Rapid changes in overnight blood pressure after transitioning to early-morning shiftwork

Risk for adverse cardiovascular events increases when blood pressure does not decrease at night (“non-dipping”, <10% decrease from daytime blood pressure). Shiftwork alters relationships between behaviors and endogenous circadian rhythms (i.e., circadian disruption along with variable sleep timing), and chronic shiftwork increases cardiovascular disease risk. To determine whether transitioning into shiftwork changes the overnight blood pressure dipping pattern, we leveraged a natural experiment that occurs when newly-hired bus operators transition from a daytime training schedule into an early-morning shiftwork or daywork schedule. Twenty participants were studied in a 90-day protocol upon new employment and underwent cardio-metabolic health assessments, including ambulatory blood pressure monitoring, and weekly sleep-wake diaries. Measurements were repeated after ~30 and 90 days after transitioning to a day or an early-morning shiftwork schedule. Newly-hired shiftworkers displayed dramatic changes in overnight blood pressure, with 62% converting from a healthy dipping blood pressure to the non-dipping pattern, resulting in 93% of shiftworkers displaying a non-dipping phenotype at 90-days. In contrast, 50% of dayworkers had a non-dipping profile at baseline and this decreased to 0% at 90-days, a significant difference from shiftworkers (p=0.001). At 90-days, overnight blood pressure dipping was ~7% less in shiftworkers than dayworkers (-6.3% [95%CI -3.7 to -8.8%] vs -13.1% [-10.3 to -15.9%]: p<0.01), with changes in dipping associated with changes in sleep timing variability (r 2=0.28, p=0.03). The observed changes in overnight blood pressure dipping in newly-hired early-morning shiftworkers, which were associated with sleep timing variability, may be an early warning sign of increased cardiovascular risk among shiftworkers.

Blood pressure dipping during REM and non-REM sleep in patients with moderate to severe obstructive sleep apnea

A limited number of papers have addressed the association between non-dipping-blood pressure (BP) obstructive sleep apnea (OSA), and no study has assessed BP-dipping during rapid eye movement (REM) and non-REM sleep in OSA patients. This study sought to noninvasively assess BP-dipping during REM and non-REM (NREM)-sleep using a beat-by-beat measurement method (pulse-transit-time (PTT)). Thirty consecutive OSA patients (men = 50%) who had not been treated for OSA before and who had > 20-min of REM-sleep were included. During sleep, BP was indirectly determined via PTT. Patients were divided into dippers and non-dippers based on the average systolic-BP during REM and NREM-sleep. The studied group had a a median age of 50 (42–58.5) years and a body mass index of 33.8 (27.6–37.5) kg/m2. The median AHI of the study group was 32.6 (20.1–58.1) events/h (range: 7–124), and 89% of them had moderate-to-severe OSA. The prevalence of non-dippers during REM-sleep was 93.3%, and during NREM-sleep was 80%. During NREM sleep, non-dippers had a higher waist circumference and waist-hip-ratio, higher severity of OSA, longer-time spent with oxygen saturation < 90%, and a higher mean duration of apnea during REM and NREM-sleep. Severe OSA (AHI ≥ 30) was defined as an independent predictor of non-dipping BP during NREM sleep (OR = 19.5, CI: [1.299–292.75], p-value = 0.03). This short report demonstrated that BP-dipping occurs during REM and NREM-sleep in patients with moderate-to-severe OSA. There was a trend of more severe OSA among the non-dippers during NREM-sleep, and severe OSA was independently correlated with BP non-dipping during NREM sleep.

The relationship between ambulatory arterial stiffness, inflammation, blood pressure dipping and cardiovascular outcomes

Background The ambulatory arterial stiffness index (AASI) is an indirect measure of arterial stiffness obtained during ambulatory blood pressuring monitoring (ABPM). Its relationship to nocturnal blood pressure dipping status and major adverse cardiovascular events (MACE) are controversial and its association with vascular inflammation has not been examined. We aimed to investigate the relationship between the AASI, inflammation and nocturnal blood pressure dipping status and its association with MACE. Methods Adults (aged 18–80 years) who underwent 24-h ABPM for the diagnosis of hypertension or its control were included. The inflammatory markers measured were the neutrophil–lymphocyte (NLR), platelet-lymphocyte (PLR) and monocyte-lymphocyte ratios (MLR). The primary MACE was a composite of cardiovascular death, acute limb ischaemia, stroke or transient ischaemic attack (TIA) or acute coronary syndrome. Results A total of 508 patients (51.2% female) aged 58.8 ± 14.0 years were included; 237 (46.7%) were normal-dippers (≥ 10% nocturnal systolic dip), 214 (42.1%) were non-dippers (0–10% dip) and 57 (11.2%) were reverse-dippers (< 0% dip). The AASI was significantly higher among reverse (0.56 ± 0.16) and non-dippers (0.48 ± 0.17) compared with normal dippers (0.39 ± 0.16; p < 0.0001) and correlated with the NLR (r = 0.20; 95% CI 0.11 to 0.29: < 0.0001) and systolic blood pressure dipping % (r = − 0.34; − 0.42 to − 0.26: p < 0.0001). Overall 39 (7.7%) patients had ≥ 1 MACE which included a total of seven cardiovascular deaths and 14 non-fatal strokes/TIAs. The mean follow up was 113.7 ± 64.0 weeks. Increasing NLR, but not AASI or systolic dipping, was independently linked to MACE (overall model Chi-square 60.67; p < 0.0001) and MLR to cardiovascular death or non-fatal stroke/TIA (overall model Chi-square 37.08; p < 0.0001). Conclusions In conclusion AASI was associated with blood pressure dipping and chronic inflammation but not independently to MACE. The MLR and NLR were independent predictors of MACE.

Association between nocturnal blood pressure dipping and chronic kidney disease among patients with controlled office blood pressure

Background Although abnormal blood pressure patterns are associated with adverse cardiorenal outcomes, their associations are yet unquantified by nocturnal dipping status. We examined the association of nocturnal blood pressure dipping pattern with albuminuria and kidney function among participants with controlled hypertension without prior advanced kidney disease. Methods Ambulatory blood pressure measurements were collected from 995 middle-aged, cardiology clinic patients with controlled office blood pressure (&lt;140/90 mmHg). The magnitude of dipping was calculated as the difference between daytime and nighttime systolic blood pressure divided by daytime systolic blood pressure. Accordingly, the participants were categorized as extreme-dipper (≥20%), dipper (10-&lt;20%), non-dipper (0-&lt;10%), or reverse-dipper (&lt;0%). We analyzed the cross-sectional associations of dipping with albuminuria (urine albumin-to-creatinine ratio ≥30 mg/g) and decreased estimated glomerular filtration rate (&lt;60 ml/min/1.73m 2), adjusting for office/ambulatory blood pressure, antihypertensive class, body mass index, total cholesterol, fasting glucose, socioeconomic status, and health behavior. Results The participants (mean age 60.2 years; 52.9% male) consisted of 13.5% extreme-dippers, 43.1% dippers, 34.7% non-dippers, and 8.7% reverse-dippers. In reference to dippers, odds ratios [95% confidence interval] for albuminuria were 1.73 [1.04-2.60] in reverse-dippers, 1.67 [1.20-2.32] in non-dippers, and 0.62 [0.38-1.04] in extreme-dippers. Likewise, abnormal dipping profile was associated with decreased kidney function: reverse-dipping, 2.02 [1.06-3.84]; non-dipping, 1.98 [1.07-3.08]; extreme-dipping, 0.69 [0.20-1.17]. The associations persisted participants with more conservatively controlled office blood pressure (&lt;130/80 mmHg). Conclusions Monitoring diurnal and nocturnal blood pressure may identify chronic kidney disease otherwise overlooked based on office blood pressure.