ABC | Volume 111, Nº1, July 2018

Original Article Wu et al Carotid sinus massage in syncope evaluation Arq Bras Cardiol. 2018; 111(1):84-91 by the classical blood pressure criteria for the diagnosis of CSH (a fall in SBP ≥ 50 mmHg), as compared with the ≤ 85 mmHg SBP cut‑off value. Therefore, they offered this standardized objective methodology of classification of the VD reflex component to be used in clinical practice. 26 Few large-scale studies have evaluated the diagnostic value of CSM. When positive, it suggests a tendency or predisposition to carotid sinus syndrome; however, this does not establish it as the cause of the patient’s syncope, with no “ideal” protocol, given that there is an inexorable trade-off between sensitivity and specificity without a “gold standard” test to prospectively validate it in populations with rigorously defined carotid sinus syndrome. Likewise, the reproduction of spontaneous symptoms to confirm the diagnosis as recommended by the European Society of Cardiology with the Method of Symptoms may be imprecise in this population, since prodromal symptoms are absent in up to 93% of patients with carotid sinus syndrome, and most of all with frequent memory and cognitive deficit, confounding the correlation. Additionally, any etiology that causes hypotension might result in symptoms similar to those determined by CSH, with the first symptoms of retinal and cerebral hypoperfusion expected in the upright position when SBP drops below 80 mmHg. An association between impaired cerebral autoregulation and the symptomatic presentation of CSH was demonstrated by Tan et al. 27 in a study using transcranial Doppler ultrasonography during lower body negative pressure-induced systemic hypotension. 27 They have demonstrated that individuals with symptomatic CSH have lower cerebral blood flow than do asymptomatic individuals with CSH in response to comparable reductions in systemic blood pressure, and have suggested that symptomatic individuals have an increased susceptibility to syncope or falls compared with individuals with asymptomatic CSH due to a lower ability to maintain cerebral blood flow in the face of a hypotensive challenge. In our study, we observed that symptoms resulting from the CSM occurred mainly when the SBP dropped below 90 mmHg and/or the RR intervals extended longer than 2500ms, regardless of the diagnosis associated with CSM. Associated with this factor, CSH is elicited by manual massage, which is a highly variable stimulus. This may be the reason for the low reproducibility of the positive response, as shown in this study. While CSH has been observed in patients with syncope, and the symptoms were reproduced during CSM, there are no reports demonstrating that the hemodynamic alterations seen in the laboratory occur in a spontaneous event. Trying to establish the relationship between CSH and falls or syncopes, Schoon et al. have tested the hypothesis that head turning triggers hypotensive episodes in elderly with CSH. They have concluded that head turning may cause hypotensive episodes in the elderly. Head turning led to hypotension in 39% (total of 96 patients) of patients, with a mean SBP drop of 36 mm Hg (SD ± 13; range 20-76) with similar occurrence compared to healthy elderly, with 44% (total of 25 patients) and a mean SBP drop of 35 mmHg (SD ± 19; range 20‑85). A drawback of the observational design is that it does not allow for conclusions about the causal relationships among head turning-triggered hypotension and syncope, and falls. They have also found a discrepancy between the occurrence of that head turning‑triggered hypotension and related symptoms. 28 Thus, the positive correlation between CSH and syncope and/or falls still needs to be redefined due to the accumulating evidence that CSM causes a similar positive response in the asymptomatic population with the current criteria to diagnose CSH. The cut-off value of symptomatic SBP ≤ 85 mmHg to identify the VD form of CSH may cause overdiagnosis, sometimes leads to misdiagnosis, with no benefits in treatment plus potential side effects outweighing the benefits. Other options, such as long‑lasting ECG monitoring with documentation of spontaneous events, are the only way to corroborate the diagnosis and its correlation with laboratorial findings. Conclusion In conclusion, no differences in the response to CSM were demonstrated between patients with and without syncope or presyncope. Carotid sinus hypersensitivity may be an unspecific condition in the evaluation of syncope. The best cut-off values of the asystolic pause and SBP based or not on the reproduction of symptoms are still a challenging task in medical practice. Consequently, clinical correlation and other methods of evaluation, such as long-lasting ECG monitoring, may be necessary to confirm CSH as a cause of syncope. Study limitations The control group was composed of not completely healthy individuals, but with no significant heart disease and in stable clinical condition. It is already known that elderly people have an average of three comorbidities per person. Asymptomatic patients in this study were recruited from an outpatient geriatric unit. The institution is a referral tertiary cardiology center, and the patients usually have substantial clinical complexity. Even with the exclusion criteria, which led to the inclusion of only patients without significant heart disease and in stable clinical conditions at the time of selection, we observed that more patients with diabetes and coronary artery disease were in the asymptomatic group. On the other hand, patients in the asymptomatic group were a little older than those in the symptomatic group, with a mean age of 73.0 and 69.6 years, respectively. Despite this difference, patients in both groups are representative of the elderly population, in whom a positive vagal maneuver is believed to define the etiologic diagnosis of syncope. The presence of systemic underlying comorbidities in the asymptomatic group may be an important concern. The advanced age and the presence of simultaneous underlying diseases in these patients reinforce the hypothesis that CSH could be not much more than a laboratory finding related to aging and vascular diseases. We recognize that the difference in age and in comorbidities between groups could constitute a bias, but we are sure that both groups are representative of the elderly population in which unexplained syncope is a great challenge. In this study the CSM was performed with the patient in the 70° upright position after 5 minutes in the orthostatic position different from other studies performed in the supine position. Thus, our findings may be different and, therefore, could not be applied to the CSM in supine position. We chose the orthostatic position because it is the most sensitive to detect CSH according to the study performed by Parry et al., 29 who have demonstrated that the specificity and sensitivity of 89