Diabetes care · 2011
Baroreflex sensitivity and its response to deep breathing predict increase in blood pressure in type 1 diabetes in a 5-year follow-up.
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Rosengård-Bärlund Milla, Bernardi Luciano, Sandelin Anna, Forsblom Carol, Groop Per-Henrik, FinnDiane Study Group
Аннотация
OBJECTIVE: We have recently demonstrated that early autonomic dysfunction, defined as low baroreflex sensitivity (BRS), could be functional and reversible. However, potential temporal changes in BRS have not yet been addressed by longitudinal studies in type 1 diabetes. Moreover, it is not known whether low BRS predisposes to hypertension or other nonfatal diabetes complications.
RESEARCH DESIGN AND METHODS: We conducted a 5-year prospective study including 80 patients with type 1 diabetes. We measured ambulatory blood pressure and autonomic function tests. BRS was assessed by six different methods during spontaneous, controlled, and slow deep breathing at baseline and follow-up.
RESULTS: Spontaneous BRS declined over time (BRS(average) 16.2 ± 0.8 vs. 13.2 ± 0.8 ms/mmHg; P < 0.01), but the change was not significant when adjusted for time of follow-up. Low BRS at baseline did not progress to cardiac autonomic neuropathy but predicted an increase in the nighttime systolic blood pressure (BRS(average) r = -0.37; P < 0.05). Additionally, BRS response to deep breathing at baseline predicted an increase in 24-h ambulatory blood pressure (BRS-αLF r = 0.323-0.346; P < 0.05).
CONCLUSIONS: The decline in spontaneous BRS over time in patients with type 1 diabetes seems to be due to normal aging, which supports a functional etiology behind early autonomic derangements. Decreased resting BRS and the magnitude of improvement by deep breathing may be due to sympathovagal imbalance, a well-known mechanism in the development of hypertension. Early interventions aiming to reduce sympathetic overactivity in patients with low BRS might delay the development of hypertension.
RESEARCH DESIGN AND METHODS: We conducted a 5-year prospective study including 80 patients with type 1 diabetes. We measured ambulatory blood pressure and autonomic function tests. BRS was assessed by six different methods during spontaneous, controlled, and slow deep breathing at baseline and follow-up.
RESULTS: Spontaneous BRS declined over time (BRS(average) 16.2 ± 0.8 vs. 13.2 ± 0.8 ms/mmHg; P < 0.01), but the change was not significant when adjusted for time of follow-up. Low BRS at baseline did not progress to cardiac autonomic neuropathy but predicted an increase in the nighttime systolic blood pressure (BRS(average) r = -0.37; P < 0.05). Additionally, BRS response to deep breathing at baseline predicted an increase in 24-h ambulatory blood pressure (BRS-αLF r = 0.323-0.346; P < 0.05).
CONCLUSIONS: The decline in spontaneous BRS over time in patients with type 1 diabetes seems to be due to normal aging, which supports a functional etiology behind early autonomic derangements. Decreased resting BRS and the magnitude of improvement by deep breathing may be due to sympathovagal imbalance, a well-known mechanism in the development of hypertension. Early interventions aiming to reduce sympathetic overactivity in patients with low BRS might delay the development of hypertension.