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Heart rate and blood pressure responses to carotid sinus massage in healthy elderly subjects.


The purpose of the study was to define heart rate and blood pressure responses to surpine and upright carotid sinus massage in healthy elderly subjects and thus to establish the validity of current diagnostic criteria for carotid sinus syndrome in this age group.

Twenty-five healthy asymptomatic subjects (61-87 years) had carotid sinus massage carried out following a standardized technique employing previously defined criteria for abnormal heart rate and blood pressure responses: 3 s asystole and a 50 mmHg fall in systolic blood pressure independent of any heart rate slowing (after intravenous atropine).

No cardioinhibitory responses of greater than 3 s were documented. The mean maximal cardioinhibitory response was 1038 [+ or -] 195 msec. Right-sided responses were more marked than left when upright (1040 [+ or -] 202 vs. 946 [+ or -] 135 msec; p [less than] 0.01) but not when surpine (1094 [+ or -] 215 vs. 1074 [+ or -] 197 msec; NS).

After atropine three subjects (12%) had a significant vasodepressor response when upright, but none when supine. The mean maximal vasodepressor response was 21 [+ or -] 14 mmHg. Right-sided blood pressure responses were more marked than left (p [less than] 0.01). There was no fixed relationship between maximum heart rate slowing and the degree of vasodepression during massage (range 2-80 msec/mmHg).

The diagnostic criteria for heart rate and blood pressure responses in carotid sinus syndrome are appropriate for surpine carotid sinus massage in elderly subjects. Asymptomatic vasodepressor responses occur in a small proportion of healthy elderly when upright.


Carotid sinus syndrome is an underdiagnosed cause of dizziness and syncope particularly in elderly patients. Three clinical subtypes of the syndrome are defined by heart rate and systolic blood pressure responses to carotid sinus massage [1]: (1) cardioinhibition--3 s or more of asystole, (2) vasodepression--a 50 mmHg or more fall in systolic blood pressure whilst surpine or upright, (3) mixed response--a combination of cardioinhibition and vasodepression.

The afferent limb of the reflex is predominantly via the glossopharyngeal nerve. Impulses are modulated at the cardiovascular centre in the brain-stem. The efferent limb of the reflex is twofold: vagal excess to cardiac nerves (and hence sinoatrial and atrioventricular nodes) and withdrawal of sympathetic activity to the peripheral vasculature (resulting in peripheral vasodilatation and hypotension). The cardioinhibitory respose is abolished by atropine which affords definition of the vasodepressor response independent to heart rate slowing [2].

Recent prospective studies of elderly patients attending a syncope clinic with recurrent unexplained symptoms have reported abnormal cardioinhibitory responses in 25% and abnormal vasodepressor responses (predominantly during upright carotid sinus massage) in 40% [3, 4]. In view of these high diagnostic rates in selected patients, we considered the possibility that haemodynamic responses to massage might be modified by ageing alone and that the accepted diagnostic criteria in particular for vasodepressor carotid sinus syndrome may require re-evaluation in elderly patients. Moreover there are no data for normal heart rate and blood pressure responses to carotid sinus massage during upright posture or for the reproducibility of the response.

The purpose of this study was to define heart rate and blood pressure responses to surpine and upright carotid sinus massage in healthy elderly subjects and thus to assess the validity of accepted diagnostic criteria for carotid sinus syndrome in this age group.


Twenty-five healthy elderly subjects (11 men) with no previous history of dizziness, falls or syncope were studied. They had no intercurrent illness and were not taking any medications. All had a normal 12-lead surface electrocardiograph (ECG). Subjects were restricted by poster advertising in public areas; their mean age was 69 years, range 61-87 years.


Local ethical committee approval for the study was obtained.

Longitudinal massage of the carotid sinus (level with the upper border of the thyroid cartilage) was performed for 5 s on right and left sides allowing a minimum interval of 1 min between tests (for return of the baroreflex gain to baseline). Right- and left-side carotid sinus massage was repeated during 70 [degrees] head-up tilt (Akron automated tilt table: footplate support). Surface ECG and non-invasive beat-to-beat blood pressure measurements (Finapres: digital photoplethysmography) were made throughout.

The entire procedure was repeated following the administration of 600 [mu]g intravenous atropine which abolished cardioinhibition and allowed definition of the pure vasodepressor response. Carotid sinus massage was performed by the same investigator in all subjects. It was repeated at least once in each position and the greater response was used for analysis. In six individuals massage was repeated three times in each position to allow assessment of the reproducibility of the response.

Data Analysis

The mean of 10 consecutive R-R intervals (ms) and systolic blood pressure readings mmHg prior to the onset of massage were used as baseline measurements. The cardioinhibitory response was defined as the maximum heart rate slowing (expressed as the longest R-R interval) during carotid sinus massage. The change in the R-R interval from baseline was also calculated. The vasodepressor response was the maximum fall in systolic blood pressure from baseline. Changes were analysed for statistical significance using paired t tests. The times from the onset of massage to the blood pressure nadir and to the recovery of baseline levels were also measured. Reproducibility was assessed by calculating the coefficient of variation for cardioinhibitory and vasodepressor responses in each position in the six subjects who underwent repeated carotid sinus massage. Correlation coefficients were calculated for baseline R-R versus change to maximum R-R and maximum R-R versus maximum vasodepression.


No subject had asystole of 3 s or more during carotid sinus massage. The average maximum R-R interval was 1038 [+ or -] 195 ms (range 700-1540 ms). Right and left supine responses were similar (1094 [+ or -] 215 vs 1073 [+ or -] 194 ms; NS]. Posture did not influence heart rate responses on the right (supine 1094 [+ or -] 215 vs upright 1040 [+ or -] 202 ms; NS] but upright responses were less than supine on the left side (supine 1073 [+ or -] 194 vs. upright 946 [+ or -] 135 ms; p [less than] 0.01) (Figure 1). There was no fixed correlation between the baseline heart rate and degree of heart rate slowing during carotid sinus massage (r = 0.30; NS).

In no subject was the vasodepressor response 50 mmHg or greater when supine after atropine. When upright, three (12%) had a reproducible vasodepressor response excluding 50 mmHg; two with right-sided and one with left-sided massage. The average response was 21 [+ or -] 14 mmHg (range 1-89 mmHg). Right-sided blood pressure responses were greater than left both supine and upright (right supine 19 [+ or -] 11 vs. left supine 14 [+ or -] 7 mmHg; p [less than] 0.01, and right upright 29 [+ or -] 19 vs. left upright 21 [+ or -] 13 mmHg; p [less than] 0.01). Upright responses were greater than supine for both sides (p [less than 0.01) (Figure 2).

The mean time to the blood pressure nadir was 17 [+ or -] 4 s was recovery to baseline levels at 30 [+ or -] 6 s. Before the administration of atropine the median change in R-R interval per mmHg fall in systolic blood pressure was 9 ms. Although heart rate responses correlated with falls in blood pressure (r = 0.62; p [less than] 0.001), the relationship for individual subjects between the degree of heart rate slowing and the fall in systolic blood pressure varied between extremes of 2 and 80 ms mmHg vasodepression. For repeated episodes of carotid sinus massage, the coefficients of variation for cardioinhibitory responses were: right supine 6% (range 2-10%) and left supine 7% (range 3-10%). Corresponding values for vasodepressor responses were more variable: 35% (range 15-66%) and 65% (range 23-132%). There was no sex differrence in cardioinhibitory or vasodepressor responses.


Carotid sinus syndrome is an important but frequently overlooked cause of dizziness and syncope [5]. It is diagnosed in a symptomatic individual when carotid sinus massage produces asystole exceeding 3 s (a cardioinhibitory response), fall in systolic blood pressure exceeding 50 mmHg (a vasodepressor response) or a combination of the two (a mixed response) [1]. Recent studies have demonstrated a clear link between carotid sinus hypersensitivity and previously unreported symptoms of bradycardia [6]. Moreover, in centres which routinely assess patients with such symptoms for abnormal cardioinhibitory responses, the pacing rates for carotid sinus syndrome exceed those for sinus node disease: 40 versus 37 cardiac pacemaker implants per million population per year [7].

The incidence of carotid sinus syndrome increases with age [8]. The cardioinhibitory subtype which is reported to account for up to 80% of cases [1] was recently diagnosed in 25% of elderly patients attending a syncope clinic with recurrent, unexplained symptoms [3]. Abnormal prolongation of the cardioinhibitory response to carotid sinus massage does not, however, occur as a part of the normal ageing process: previous investigators have shown that although responses exceeding 3 s occur more frequently in the presence of coronary artery disease and hypertension [8, 9] they do not occur in healthy elderly people when the duration of massage is standardized to 5 s [10]. The results of the present study are in keeping with these findings. None of the healthy controls had an abnormal cardioinhibitory response to carotid sinus massage either supine or upright--the mean maximal R-R interval during massage was approximately 1 s. Additionally, no correlation was foiund between the baseline heart rate and subsequent change during carotid sinus massage.

Previously published data suggest that pure vasodepressor carotid sinus syndrome is a rare condition accounting for only 5-10% of cases [1]. The rapid blood pressure response following massage has until recently proved difficult to measure routinely without intra-arterial cannulation and investigators have been reluctant to do this on a large scale in symptomatic patients. Using the non-invasive technique of digital photoplethysmography, abnormal vasodepressor respoinses to either supine or, more frequently, upright carotid sinus massage have recently been demonstrated in up to 40% or elderly patients referred to a syncope clinic with recurrent unexplained symptoms [4]. This high frequency of response exceeding 50 mmHg led to speculation regarding the validity of the accepted diagnostic criteria for vasodepressor carotid sinus syndrome in elderly subjects. No previous studies have examined age-associated changes in the vasodepressor response to carotid sinus massage. Moreover, although upright carotid sinus massage is increasingly being used as a means of assessing symptoms reproduction (in itself a controversial issue) [11, 12], there is a paucity of data regarding normal blood pressure and, indeed, heart rate responses to upright carotid sinus massage.

In the present study, none of the healthy controls had an abnormal vasodepressor response during carotid sinus massage when supine, suggesting that the accepted criteria are applicable to elderly patients when massage is performed in this position. Blood pressure responses were significantly greater following carotid sinus massage performed during head-up tilt, when reproducibly abnormal (although asymptomatic) responses were demonstrated in 12a%. Follow-up of these subjects will help to clarify the significance of these responses.

Previous investigators have demonstrated abnormal cardioinhibitory responses more frequently with right-compared with left--sided carotid sinus massage [1]. In the present study although no abnormal heart rate responses were documented, right-sided responses were greater than left during upright but not supine massage. Of note was the previously unreported finding that vasodepressor responses in healthy subjects are also greater on the right during both supine and upright carotid sinus massage. The reproducibility of the response was more consistent for heart rate than for blood pressure responses.

The exact site of the lesion in carotid sinus syndrome is not known. It is unlikely that the abnormality lies within the carotid sinus itself, since symptoms are not invariably triggered by head movement but may be precipitated by vagal stimuli [13]. Likewise, afferent baroreceptor pathways appear to be intact since the release of arginine vasopressin during hypotension (which is dependent upon intact connections with the hypothalamus) remains normal in patients with the syndrome [14]. Efferent pathway function in this condition has been less extensively studied but there is no evidence of target organ hypersensitivity to cholingeric stimulation [15]. By a process of exclusion it would appear most likely that carotid sinus syndrome results from a central abnormality of baroreflex gain. Although the cause of this abnormality is also ill-understood, the frequent association of carotid sinus syndrome with arteriosclerotic diagnoses has led to speculation that ischaemia may play an important role in its pathogenesis [9]. This might act at either myocardial level causing activation of vagal afferents capable of modulating central baroreflex pathways or directly at brain-stem level resulting in abnormalities of neurotransmitter function [9, 16].

In conclusion, prolonged slowing of the heart rate in response to carotid sinus massage does not occur in healthy elderly subjects. Furthermore, significant vasodepressor responsed do not occur when supine and occur in only 12% when upright. The diagnostic criteria for carotid sinus syndrome are valid for supine carotid sinus massage in elderly subjects. The significance of vasodepressor responses elicited in patients in the upright position requires further definition.


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[2.] Walter PF, Crawley IS, Dorney ER. Carotid sinus hypersensitivity and syncope. Am J Cardiol 1978;41:396-403.

[3.] Kenny RA, Traynor G. Carotid sinus syndrome: clinical characteristics in elderly patients. Age Ageing 1991;20:449-54.

[4.] McIntosh SJ, Da Costa D, Kenny RA. Outcome of an integrated approach to the investigation of dizziness, falls and syncope in elderly patients referred to a 'syncope' clinic. Age Ageing 1993;22:53-8.

[5.] Strasberg B, Sagie A, ERdman S, Kusniec J, Sclarovsky S, Agmon J. Carotid sinus hypersensitivity and the carotid sinus syndrome. Prog Cardiovasc Dis 1989;31:379-91.

[6.] Hudson WM, Morley CA, Perrins EJ, Sutton R. Is a hypersensitive carotid sinus reflex relevant? PACE 1983;6:A-18.

[7.] Brignole M, Menozzi C, Lolli G, Oddone D, Gianfranchi L, Bertulla A. Pacing for carotid sinus syndrome and sick sinus syndrome. PACE 1990;13:2071-5.

[8.] Thomas JE. Diseases of the carotid sinus: syncope. In: Vinken PJ, Bruyn GW, eds. Handbook for clinical neurology vol 11. Amsterdam: North Holland Publishing, 1972;532-51.

[9.] Brown KA, Maloney JA, Smith HC, Hartzler GO, Ilstrup DM. Carotid sinus reflex in patients undergoing coronary angiography: relationship of degree and location of coronary artery disease in response to carotid sinus massage. Circulation 1980;62:697-703.

[10.] Smiddy J, Lewis HD, Dunn M. The effect of carotid massage in older men. J Gerontol 1972;27:209-11.

[11.] Sugrue DD, Gersh Bj, Holmes DR, Wood DL, Osborn MJ, Hammill SC. Symptomatic isolated carotid sinus hypersensitivity: natural history and results of treatment with anticholingeric drugs or pacemakers. J Am Coll Cardiol 1986;7:158-62.

[12.] Morley CA, Sutton R. Carotid sinus syncope. Int J Cardiol 1984;6:287-93.

[13.] McIntosh SJ, Lawson J, Kenny RA. The clinical characteristics of vasodepressor, cardioinhibitory and mixed carotid sinus syndrome in the elderly. Am J Med (In Press).

[14.] Kenny RA, Lyon CC, Ingram AM, Bayliss J, Lightman SL, Sutton R. Enhanced vagal activity and normal arginine vasopressin response in carotid sinus syndrome: implications for a central abnormality in carotid sinus hypersensitivity. Cardiovasc Res 1987;21:545-50.

[15.] Morley CA. A study of the mechanism of carotid sinus hypersensitivity and the treatment of carotid sinus syndrome. DM Thesis. University of Oxford 1985;173-80.

[16.] Baig MW, Kaye GC, Perrins EJ. Can central neuropeptides be implicated in carotid sinus reflex hypersensitivity? Med Hypotheses 1989;28:255-9.
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Author:McIntosh, Shona J.; Lawson, Joanna; Kenny, Rose Anne
Publication:Age and Ageing
Date:Jan 1, 1994
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