In resistant hypertensive patients acute carotid baroreflex stimulation is associated with a blood pressure (BP) reduction, believed to be mediated by a central sympathoinhbition.The evidence for this sympathomodulatory effect is limited, however. This meta-analysis is the first to examine the sympathomodulatory effects of acute carotid baroreflex stimulation in drug-resistant and uncontrolled hypertension, based on the results of microneurographic studies. The analysis included 3 studies assessing muscle sympathetic nerve activity (MSNA) and examining 41 resistant uncontrolled hypertensives. The evaluation included assessment of the relationships between MSNA and clinic heart rate and BP changes associated with the procedure. Carotid baroreflex stimulation induced an acute reduction in clinic systolic and diastolic BP which achieved statistical significance for the former variable only [systolic BP: −19.98 mmHg (90% CI, −30.52, −9.43), P < 0.002], [diastolic BP: −5.49 mmHg (90% CI, −11.38, 0.39), P = NS]. These BP changes were accompanied by a significant MSNA reduction [−4.28 bursts/min (90% CI, −8.62, 0.06), P < 0.07], and by a significant heart rate decrease [−3.65 beats/min (90% CI, −5.49, −1.81), P < 0.001]. No significant relationship was detected beween the MSNA, systolic and diastolic BP changes induced by the procedure, this being the case also for heart rate. Our data show that the acute BP lowering responses to carotid baroreflex stimulation, although associated with a significant MSNA reduction, are not quantitatively related to the sympathomoderating effects of the procedure. This may suggest that these BP effects depend only in part on central sympathoinhibition, at least in the acute phase following the intervention.
Biffi, A., Quarti-Trevano, F., Vanoli, J., Dell'Oro, R., Corrao, G., Mancia, G., et al. (2024). Effects of acute carotid baroreceptor stimulation on sympathetic nerve traffic in resistant and uncontrolled hypertension: a systematic review and meta-analysis. HYPERTENSION RESEARCH, 47(7), 1962-1969 [10.1038/s41440-024-01704-9].
Effects of acute carotid baroreceptor stimulation on sympathetic nerve traffic in resistant and uncontrolled hypertension: a systematic review and meta-analysis
Biffi A;Quarti-Trevano F;Vanoli J;Dell'Oro R;Corrao G;Mancia G;Grassi G.
2024
Abstract
In resistant hypertensive patients acute carotid baroreflex stimulation is associated with a blood pressure (BP) reduction, believed to be mediated by a central sympathoinhbition.The evidence for this sympathomodulatory effect is limited, however. This meta-analysis is the first to examine the sympathomodulatory effects of acute carotid baroreflex stimulation in drug-resistant and uncontrolled hypertension, based on the results of microneurographic studies. The analysis included 3 studies assessing muscle sympathetic nerve activity (MSNA) and examining 41 resistant uncontrolled hypertensives. The evaluation included assessment of the relationships between MSNA and clinic heart rate and BP changes associated with the procedure. Carotid baroreflex stimulation induced an acute reduction in clinic systolic and diastolic BP which achieved statistical significance for the former variable only [systolic BP: −19.98 mmHg (90% CI, −30.52, −9.43), P < 0.002], [diastolic BP: −5.49 mmHg (90% CI, −11.38, 0.39), P = NS]. These BP changes were accompanied by a significant MSNA reduction [−4.28 bursts/min (90% CI, −8.62, 0.06), P < 0.07], and by a significant heart rate decrease [−3.65 beats/min (90% CI, −5.49, −1.81), P < 0.001]. No significant relationship was detected beween the MSNA, systolic and diastolic BP changes induced by the procedure, this being the case also for heart rate. Our data show that the acute BP lowering responses to carotid baroreflex stimulation, although associated with a significant MSNA reduction, are not quantitatively related to the sympathomoderating effects of the procedure. This may suggest that these BP effects depend only in part on central sympathoinhibition, at least in the acute phase following the intervention.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.