hypotensive stimulus. METHODS: We used transcranial Doppler monitoring of blood flow velocity in the middle cerebral artery and noninvasive monitoring of arterial blood pressure and heart rate before, during, and after acute arterial hypotension induced by reactive hyperemia of the lower limbs. RESULTS: After maximum hypotension, the mean blood flow velocity was higher in the healthy volunteers than in the patients. In the healthy subjects mean velocity rose significantly (P < .01) higher than arterial blood pressure after 30 seconds and 60 seconds; in the patients mean velocity and arterial pressure moved in parallel fashion. The diastolic blood flow velocity increased more in the control group than in the patients during the early stages of the test; furthermore, only in the healthy volunteers did it increase significantly more than arterial pressure after 30 seconds and 60 seconds. Regarding the pulsatility index, the differences between the two groups were similar to the diastolic velocity results. CONCLUSIONS: (1) Monitoring of mean blood flow velocity showed the ability to maintain an adequate cerebral blood flow in healthy subjects; this mechanism was not efficient in the patients with autonomic failure. (2) Diastolic velocity and pulsatility index values clearly showed that only in healthy subjects were cerebral hemodynamics relatively independent of pressure values.