Impact of nocturnal hemodialysis on the variability of heart rate and duration of hypoxemia during sleep

Impact of nocturnal hemodialysis on the variability of heart rate and duration of hypoxemia during sleep.BackgroundNocturnal hemodialysis (NHD) alleviates uremia-related sleep apnea, a condition characterized by increased sympathetic activity and diminished heart rate (HR) variability. We tested the hypothesis that NHD reduces both hypoxemia and sympathetic neural contributions to HR variability during sleep.MethodsEpisodes of apnea and hypopnea and the duration of nocturnal hypoxemia during sleep were determined in 9 end-stage renal disease (ESRD) patients (age: 44 ± 2) (mean ± SEM) before and after conversion from conventional hemodialysis (CHD) to NHD, and in 10 control subjects (age: 45 ± 3) with normal renal function and without sleep apnea. Low frequency (LF) (0.05-0.15 Hz) and high frequency (HF) (0.15-0.5 Hz) HR spectral power during stage 2 sleep was calculated (Fast Fourier transformation). Patients were studied 4 times (1day before and on the night after their CHD session) and 6–15months after conversion to NHD, while receiving NHD and on a non-dialysis night.ResultsNHD decreased the frequency of apnea and hypopnea (from 29.7 ± 9.3 to 8.2 ± 2.0 episodes per hour, P = 0.02), and duration of nocturnal hypoxemia (from 13.9 ± 5.2 to 2.6 ± 1.9% of total sleep time, P = 0.02). As CHD recipients, ESRD patients had faster nocturnal heart rates (79 ± 2 vs. 58 ± 1min-1, P = 0.03) and lower HF (vagal) (78 ± 27 vs. 6726 ± 4556ms2, P = 0.001) spectral power than control subjects. After conversion to NHD, HR fell (from 79 ± 2 to 66 ± 1min-1, P = 0.03) and HF power increased (from 78 ± 27 to 637 ± 139ms2, P = 0.001). The HF/HF+LF ratio, an index of vagal HR modulation, was lower during CHD (0.16 ± 0.03 vs. 0.42 ± 0.05 in control subjects, P < 0.05) and increased (to 0.45 ± 0.05, P < 0.001) after conversion to NHD. The LF/HF ratio, a representation of sympathetic HR modulation, which was significantly higher during CHD than in control subjects (2.77 ± 0.82 vs. 0.71 ± 0.11, P < 0.05), was also normalized by NHD (0.74 ± 0.12, P < 0.05, compared with CHD).ConclusionHigher heart rates and impaired vagal and augmented sympathetic HR modulation during sleep in ESRD patients are normalized by NHD. Potential mechanisms for these observations include attenuation of surges in sympathetic outflow elicited by apnea and hypoxia during sleep, normalization of nocturnal breathing patterns that influence HRV, and removal, by increased dialysis, of a sympatho-excitatory stimulus of renal origin

Regression of left ventricular hypertrophy after conversion to nocturnal hemodialysis

Regression of left ventricular hypertrophy after conversion to nocturnal hemodialysis.BackgroundLeft ventricular hypertrophy (LVH) is an independent risk factor for mortality in the dialysis population. LVH has been attributed to several factors, including hypertension, excess extracellular fluid (ECF) volume, anemia and uremia. Nocturnal hemodialysis is a novel renal replacement therapy that appears to improve blood pressure control.MethodsThis observational cohort study assessed the impact on LVH of conversion from conventional hemodialysis (CHD) to nocturnal hemodialysis (NHD). In 28 patients (mean age 44 ± 7 years) receiving NHD for at least two years (mean duration 3.4 ± 1.2 years), blood pressure (BP), hemoglobin (Hb), ECF volume (single-frequency bioelectrical impedance) and left ventricular mass index (LVMI) were determined before and after conversion. For comparison, 13 control patients (mean age 52 ± 15 years) who remained on self-care home CHD for one year or more (mean duration 2.8 ± 1.8 years) were studied also. Serial measurements of BP, Hb and LVMI were also obtained in this control group.ResultsThere were no significant differences between the two cohorts with respect to age, use of antihypertensive medications, Hb, BP or LVMI at baseline. After transfer from CHD to NHD, there were significant reductions in systolic, diastolic and pulse pressure (from 145 ± 20 to 122 ± 13mm Hg, P < 0.001; from 84 ± 15 to 74 ± 12mm Hg, P = 0.02; from 61 ± 12 to 49 ± 12mm Hg, P = 0.002, respectively) and LVMI (from 147 ± 42 to 114 ± 40 g/m2, P = 0.004). There was also a significant reduction in the number of prescribed antihypertensive medications (from 1.8 to 0.3, P < 0.001) and an increase in Hb in the NHD cohort. Post-dialysis ECF volume did not change. LVMI correlated with systolic blood pressure (r = 0.6, P = 0.001) during nocturnal hemodialysis. There was no relationship between changes in LVMI and changes in BP or Hb. In contrast, there were no changes in BP, Hb or LVMI in the CHD cohort over the same time period.ConclusionsReductions in BP with NHD are accompanied by regression of LVH

Contrasting Effects of Lower Body Positive Pressure on Upper Airways Resistance and Partial Pressure of Carbon Dioxide in Men With Heart Failure and Obstructive or Central Sleep Apnea

ObjectivesThis study sought to test the effects of rostral fluid displacement from the legs on transpharyngeal resistance (Rph), minute volume of ventilation (Vmin), and partial pressure of carbon dioxide (PCO2) in men with heart failure (HF) and either obstructive (OSA) or central sleep apnea (CSA).BackgroundOvernight rostral fluid shift relates to severity of OSA and CSA in men with HF. Rostral fluid displacement may facilitate OSA if it shifts into the neck and increases Rph, because pharyngeal obstruction causes OSA. Rostral fluid displacement may also facilitate CSA if it shifts into the lungs and induces reflex augmentation of ventilation and reduces PCO2, because a decrease in PCO2 below the apnea threshold causes CSA.MethodsMen with HF were divided into those with mainly OSA (obstructive-dominant, n = 18) and those with mainly CSA (central-dominant, n = 10). While patients were supine, antishock trousers were deflated (control) or inflated for 15 min (lower body positive pressure [LBPP]) in random order.ResultsLBPP reduced leg fluid volume and increased neck circumference in both obstructive- and central-dominant groups. However, in contrast to the obstructive-dominant group in whom LBPP induced an increase in Rph, a decrease in Vmin, and an increase in PCO2, in the central-dominant group, LBPP induced a reduction in Rph, an increase in Vmin, and a reduction in PCO2.ConclusionsThese findings suggest mechanisms by which rostral fluid shift contributes to the pathogenesis of OSA and CSA in men with HF. Rostral fluid shift could facilitate OSA if it induces pharyngeal obstruction, but could also facilitate CSA if it augments ventilation and lowers PCO2

Arterial stiffness is decreased in estrogen deficient physically active women with functional hypothalamic amenorrhea [abstract]

Arterial stiffness is decreased in estrogen deficient physically active women with functional hypothalamic amenorrhea [abstract

Elevated cardiac vagal tone in hypoestrogenic active premenopausal women with functional hypothalamic amenorrhea

Elevated cardiac vagal tone in hypoestrogenic active premenopausal women with functional hypothalamic amenorrhe

Augmented vagal heart rate modulation in active hypoestrogenic pre-menopausal women with functional hypothalamic amenorrhoea

Compared with eumenorrhoeic women, exercise-trained women with functional hypothalamic amenorrhoea (ExFHA) exhibit low heart rates (HRs) and absent reflex renin-angiotensin-system activation and augmentation of their muscle sympathetic nerve response to orthostatic stress. To test the hypothesis that their autonomic HR modulation is altered concurrently, three age-matched (pooled mean, 24 ± 1 years; mean ± S.E.M.) groups of women were studied: active with either FHA (ExFHA; n=11) or eumenorrhoeic cycles (ExOv; n=17) and sedentary with eumenorrhoeic cycles (SedOv; n=17). Blood pressure (BP), HR and HR variability (HRV) in the frequency domain were determined during both supine rest and graded lower body negative pressure (LBNP; -10, -20 and -40 mmHg). Very low (VLF), low (LF) and high (HF) frequency power spectra (ms(2)) were determined and, owing to skewness, log10-transformed. LF/HF ratio and total power (VLF + LF + HF) were calculated. At baseline, HR and systolic BP (SBP) were lower (P0.05). At each stage, HR correlated inversely (P<0.05) with HF. In conclusion, ExFHA women demonstrate augmented vagal yet unchanged sympathetic HR modulation, both at rest and during orthostatic stress. Although the role of oestrogen deficiency is unclear, these findings are in contrast with studies reporting decreased HRV in hypoestrogenic post-menopausal women

Influence of Sex and Age on Muscle Sympathetic Nerve Activity of Healthy Normotensive Adults

As with blood pressure, age-related changes in muscle sympathetic nerve activity (MSNA) may differ nonlinearly between sexes. Data acquired from 398 male (age: 39±17; range: 18-78 years [mean±SD]) and 260 female (age: 37±18; range: 18-81 years) normotensive healthy nonmedicated volunteers were analyzed using linear regression models with resting MSNA burst frequency as the outcome and the predictors sex, age, MSNA, blood pressure, and body mass index modelled with natural cubic splines. Age and body mass index contributed 41% and 11%, respectively, of MSNA variance in females and 23% and 1% in males. Overall, changes in MSNA with age were sigmoidal. At age 20, mean MSNA of males and females were similar, then diverged significantly, reaching in women a nadir at age 30. After 30, MSNA increased nonlinearly in both sexes. Both MSNA discharge and blood pressure were lower in females until age 50 (17±9 versus 25±10 bursts·min-1; P\u3c1×10-19; 106±11/66±8 versus 116±7/68±9 mm Hg; P\u3c0.01) but converged thereafter (38±11 versus 35±12 bursts·min-1; P=0.17; 119±15/71±13 versus 120±13/72±9 mm Hg; P\u3e0.56). Compared with age 30, MSNA burst frequency at age 70 was 57% higher in males but 3-fold greater in females; corresponding increases in systolic blood pressure were 1 (95% CI, -4 to 5) and 12 (95% CI, 6-16) mm Hg. Except for concordance in females beyond age 40, there was no systematic change with age in any resting MSNA-blood pressure relationship. In normotensive adults, MSNA increases after age 30, with ascendance steeper in women

After-exercise heart rate variability is attenuated in postmenopausal women and unaffected by estrogen therapy

Delayed heart rate (HR) recovery in the immediate postexercise period has been linked to adverse cardiovascular prognosis. The after effects of an acute bout of exercise on HR modulation in postmenopausal women (PMW) and the influence of estrogen therapy are unknown.In 13 sedentary PMW (54 ± 2 y, mean ± SEM), we assessed HR variability (HRV) -an index of HR modulation-and the influence of estrogen therapy on HRV. HRV in the frequency domain was quantified during supine rest and again 60 minutes after treadmill exercise for 45 minutes, at 60% VO2peak. PMW were studied before and after 4 weeks of oral estradiol. To obtain reference values for the after effects of exercise on HRV in healthy young women, 14 premenopausal women (PreM) completed the identical exercise protocol.Compared with PreM, PMW demonstrated lower high frequency (vagal modulation) and total HRV (P < 0.05) at rest. In PreM, all HRV values were similar before and after exercise. In contrast, in PMW after exercise, despite having identical HR to PreM, high frequency and total HRV were all lower (all P ≤ 0.01) compared with pre-exercise HRV values. Estrogen therapy had no effect on pre or postexercise values for HRV.When compared with PreM, PMW have identical HR, but lower vagal HR modulation at rest and delayed HRV recovery after exercise. Estrogen does not restore baseline HRV or accelerate HRV recovery postexercise, suggesting aging rather than estrogen deficiency per se may lower HRV in PMW

Discordant orthostatic reflex renin-angiotensin and sympathoneural responses in premenopausal exercising-hypoestrogenic women

Our prior observations in normotensive postmenopausal women stimulated the hypotheses that compared with eumenorrheic women, active hypoestrogenic premenopausal women with functional hypothalamic amenorrhea would demonstrate attenuated reflex renin-angiotensin-aldosterone system responses to an orthostatic challenge, whereas to defend blood pressure reflex increases in muscle, sympathetic nerve activity would be augmented. To test these hypotheses, we assessed, in recreationally active women, 12 with amenorrhea (ExFHA; aged 25 ± 1 years; body mass index 20.7 ± 0.7 kg/m(2); mean ± SEM) and 17 with eumenorrhea (ExOv; 24 ± 1 years; 20.9 ± 0.5 kg/m(2)), blood pressure, heart rate, plasma renin, angiotensin II, aldosterone, and muscle sympathetic nerve activity at supine rest and during graded lower body negative pressure (-10, -20, and -40 mm Hg). At baseline, heart rate and systolic blood pressure were lower (P0.05). In response to graded lower body negative pressure, heart rate increased (P0.05). Muscle sympathetic nerve activity burst incidence increased reflexively in both groups, but more so in ExFHA (P<0.05). Otherwise, healthy hypoestrogenic ExFHA women demonstrate low blood pressure and disruption of the normal circulatory response to an orthostatic challenge: plasma renin, angiotensin II, and aldosterone fail to increase and blood pressure is defended by an augmented sympathetic vasoconstrictor response

Microneurographic characterization of sympathetic responses during 1-leg exercise in young and middle-aged humans

Muscle sympathetic nerve activity (MSNA) at rest increases with age. However, the influence of age on MSNA recorded during dynamic leg exercise is unknown. We tested the hypothesis that aging attenuates the sympatho-inhibitory response observed in young subjects performing mild to moderate 1-leg cycling. After pre-determining peak oxygen uptake (VO2peak), we compared contra-lateral fibular nerve MSNA during 2 minutes each of mild (unloaded) and moderate (30-40% of the work rate at peak VO2, halved for single leg) 1-leg cycling in 18 young (23±1 years [mean±SE]) and 18 middle-aged (57±2 years) sex-matched healthy subjects. Mean height, weight, resting heart rate (HR), systolic blood pressure (BP) and percent predicted VO2peak were similar between groups. Middle-aged subjects had higher resting MSNA burst frequency and incidence (P<0.001) and diastolic BP (P=0.04). During moderate 1-leg cycling, older subjects’ systolic BP increased more (+21±5 vs.+10±1 mmHg; P=0.02) and their fall in MSNA burst incidence was amplified (-19±2 vs. -11±2 bursts/100heartbeats; P=0.01) but because HR rose less (+153 vs.+192 bpm; P=0.03), exercise induced similar reductions in burst frequency (P=0.25). Contrary to our initial hypothesis, with advancing age, mild to moderate intensity dynamic leg exercise elicits a greater rise in systolic BP and a larger fall in MSNA