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Resistant hypertension is associated with increased risk of cognitive decline, stroke, and dementia. Lifestyle modification has been suggested to improve cognitive function through its salutary effects on vascular function.Participants included 140 patients with resistant hypertension participating in the TRIUMPH trial. Participants were randomized to a cardiac rehabilitation-based lifestyle program (C-LIFE) or a standardized education and physician advice condition (SEPA). Participants completed a 45-min cognitive test battery consisting of tests of Executive Functioning and Learning, Memory, and Processing Speed. Biomarkers of vascular [flow mediated dilation of the brachial artery (FMD)], microvascular, and cerebrovascular function were also collected, in addition to weight, fitness, and ambulatory blood pressure.Participants averaged 63 years of age, 48% women, 59% black, and obese [mean BMI = 36 kg/m 2 (SD = 4)]. Cognitive performance improved across the entire cohort during the 4-month trial [ t -scores pretreatment = 48.9 (48, 50) vs. posttreatment = 50.0 (49, 51), P 0.001]. Postintervention Executive Function/Learning composite performance was higher for participants in C-LIFE compared to SEPA ( d = 0.37, P = 0.039). C-LIFE intervention effects on Memory and Processing Speed were moderated by sex and baseline stroke risk, respectively ( P = 0.026 and P = 0.043 for interactions), such that males and participants with greater stroke risk showed the greatest cognitive changes. FMD [C-LIFE: +0.3% (-0.3, 1.0) vs. SEPA: -1.4% (-2.5, -0.3), P = 0.022], and microvascular function [C-LIFE: 97 (65, 130) vs. SEPA: 025 (-75, 23), P 0.001] were improved in C-LIFE compared with SEPA, whereas cerebrovascular reactivity was not [C-LIFE: -0.2 (-0.4, 0) vs. SEPA: 0.1 (-0.2, 0.4), P = 0.197). Mediation analyses suggested that increased executive function/learning was associated with reduced ambulatory SBP levels secondary to weight loss [indirect effect: B = 0.25 (0.03, 0.71)].Lifestyle modification individuals with resistant hypertension improves cognition, which appeared to be associated with reduced ambulatory SBP changes through weight loss. Cognitive improvements were accompanied by parallel improvements in endothelial and microvascular function.

Prior research has demonstrated that individuals exposed to trauma have shown impaired autonomic function. We sought to determine if heart rate variability (HRV), a marker of impaired autonomic function, differed across periods of wake, rest, and sleep as a function of the level of symptoms of posttraumatic stress disorder (PTSD). A sample of young adults (N = 209), 95 of whom met full criteria for current PTSD based on the Clinician Administered PTSD Scale (CAPS; Blake et al., 1995), were evaluated for ≈ 24 hr using actigraphy and electrocardiogram. Actigraphy data were categorized as active, rest, or sleep. Multilevel modeling analyses showed that individuals with high PTSD symptom severity had lower high-frequency HRV than individuals with low PTSD symptom severity during periods of sleep, t(1083) = 2.20, p = .028, Cohen's d = 0.12. No differences were found during periods of activity, t(1083) = 1.34, p = .499, d = 0.05, or rest, t(1083) = 1.34, p = .180, d = 0.09. Our findings extended the import of prior studies to suggest that those with elevated PTSD symptoms may have decreased parasympathetic control during sleep. Moreover, relative to periods of wake and rest, sleep may represent a state of increased vulnerability for decreased parasympathetic cardiac control. Individuals with elevated PTSD symptoms may benefit from early screening for detection of cardiovascular disease.

Posttraumatic stress disorder (PTSD) has been linked to elevated heart rate (HR) and reduced heart rate variability (HRV) in cross-sectional research. Using ecological momentary assessment and minute-to-minute HRV/HR monitoring, we examined whether cross-sectional associations between PTSD symptom severity and HRV/HR were due to overall elevations in distress levels or to attenuated autonomic regulation during episodes of acute distress.Two hundred nineteen young adults (18-39 years old), 99 with PTSD, underwent 1 day of Holter monitoring and concurrently reported distress levels via ecological momentary assessment. Using multilevel modeling, we examined the associations between momentary distress and the 5-minute means for low-frequency (LF) and high-frequency (HF) HRV and HR immediately following distress ratings, and whether PTSD symptom severity moderated these associations.Compared with the controls, participants with PTSD recorded higher ambulatory distress (mean [standard deviation] = 1.7 [0.5] versus 1.2 [0.3], p.001) and HR (87.2 [11.8] versus 82.9 [12.6] beats/min, p = .011), and lower ambulatory LF HRV (36.9 [14.7] versus 43.7 [16.9 ms, p = .002) and HF HRV (22.6 [12.3] versus 26.4 [14.6] milliseconds, p = .043). Overall distress level was not predictive of HR or HRV (p values.27). However, baseline PTSD symptom severity was associated with elevated HR (t(1257) = 2.76, p = .006) and attenuated LF (t(1257) = -3.86, p.001) and HF (t(1257) = -2.62, p = .009) in response to acute momentary distress.Results suggest that PTSD is associated with heightened arousal after situational distress and could explain prior findings associating PTSD with HR/HRV. Implications for treatment and cardiovascular risk are discussed.