Acute and Short-Term Autonomic and Hemodynamic Responses to Transcranial Direct Current Stimulation in Patients With Resistant Hypertension

Abstract

Previously, we demonstrated that acute transcranial direct current stimulation (tDCS) reduced blood pressure (BP) and improved autonomic modulation in hypertensives. We hypothesized that acute and short-term tDCS intervention can promote similar benefits in resistant hypertensive patients (RHT). We assessed the impact of one (acute intervention) and ten (short-term intervention) tDCS or SHAM (20 min, each) sessions on BP, pulse interval (PI) and systolic blood pressure variabilities, humoral mechanisms associated with BP regulation, and cytokines levels. True RHT subjects (n = 13) were randomly submitted to one and ten SHAM and tDCS crossing sessions (1 week of "washout"). Hemodynamic (Finometer^®, Beatscope), office BP, and autonomic variables (accessed through spectral analysis of the pulse-to-pulse BP signal, in the time and frequency domain - Fast Fourrier Transform) were measured at baseline and after the short-term intervention. 24 h-ambulatory BP monitoring was measured after acute and short-term protocols. Acute intervention: tDCS reduced BP, cardiac output, and increase high-frequency band of PI (vagal modulation to the heart). Short-term protocol: tDCS did not change BP and cardiac output parameters. In contrast, central systolic BP (-12%), augmentation index (-31%), and pulse wave velocity (34%) were decreased by the short-term tDCS when compared to SHAM. These positive results were accompanied by a reduction in the low-frequency band (-37%) and an increase of the high-frequency band of PI (+62%) compared to SHAM. These findings collectively indicate that short-term tDCS concomitantly improves resting cardiac autonomic control and pulse wave behavior and reduces central BP in RHT patients, https://ensaiosclinicos.gov.br/rg/RBR-8n7c9p.

Keywords: autonomic nervous system; biochemical analyses; blood pressure; resistant hypertension; transcranial direct current stimulation (tDCS).

Figure 1

Experimental design. BMI, body mass index; ABPM, ambulatory blood pressure measurement.

Figure 2

Short-term intervention (10 sessions): Applanation tonometry method to determine whether short-term tDCS (10 sessions) could affect the central blood pressure and pulse waves behavior. (A) Central SBP [P = 0.0225 vs. SHAM; Interaction – P = 0.0016]; (B) Central diastolic blood pressure [p = 0.2655 vs. SHAM; Interaction – P = 0.0106]; (C) Central mean blood pressure [P = 0.0320 vs. SHAM; Interaction – P = 0.0002]; (D) Augmentation Index (AIx) expressed in % [P = 0.0421 vs. SHAM; Interaction – P = 0.0002]; (E) AIx normalized for a heart rate of 75 bpm [P = 0.0010 vs. SHAM; Interaction – P < 0.0001]; (F) PWV – pulse wave velocity [P = 0.0093 vs. SHAM; Interaction – P < 0.0001]. Repeated-measures two-way ANOVA, followed by Bonferroni post-test. *Difference vs. SHAM at final moment; ^†P < 0.05 vs. tDCS baseline in the same condition.

Figure 3

Short-term intervention (10 sessions): tDCS or SHAM effects on pulse interval and systolic blood pressure variability. Repeated measures ANOVA with Bonferroni post-test. (A) PI Variance - pulse interval variance [P = 0.0006 vs. SHAM; Interaction – P = 0.0002]; (B) RMSSD - square root of the mean of the square of the differences between adjacent standard RR intervals [P = 0.0421 vs. SHAM; Interaction – P = 0.0033]; (C) LF-PI - low-frequency band of the pulse interval expressed in n.u. [P = 0.0002 vs. SHAM; Interaction – P = 0.0003]; (D) HF-PI - a high-frequency band of the pulse interval expressed in n.u. [P < 0.0001 vs. SHAM; Interaction – P < 0.0001]; (E) LF/HF ratio - autonomic balance [P < 0.0001 vs. SHAM; Interaction – P < 0.0001]; (F) SBP Variance - variance of systolic blood pressure [P = 0.0018 vs. SHAM; Interaction – P < 0.0001]; (G) LF-SBP - low-frequency band of systolic blood pressure [P = 0.0012 vs. SHAM; Interaction – P < 0.0001]. *Difference vs. SHAM at the final moment; ^†P < 0.05 vs. tDCS baseline.

Figure 4

Short-term intervention (10 sessions): Humoral mechanisms associated with BP regulation {(A) cortisol [P = 0.0056 vs. SHAM; Interaction – P = 0.0072]; (B) noradrenaline [P = 0.0004 vs. SHAM; Interaction – P < 0.0001]; (C) acetylcholinesterase [P < 0.0001 vs. SHAM; Interaction – P < 0.0001]} and inflammatory cytokines {(D) TNF-α [P=0.5774 vs. SHAM; Interaction – P=0.8195], and (E) IL-10 [P = 0.0053 vs. SHAM; Interaction – P = 0.0062]}. ^#Difference vs. SHAM baseline; ^†P < 0.05 vs. tDCS baseline; *Difference vs. SHAM at final moment.

Figure 5

Short-term intervention (10 sessions): Linear regression analysis was carried out and, if the slope of the regression line is significantly larger than 0 with P < 0.05, the linear regression (solid line) and its 95% confidence interval (dotted lines) are plotted as well. (A) LF-PI and Central SBP [r = 0.5315; P =0.0063]; (B) LF-PI and Cortisol levels [r = 0.7058; P < 0.0001]; (C) HF-PI and IL-10 levels [r = 0.5344; P = 0.0049]; (D) IL-10 and AIx (@HR75%) [r = −0.6522; P = 0.0003].