A M Humm1, C J Mathias. 1. Neurovascular Medicine Unit, Imperial College London at St Mary's Hospital and Institute of Neurology, University College London, London, UK. andrea.humm@insel.ch
Abstract
BACKGROUND AND PURPOSE: Carotid sinus massage (CSM) is commonly used to identify carotid sinus hypersensitivity (CSH) as a possible cause for syncope, especially in older patients. However, CSM itself could provoke classical vasovagal syncope (VVS) in pre disposed subjects. METHODS: Retrospective analysis of CSM, cardiovascular autonomic function tests (including tilt table testing) and medical history in 388 patients with recurrent syncope to identify and characterize patients in whom an abnormal response to CSM was more likely to reflect VVS than CSH. RESULTS: CSM was abnormal in 79 patients. In 53 patients (77.2 +/- 8.7 years), CSH was the likely cause of syncope. VVS was the more likely diagnosis in 26 younger patients (59.7 +/- 12.6 years) with longstanding syncope from youth, in whom fear or pain was as a trigger; 7/26 suffered from intense chronic or intermittent neck pain and one exacerbation of syncopal attacks followed a physical and emotional trauma to the neck. In VVS, 4/26 had spontaneous VVS during head-up tilt, another six after venepuncture (performed in 17/26). In 6/26, the abnormal response to CSM was delayed, occurring 62.8 +/- 28.4 s after completion of CSM. The response to CSM was predominantly of the mixed type (20/26) and abnormal on both sides in 14/26. CONCLUSIONS: An abnormal response to CSM may not indicate syncope caused by CSH and needs to be considered in the light of the patient's age, duration of syncopal episodes and detailed history of provocative stimuli. Differentiating CSH from VVS with an abnormal response to CSM has various implications from advice on driving to treatment strategies.
BACKGROUND AND PURPOSE: Carotid sinus massage (CSM) is commonly used to identify carotid sinus hypersensitivity (CSH) as a possible cause for syncope, especially in older patients. However, CSM itself could provoke classical vasovagal syncope (VVS) in pre disposed subjects. METHODS: Retrospective analysis of CSM, cardiovascular autonomic function tests (including tilt table testing) and medical history in 388 patients with recurrent syncope to identify and characterize patients in whom an abnormal response to CSM was more likely to reflect VVS than CSH. RESULTS: CSM was abnormal in 79 patients. In 53 patients (77.2 +/- 8.7 years), CSH was the likely cause of syncope. VVS was the more likely diagnosis in 26 younger patients (59.7 +/- 12.6 years) with longstanding syncope from youth, in whom fear or pain was as a trigger; 7/26 suffered from intense chronic or intermittent neck pain and one exacerbation of syncopal attacks followed a physical and emotional trauma to the neck. In VVS, 4/26 had spontaneous VVS during head-up tilt, another six after venepuncture (performed in 17/26). In 6/26, the abnormal response to CSM was delayed, occurring 62.8 +/- 28.4 s after completion of CSM. The response to CSM was predominantly of the mixed type (20/26) and abnormal on both sides in 14/26. CONCLUSIONS: An abnormal response to CSM may not indicate syncope caused by CSH and needs to be considered in the light of the patient's age, duration of syncopal episodes and detailed history of provocative stimuli. Differentiating CSH from VVS with an abnormal response to CSM has various implications from advice on driving to treatment strategies.