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Clinical context and outcome of carotid sinus syndrome diagnosed by means of the ‘method of symptoms’

Diana Solari, Roberto Maggi, Daniele Oddone, Alberto Solano, Francesco Croci, Paolo Donateo, Michele Brignole
DOI: http://dx.doi.org/10.1093/europace/eut283 928-934 First published online: 20 September 2013

Abstract

Aims The prevalence and outcome of carotid sinus syndrome (CSS) reported in the literature vary owing to differences in indications and methods of carotid sinus massage (CSM).

Methods and results We performed CSM on all patients aged 40 years and above with unexplained syncope after the initial evaluation. Carotid sinus massage was performed in the supine and standing positions on both sides for 10 s during continuous electrocardiogram and blood pressure monitoring; CSS was diagnosed in the event of an abnormal response to CSM in association with reproduction of spontaneous symptoms (‘method of symptoms’). From July 2005 to July 2012, CSS was found in 164 (8.8%) of 1855 patients (mean age 77 ± 9 years, 73% males): 81% had an asystolic reflex (mean pause 7.6 ± 2.2 s) and 19% a vasodepressor reflex (mean lowest systolic blood pressure 65 ± 15 mmHg). Potential multifactorial causes of syncope (orthostatic hypotension, bundle branch block, bradycardia, tachyarrhythmias) were found in 74% of patients. One hundred forty-one patients received the proper care [advice on lifestyle measures in all, discontinuation (#40) or reduction (#17) of antihypertensive drugs, pacemaker implantation (#57)] and were followed up for 39 ± 25 months. Syncope recurred in 23 patients; the actuarial syncopal recurrence rate was 7% at 1 year and 26% at 5 years. Total syncopal episodes decreased from 91 per year during the 2 years before evaluation to 21 episodes per year during follow-up (P = 0.001). On Cox proportional-hazards regression, a mixed or vasodepressor response to tilt testing was the only independent predictor of syncopal recurrence (hazard ratio = 1.8; P = 0.01).

Conclusion Carotid sinus massage by means of the ‘method of symptoms’ indentifies a clinical syndrome with definite features and outcome. A treatment strategy involving lifestyle measures, reduction of antihypertensive drugs and cardiac pacing when appropriate is effective in reducing the syncopal recurrence rate.

  • Carotid sinus syndrome
  • Carotid sinus massage
  • Syncope
  • Tilt table testing

What's new?

  • Carotid sinus massage by means of the ‘method of symptoms’ indentifies a clinical syndrome with definite prevalence, clinical features and outcome.

  • One or more potential multifactorial causes of syncope are present in 74% of CSS patients. Carotid sinus massage provides an additive diagnostic value to diagnosis based on initial evaluation because it is able to document the susceptibility to an abnormal or impaired reflex and is of help to guide therapy.

  • We were able to evaluate the overall long-term outcome of CSS patients. A treatment strategy involving lifestyle measures, the reduction of antihypertensive drugs and cardiac pacing determined a 77% reduction in the syncope burden after treatment compared with that of 2 preceding years. The fact that treatments modified the natural history of the disease—as indicated by the reduction in syncope burden after treatment—supports the definition of the clinical syndrome of CSS.

  • No prior study has evaluated the effect of hypotensive therapy in CSS during long-term follow-up.

Introduction

In its rare ‘spontaneous’ form, carotid sinus syndrome (CSS) is triggered by accidental mechanical manipulation of the carotid sinuses. In the more common form, no mechanical trigger is found and CSS is diagnosed in patients with unexplained syncope who show carotid sinus hypersensitivity (CSH) triggered by carotid sinus massage (CSM).1,2 The prevalence and outcome of ‘induced’ CSS vary widely in the literature, owing to differences in indications, methods of execution of CSM3, and the definition of CSS.

In our centre, CSM according to the ‘method of symptoms’1,2,4,5 is performed systematically on patients aged 40 years or above with syncope which remains unexplained after the initial evaluation. In this study, we assessed the prevalence, clinical context, and outcome of CSS in a large series of consecutive patients.

Methods

We analysed all consecutive patients who underwent CSM from July 2005 to July 2012 at the Syncope Unit of Ospedali del Tigullio, Lavagna. This is the only Syncope Unit of the district and has an estimated referral population of 180 000 inhabitants. It is located inside a general hospital endowed with 24 h emergency department and a cardiology ward with a coronary care unit. Patients are referred from the emergency room and from in-hospital and out-of-hospital services. The Unit is led by three syncope experts, with a more than 5 year expertise in syncope management who lead the comprehensive management of the patient from risk stratification to diagnosis, therapy, and follow-up.6

The only patients excluded were those with permanent pacemakers. During that period, the Syncope Unit applied a standardized protocol of management of syncope, drawn up in accordance with the 2004 guidelines of the European Society of Cardiology.1 According to this protocol, CSM was performed on all patients aged 40 years and above with syncope whose diagnosis had remained uncertain after the initial evaluation or because no cause could be found or because contrasting findings were present. The initial evaluation consisted of history, physical examination, standard electrocardiogram, systemic blood pressure (BP) measurement in the supine and upright positions, and, if appropriate, echocardiogram and electrocardiogram monitoring. The diagnosis was considered established—and CSM was not performed—when the criteria for certain diagnosis defined by the above guidelines were met. In particular, CSM was not performed in case of

  • Reflex, classical vasovagal syncope if the syncope was precipitated by emotional distress (fear, severe pain, and instrumentation) or prolonged standing and was associated with typical prodromes.

  • Reflex, situational syncope if the syncope occurred during or immediately after urination, defecation, coughing, laughing, or swallowing.

  • Orthostatic hypotension if syncope occurred after standing up and symptomatic orthostatic hypotension was documented.

  • Cardiac arrhythmia if there was documentation of persistent sinus bradycardia less than 40 beats/min or repetitive sinoatrial blocks or sinus pauses >3 s; Mobitz II second or third degree atrioventricular block; alternating left and right bundle branch block; rapid paroxysmal supraventricular tachycardia or ventricular tachycardia.

  • Structural cardiac or cardiopulmonary disease if the patient was affected by acute cardiac ischaemia or other acute cardiopulmonary diseases or prolapsing atrial myxoma or severe aortic stenosis.

Thus, CSM was performed immediately after an unremarkable initial evaluation; if CSS was found, the investigation was stopped and therapy started. Moreover, potential multifactorial causes of syncope were assessed.

Carotid sinus massage was performed during continuous electrocardiographic and non-invasive BP monitoring with the Task Force Monitor® (CNSystem),7 and consisted of manual compression with the tips of the second, third, and fourth fingers of one hand, at the site of the maximum carotid pulse, between the angle of the jaw and the cricoid cartilage on the anterior margin of the sternocleidomastoid muscle, with the face rotated contralaterally. The massage was applied up and down the carotid artery on the right and left sides in both the supine and upright positions for 10 s, to allow symptoms to develop; the time interval between massages had to be long enough for baseline heart and BP values to be restored.

By means of the ‘Method of Symptoms’, CSH was diagnosed when CSM elicited abnormal cardioinhibition (i.e. asystole >3 s) and/or vasodepression (i.e. fall in systolic BP >50 mmHg); CSS was established when spontaneous symptoms (syncope or pre-syncope) were reproduced in the presence of CSH.1,2,4,5 Thus, CSH alone was not considered diagnostic owing to its low specificity,2,3,8 since it can be frequently observed in the general older population.8 Once CSS was established, the evaluation was usually completed by means of tilt table testing, which was performed according to the Italian protocol9 in order to investigate the susceptibility of patients to orthostatic stress.

Treatment and follow-up

In all patients, initial treatment comprised education regarding the awareness and possible avoidance of triggers (e.g. hot crowded environments, volume depletion), early recognition of prodromal symptoms, and the performance of maneuvers to abort the episode (e.g. supine posture, physical counterpressure maneuvers). If possible, triggers were addressed directly, such as avoiding micturition in the standing position. Patients evaluated for the first episode of syncope and those with pre-syncope in general received only the above lifestyle counseling, without any specific treatment. Patients with recurrent syncopes and those at risk of traumatic injuries underwent cardiac pacemaker implantation and/or advice on the discontinuation/reduction of antihypertensive drugs, as appropriate, in addition to the above lifestyle advice.

For the purpose of this study, the patients' outcome was analysed in October to November 2012 by retrieving their clinical records, if available. Patients were also interviewed over phone or during a clinical visit, if appropriate. This investigation concerned recurrences of syncope and/or pre-syncope and other major clinical events.

Statistical analysis

Continuous data are shown as average±SD or median (25th–75th percentile), as appropriate. The Shapiro–Wilks test was performed to check the skewness of distributions. Absolute and relative frequencies were used to show categorical data. The unpaired Student's t test and the non-parametric Mann–Whitney test were used to compare continuous variables, as appropriate. Fisher's exact test was used to compare proportions.

The primary analysis of the study was the comparison of the syncope burden, which was defined as the number of episodes of syncope per patient per year. Pre-syncope episodes were not counted in the syncope burden. For each patient, the ‘syncope burden’ during the two years before diagnostic CSM was compared with the burden during follow-up. Since the count of the referral syncope (i.e. the episode prompting the first visit) among the episodes before treatment would have biased syncope burden comparison in favour of a reduction of burden with treatment, referral syncope was not counted. Kaplan–Meier survival estimates were calculated for the time to the first syncopal recurrence and to death. The Cox proportional hazards regression technique was used to analyse the causal relationship between recurrence of syncope during follow-up and the baseline clinical variables (listed in Table 4) that, on univariate analysis, had a P value of <0.1.

Results

Carotid sinus hypersensitivity was found in 453 (24%) of 1855 patients who underwent CSM (Figure 1): of these, asystole ≥3 s was present in 258 and vasodepression alone in 195 patients. Carotid sinus syndrome was found in 164 (8.8%) patients. Carotid sinus syndrome patients had a mean age of 77 ± 9 years; 73% were males; 150 patients had a history of syncope [median 2 (IQR 1–3)], while 14 patients had pre-syncope only.

Figure 1

Screening of the patients.

The results of CSM are shown in Table 1. The massage induced a similar fall in BP in patients with an asystolic response and in those with a vasodepressor response alone, but syncope was induced more frequently in those with an asystolic response. The maximum response was obtained in the standing position in 72% of asystolic and in 100% of vasodepressor forms.

View this table:
Table 1

Carotid sinus massage results

Asystole (132 patients)No asystole (32 patients)P
Maximum RR interval (s)7.6 ± 2.21.9 ± 0.70.001
Baseline SBP (mmHg)126 ± 17120 ± 150.12
Minimum SBP (mmHg)63 ± 2265 ± 150.68
Fall in SBP (mmHg)63 ± 2456 ± 170.10
Syncope93 (70%)15 (47%)0.01
Pre-syncope39 (30%)17 (53%)
Site of maximum response
 Supine right24 (18%)0 (0%)0.002a
 Supine left13 (10%)0 (0%)
 Standing right70 (53%)19 (59%)
 Standing left25 (19%)13 (41%)
  • aChi-square test.

  • SBP, systolic blood pressure.

One or more potential multifactorial causes of syncope were present in 74% of CSS: symptomatic orthostatic hypotension in 12 patients, asymptomatic orthostatic hypotension in 34, bundle branch block in 23, suspected bradycardia (sinus bradycardia 40–50 bpm or first degree atrioventricular block) in 36, atrial tachyarrhythmias in 36, severe aortic stenosis in 2, and severe anemia in 2. In addition, tilt table testing was performed in 112 patients and was positive in 71 (63%) patients.

Follow-up data were available in 141 patients. All these patients received advice on lifestyle measures. In addition, preexisting hypotensive drug therapy was discontinued in 40 patients and reduced in 17 (Table 2), and 57 patients underwent pacemaker implantation. Of those with a pacemaker, 18 had coexisting bundle branch block and 22 had bradycardia.

View this table:
Table 2

Hypotensive drug therapy during the study

EnrolmentDischargePLast follow-up visitP (vs. enrol)
No. of patients on ≥1 hypotensive drug/s96 (68%)77 (55%)a0.00580 (57%)0.002
Total no. of drugs198146b159
Mean no. of drugs per patient (total pts)1.4 ± 1.11.0 ± 1.20.0011.2 ± 1.30.01
Mean no. of drugs per patient on treatment2.1 ± 1.11.9 ± 1.1a0.0012.0 ± 1.10.32
  • aDosage reduced in 17 of these patients.

  • b≥1 drug/s discontinued in 40 patients.

During a mean follow-up of 39 ± 25 months, syncope recurred in 22 patients and developed in 1 patient who had had pre-syncope only before enrolment; pre-syncope occurred in 25 patients. Five (3.5%) patients suffered trauma secondary to syncope recurrence. The actuarial syncopal recurrence rate was 7% [95% confidence interval (CI) ±2%] at 1 year, 12% (95% CI ±3%) at 3 years, and 26% (95% CI ±6%) at 5 years. Total syncopal episodes decreased from 91 per year during the 2 years before evaluation to 21 episodes per year during follow-up (Table 3). A diagnosis different from CSS was established during follow-up in 11 (8%) patients: paroxysmal atrioventricular block (#5), sinus arrest (#1), paroxysmal tachyarrhythmias (#4), and epilepsy (#1).

View this table:
Table 3

Yearly syncope burden

 Before diagnosisAfter diagnosisP value
Total no./yearNo. per patient/yearTotal no./yearNo. per patient/year
Total population (n = 141), median (IQR)910.5 (0–1)210 (0–0)0.001
Patients with pacemaker (n = 57), median (IQR)360.5 (0–1)140 (0–0)0.001
Patients with hypotensive drugs on enrolment (n = 96), median (IQR)740.5 (0–1)130 (0–0)0.001
  • IQR, interquartile range.

On univariate analysis, among the variables listed in Table 4, male gender, high median number of syncopes during the previous 2 years, and a non-asystolic positive response during tilt table testing were predictors of syncope recurrence during follow-up. In particular, potential cardiac causes of syncope were not predictive of pacemaker success. For example, among the eight patients who had syncope after pacemaker implantation, four had bundle branch block. On Cox proportional hazards regression, a mixed or vasodepressor response to the tilt test was the only independent predictor of syncopal recurrence [hazard ratio = 1.8 (95% CI 1.14–2.86); P = 0.01]. At 5 years, the actuarial syncope recurrence rate was 48% (95% CI ±11%) in patients who had had a positive mixed or vasodepressor tilt test, whereas it was only 7% (95% CI ±6%) in those with a positive cardioinhibitory response and 16% (95% CI ±6%) in those who had not undergone the test (Figure 2).

View this table:
Table 4

Univariate predictors of syncopal recurrences

Recurrence (23 patients)No recurrence (118 patients)P value
Mean age (years)79 ± 576 ± 90.13
Males12 (52%)88 (74%)0.04
Median no. of syncope during the 2 previous years (IQR)2 (1–3.5)1 (1–1.8)0.05
Syncopes without prodromes or short (<10 s) prodromes9 (39%)54 (46%)0.64
History of syncope ≤2 years12 (52%)69 (58%)0.65
History of syncope ≥10 years5 (22%)27 (23%)1.00
Pre-syncope7 (30%)39 (33%)1.00
Unexplained fall3 (13%)5 (4%)0.12
Any trauma secondary to syncope9 (39%)39 (33%)0.63
Hypertension12 (52%)60 (51%)1.00
Diabetes3 (13%)19 (16%)1.00
Abnormal electrocardiogram11 (48%)58 (49%)1.00
Structural heart disease8 (35%)34 (29%)0.62
Neurological diseases2 (9%)14 (12%)1.00
Baseline systolic blood pressure129 ± 16135 ± 190.58
Competing diagnoses
 Symptomatic orthostatic hypotension2 (9%)10 (8%)1.00
 Asymptomatic orthostatic hypotension5 (22%)22 (19%)0.77
 Bundle branch block4 (17%)19 (16%)1.00
 Bradycardia (sinus or first degree atrioventricular block)3 (13%)28 (24%)0.41
 Atrial tachyarrhythmias4 (4%)28 (24%)0.60
 Others (aortic stenosis, anemia)0 (0%)3 (3%)1.00
Carotid sinus syndrome forms
 Asystolic19 (83%)98 (83%)1.00
 Non-asystolic (vasodepressor only)4 (17%)20 (17%)1.00
 Tilt table test performed20 (87%)74 (63%)0.03
 Tilt-induced syncope15 (65%)44 (37%)0.02
 Non-cardioinhibitory response14 (61%)30 (13%)0.002
 Cardioinhibitory response1 (4%)14 (12%)0.46
Treatment at baseline
 Hypotensive drugs17 (74%)79 (67%)0.62
 Number of hypotensive drugs per patient2.3 ± 1.22.0 ± 1.10.34
  • IQR, interquartile range.

Figure 2

Recurrence of syncope according to tilt test results.

During follow-up, 19 patients died; the actuarial death rate was 2% (95% CI ±1%) at 1 year, 8% (95% CI ±3%) at 3 years, and 18% (95% CI ±4%) at 5 years. Other major non-fatal clinical events were stroke (#5), myocardial infarction (#3), heart failure (#11), and trauma secondary to syncope recurrence (#5).

Discussion

In this cross-sectional study, we assessed the prevalence, clinical context, and outcome of CSS, as diagnosed according to the method of symptoms. The strengths of the study are the consecutiveness of inclusion of patients, the systematic application of indications according to guidelines and the utilization of a uniform technique for CSM. Thus, the study provides a picture of the syndrome in the real world.

For the above reasons, the study is able to explain the apparent, and sometimes striking, differences in the findings reported in the literature. Manual massage of the carotid sinus is rather crude and subjective. The heterogeneity of the technique regards the duration of the stimulus applied, the force of the stimulus, how pressure is applied, i.e. phasic massage or static pressure, and the implications of carotid artery occlusion.3

The technique of performing CSM has evolved greatly over the years. Compared with the technique used before the 1980s, modern CSM involves performing massage in the standing position, usually with the aid of a tilt table, under continuous non-invasive BP monitoring. In addition to yielding a higher positivity rate than supine massage only, upright massage has the advantage of enabling better evaluation of the magnitude of the vasodepressor component, which is amplified by the standing position.5,10 In this study, the maximum response was obtained in the standing position in 72% of asystolic and in 100% of vasodepressor forms (Table 2). In the past, the vasodepressor component of the reflex was underestimated. Now, however, with the introduction of continuous BP measurement and execution of CSM in the standing position, a vasodepressor component can be identified in most patients with an asystolic response.11,12 In this study, the minimum BP observed and the magnitude the fall in BP were indistinguishable between asystolic and pure vasodepressor forms (Table 2). A study by Krediet et al.13 suggests that a fall in cardiac output is the mechanism responsible for the vasodepressor effect observed during upright massage.

Reproduction of symptoms is required in order to diagnose CSS by means of the method of symptoms. This is the main difference from the classical method, according to which the induction of asystole >3 s and/or fall in BP >50 mmHg (here defined as CSH) is considered sufficient for diagnosis. Indeed, the classical method is regarded as too lenient, owing to its low specificity.2,3,12 It is well known that CSH is observed up to 38% in patients without syncope who are affected by various types of cardiovascular diseases.1 In a recent study by Kerr et al.,8 in which CSM was performed in an unselected community sample of 272 older people, CSH was found in 39% of subjects and in 35% of a subset of 80 previously asymptomatic individuals. Similar positivity rates have been reported in the literature in patients with unexplained syncope. For example, pooled data from four studies performed in elderly patients with syncope showed a positive response rate of 35% (235 of 663 patients).1 Thus, the authors correctly questioned the clinical utility of the classical method of CSM. However, in Kerr et al.'s study,8 syncope was induced only in a minority of CSH patients (6.7% of unselected community sample and 5% of asymptomatic subset). These figures are consistent with the findings of this study. Indeed, we found CSH in 24% of our patients and CSS in about one-third of these (8.8%). Thus, a minority of CSH patients are affected by CSS, as defined according to the method of symptoms. In this study, we did not evaluate the specificity of the method of symptoms. This has previously been calculated to be 4% in control subjects without syncope.1

An important original feature of this study is that we were able to evaluate the overall long-term outcome of the patients. We observed a 77% overall reduction in the syncope burden after treatment compared with that of 2 preceding years. The fact that treatments modified the natural history of the disease—as indicated by the reduction in syncope burden after treatment—support the definition of the clinical syndrome of CSS. Owing to the lack of a control group, we could not evaluate the efficacy of any single therapy. This reduction was marked in patients who received a pacemaker (61% reduction) and in those whose hypotensive therapy was withdrawn/reduced (82% reduction). To the best of our knowledge, no prior study has evaluated the effect of hypotensive therapy in CSS during long-term follow-up. The present findings are consistent with those of a randomized acute cross-over trial which showed that chronic vasodilator therapy determined a persistence of hypotension for a longer time after CSM and that this could indirectly potentiate the severity of the clinical manifestations of the syndrome.14 The present findings are also consistent with the study of van der Velde et al.,15 who showed that withdrawal of fall-risk drugs determined a significant reduction of orthostatic hypotension and CSS. A meta-analysis16 of three controlled trials4,17,18 of the efficacy of pacemaker therapy, in which CSM was performed according to the ‘method of symptoms’, showed that, during an observation period of up to 3.3 years, syncope recurred in 9% of patients treated with a pacemaker and in 38% of untreated control patients. The cumulative odds ratio was 0.15 (95% CI 0.06–0.36). In this study, syncope recurred in 14% of patients during 3.2 years of follow-up. Finally, a beneficial effect of lifestyle measures as consequence of education regarding awareness and possible avoidance of triggers, early recognition of prodromal symptoms, and performing maneuvers to abort the episodes is likely, even though never previously assessed, and is consistent with a similar benefit observed by Romme et al.19 in patients affected by vasovagal syncope. These authors found a significant decrease of the syncope burden from a median of three episodes during the year before to a median of zero episode in the first year of non-pharmacological treatment.

Admittedly, the cross-sectional design and the lack of a control group do not allow us to draw definite conclusions regarding the efficacy of therapy. Indeed, we cannot exclude the alternative explanation that the reduction in syncope burden might have been due to the natural history of the syndrome and not to the effect of the treatments. It is known that syncopal recurrence is not constant but rather fluctuates over time, peaking at the time of evaluation. In order to minimize this phenomenon, we excluded from the calculation the referral syncope (i.e. the episode prompting the first visit). Moreover, we considered a sufficiently long period (2 years before and more than 3 years after evaluation), which should limit the effect of spontaneous fluctuation.

The consecutiveness of the population offers a reliable picture of the prevalence and clinical context of CSS and suggests some possible reasons for syncopal recurrence during follow-up. Given an estimated referral population of 180 000 inhabitants and the observed prevalence of CSM of 1855 patients and of CSS of 164 patients (Figure 1), CSM was performed to 1.5 per 1000 person/year and CSS was found in 0.13 per 1000 person/year. Since the yearly prevalence of syncope in the general population aged 70–79 years can approximately be estimated to range from 11 per 1000 person/year in the Framingham study20 to 28 per 1000 person/year in the Utah study,21 our figures mean that CSM was performed in one patient every 7–19 affected by syncope and CSS was finally diagnosed in one patient every 85–215 affected by syncope.

Who underwent CSM in this study? Carotid sinus massage was performed immediately after an unremarkable initial evaluation. Even if a formal screening log was not kept for this population, we estimare that CSM was not performed in about 20% of patients aged above 40 years who had already a certain diagnosis made at initial evaluation.6 Thus, CSM was performed in patients aged above 40 years not only with no explanation of the cause of syncope but also in patients in whom the initial evaluation already suggested a possible cause of syncope. One or more potential multifactorial causes of syncope were present in 74% of CSS patients (Table 4). The association with sinus node disease and orthostatic hypotension is well known in the literature.22,23 The relative role of associated potential causes of syncope is uncertain. Although no evident correlation emerged between associated potential causes of syncope and syncopal recurrence during follow-up, therapy could have masked the effects of such comorbidities. Conversely, a different diagnosis was made during follow-up in 8% of patients, which partly explains syncopal recurrences. Assuming that these cases were false-positive responses to CSM, this figure could be an approximate measure of the true specificity of the ‘method of symptoms’. A mixed or vasodepressor response during tilt table testing was the only predictor of syncopal recurrence. This fact has already been established24 and suggests that a more complex impairment of autonomic regulation of systemic BP is present in CSS patients.

Limitations

History taking and CSM are highly operator-dependent diagnostic tests. In this study the evaluation was performed by a small number of expert operators with a precise standardized protocol inside a structured organization. Results might be different if the tests were performed in different settings.

We were unable to provide a screening log and the final diagnosis of all syncope patients referred to our hospital and evaluated by our Syncope Unit during the study period. The description of the organizational model and some demographical data reported in the Methods section may be of help in order to provide a perspective of the selection of the population who underwent CSM.

Conclusions

In the literature, the technique of CSM is heterogeneous, making comparison difficult. According to the ‘method of symptoms’, a minority of CSH patients are affected by CSS. Carotid sinus massage performed by means of such method indentifies a clinical syndrome with definite features and outcome. The low rate of competing diagnoses during long-term follow-up indicates a good specificity. A treatment strategy involving lifestyle measures, the reduction of antihypertensive drugs and cardiac pacing when appropriate is effective in reducing the syncopal recurrence rate. The results of this study do not apply to CSS diagnosed by means of other techniques.

The bottom line is that a large symptomatic fall in BP induced by CSM is an indicator of a susceptibility to reflex syncope in the elderly that can be triggered in various ways. It is not a specific condition. By applying the label CSS to all patients aged above 40 years with symptomatic CSM who do not have a certain diagnosis after the initial evaluation regardless of the medical history an overlap between CSS and a likely clinical diagnosis based on the clinical history is inevitable. Many of these patients might be diagnosed as having a possible reflex syncope or orthostatic (drug-induced) hypotension. We do believe that the two diagnoses can co-exist. Carotid sinus massage provides an additive diagnostic value to diagnosis based on initial evaluation because it is able to document the susceptibility to an abnormal or impaired reflex and, as suggested by the result of this study, is of help to guide therapy. On the other hand, however, CSS should be interpreted in the clinical context of the comprehensive clinical evaluation.

Authors' contributions

All authors had full access to all the data in the study, Dr Solari and Dr Brignole take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Solari, Brignole, Maggi.

Acquisition of data: Solari, Maggi.

Analysis and interpretation of data: All authors.

Drafting of the manuscript: Solari, Brignole.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Brignole.

Disclaimer: The authors take full responsibility for the accuracy and completeness of the ideas presented and the interpretation and reporting of the data.

Conflict of interest: none declared.

References

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