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Sleep Disorder and

Risk of Hypertension
Dr.dr. Rimawati Tedjasukmana, SpS, RPSGT,
FICA
Medistra Hospital
INA-Sleep
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Introduction
• A large number of observational studies link sleep disorders,
particularly obstructive sleep apnea (OSA) and insomnia, to risk of
cardiovascular (CV) disease, including hypertension, ischemic
heart disease, stroke and sudden death.
• Sleep alters autonomic nervous system function and other
physiologic events that influence BP.
• Sleep disorders alter the BP response and increase hypertension
risk
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Sleep Disorders and Risk of
Hypertension
Sleep RLS/PLMD
Sleep and
duration and and
nocturnal BP
hypertension hypertension

Insomnia
OSA and
and
hypertension
hypertension
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Sleep and nocturnal BP
• During normal sleep, there is a 10-20% decrease in BP (nocturnal dipping). It is
partly caused by decreases in sympathetic output.
• Absence of nocturnal dipping (non-dipping) is <10% decrease in nocturnal BP.
• Lack or diminished nocturnal dipping of BP is a strong, independent predictor of
cardiovascular risk
• The Ohasama study: each 5% deficiency in the normal decline in nocturnal BP
was associated with 20% greater risk in cardiovascular mortality.
• Diseases with non-dipping: most secondary causes of hypertension, chronic
kidney disease, diabetes, older age, resistant hypertension, and OSA

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Predictors of All-Cause Mortality in Clinical
Ambulatory Monitoring:
Unique Aspects of Blood Pressure During Sleep

The independent predictive ability of


sleep BP appeared to be superior to
that of the corresponding awake BP in
all of the patients,

Ben-Dov et al, 2007

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Sleep duration and hypertension

• Habitual sleep duration over the past 50 years has decreased by 1.5 to 2 h/day,
and >30% of Americans report sleeping less than 6 h/night.
• The Sleep Heart Health Study: subjects sleeping <5 h/night had a higher
frequency of prevalent hypertension (adjusted OR 1.66; 95% CI, 1.35-2.04)
• Whitehall II Study:
• Baseline: no association was noted in men; however, women sleeping <5
h/night had a higher risk of hypertension compared with those sleeping 7
h/night
• Prospective: incident hypertension risk was attenuated after confounding for
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Sleep duration and hypertension
• National Health and Nutrition Examination Survey:
• short sleep duration (< 5 h/night) in middle aged people (32-59 years) was associated with a
60% higher risk of incident hypertension over an 8-10-year follow-up period. No association was
found in individuals aged >60 years
• The population-based Rotterdam study, and a Spanish prospective cohort study:
• no association was found in prevalent or incident hypertension. Note that most of these cross-
sectional population studies use subjective reports of sleep duration and not objective data
(actigraphy).
• The association between short sleep duration and hypertension appears to be most
significant during middle age.
• The Sleep Heart Health Study noted that long sleep duration ( >9 h) is associated
with prevalent hypertension compared with individuals sleeping 7 to 8 h.
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RLS/PLMD and Hypertension

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RLS and PLMD
The 2 most common movement disorder of sleep are:
• Restless Legs Syndrome (RLS):
• Almost irresistible urge to move the legs
• Caused by disagreeable sensations in the legs
• Worse during inactivity
• Periodic Limb Movement Disorder (PLMD):
• Repetitive stereotyped movements of the limbs during sleep
• Involve flexion of the limbs (legs > arms)
• Duration 0.5-5 seconds

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RLS and PLMD
• 80-90% of patients with RLS also have periodic limb movement in
sleep (PLMS).
• PLMS: periodic involuntary limb movement comprising extension of
the big toe, and triple flexion at the ankle, knee, sometimes hip.
• Both RLS and PLMD are associated with PLMS.

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RLS and hypertension
• Epidemiologic studies have suggested that a relationship may exist
between self-reported RLS and hypertension.
Ohayon &Roth Phillips et al Ulfberg et al Conflicting data
• 18,980 • 1,506 adults • 4,000 men • Italy, Austria,
subjects • USA • Sweden Wisconsin
• Europe • Ht was • subjects with Sleep Cohort
• Ht correlated associated RLS more Study.
with RLS with RLS frequently has • No association
hypertension • Age maybe
confounding
factor
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Rise of blood pressure with periodic limb
movements in sleep and wakefulness
PLMS not Fake PLMS during
PLMS with
PLMW associated with an
microarousals wakefulness
arousal
• SBP elevation of • SBP elevation of • SBP increased • SBP increase of
11.7 + 7.6 mmHg 16.7 + 9.4 mmHg 11.2 + 8.7 mmHg 3.2 + 3.1 mmHg

Individual movements are associated with significant elevations of systolic and diastolic BP,
and these elevations are greater if the PLMS is associated with a cortical arousal

Siddiqui F et al, 2007


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Insomnia and Hypertension

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Insomnia
• 10 to 15 % of the adult population suffers from chronic insomnia.
• 25 to 35 % has transient or occasional insomnia.
• Insomnia is associated with significant personal and socioeconomic
burden.
• Activation of the hypothalmic-pituitary-adrenal axis and the
sympathetic nervous system as seen in insomnia may predispose
to hypertension development

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Insomnia in ICSD-3
• Insomnia is defined as a persistent difficulty with sleep initiation,
duration, consolidation, or quality that occurs despite adequate
opportunity and circumstances for sleep, and results in some form
of daytime impairment.

Persistent Adequate
Daytime
sleep sleep
dysfunction
difficulty opportunity
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A combination of 3 sleep complaints
(DFA, SCD, NRS) predicted a slightly
increased risk of cardiovascular disease
but not hypertension, and a complaint of
either DFA or SCD predicted increased
hypertensive risk

Phillips and Mannino, J Clin Sleep Med 2007

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Insomnia Did Not Predict Incident Hypertension in
Older Adults in the Cardiovascular Health Study

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Phillips et al, SLEEP 2009


The subjects with insomnia had higher
nighttime systolic BP and a decrease in the
day-to-night systolic BP dipping compared
with the good sleepers (both P = .01).
Daytime diastolic BP ( P = .02) and nighttime
diastolic BP ( P = .01) were higher in the
subjects with insomnia,

Lanfranchi et al, SLEEP 2009

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Insomnia with Objective Short Sleep Duration is Associated with a
High Risk for Hypertension

Vgontzas et al, SLEEP 2009


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OSA and Hypertension

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Prevalence of hypertension in OSA
OSA and hypertension commonly coexist.

50% of OSA patients are hypertensive

30-40% of hypertensive patients have OSA

Strong implication of a modest causal association between OSA and


BP from well-designed observational and experimental studies
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Obstructive Sleep Apnea (OSA)
Open Airway Recurrent partial or
complete obstruction
of the airway during
sleep
Most common form of
SDB
FLOW
Muscles at back of airway
relax and obstruct upper
Closed (obstructed) airway
Breathing stops but
Airway = OSA

respiratory effort
continues
Frequent arousals
Not all snorers have OSA
NO FLOW

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Wisconsin Sleep Cohort Study

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Peppard, et al, 2000
Wisconsin Sleep Cohort Study

• Conclusion:
• There is a dose-response association between
SDB at baseline and the presence of hypertension
4 years later independent of confounding factors.

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Prevalence of hypertension (The Sleep
Heart Health Study)
 AHI <1.5 per hour - 43%
 AHI 1.5-4.9 per hour - 53%
 AHI 5.0-14.9 per hour - 59%
 AHI 15.0-29.9 per hour - 62%
 AHI >30.0 per hour - 67%Nieto et al, JAMA 2000
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The Sleep Heart Health Study

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Obstructive sleep apnoea syndrome as a risk factor for
hypertension: population study
BMJ 2000;320:479

Fig 1. Odds ratios and Wald 95% confidence intervals for hypertension
associated with apnoea-hypopnoea index level of 5, 15, 30, 40, 50, 60,
and 70 predicted by best fitting multiple logistic model: T=e.012apnoea-hypopnoea
index+.081age+.161male+.067body mass index (n=2452)
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Sleep and Biological
Rhythms 2011

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CPAP therapy
• Reduces nocturnal sympathetic nerve traffic, blunts blood
pressure surges, decreases nocturnal blood pressure surge,
and improves cardiovascular prognosis in many OSAS
patients.
• Some studies found BP change small (1.69-2.46 mmHg) or
non significant.
• Although CPAP has been the first line therapeutic strategy for
OSAS, the beneficial effect of CPAP on hypertension remains
an open question
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Schematic outlining proposed pathophysiological components of OSA, activation of
cardiovascular disease mechanisms, and consequent development of established
cardiovascular disease

Somers, V. K. et al. J Am Coll Cardiol 2008;52:686-717

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Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply.


Arnadottir, 2009

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Resistant hypertension in SDB
• Resistant hypertension is defined as BP that requires four or
more antihypertensive medications.
• Patients with resistant HT have increased likelihood of
comorbidities (obesity, diabetes, left ventricular hypertrophy,
chronic kidney disease, higher cardiovascular risk)
• The prevalence of OSA is extraordinarily high in patients with
resistant HT.
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Resistant hypertension in SDB
• In studies of general hypertensive cohorts, the prevalence of OSA
has been found to be around 30–40%.
• In studies of patients with resistant HT, the prevalence of OSA has
been found to be 70–90%.
• Logan et al. found the prevalence of OSA to be 83% among
consecutive patients diagnosed with resistant HT.

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Resistant patients has
increased OSA severity

Goncalves,
Chest 2007

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Role of aldosterone excess
AHI (r=0.44, P=0.0002)
correlates with plasma
aldosterone concentration
(PAC) in subjects with
RHTN
Pratt-Ubunama, et al.
Chest 2007

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Role of aldosterone excess
• Both OSA and hyperaldosteronism are common in patients with
RHTN.
• Aldosterone excess likely contributes to the severity of OSA.
• Worsening of OSA is probably due to aldosterone-induced fluid
retention, leading to parapharyngeal oedema and increased upper
airway resistance.
Dudenbostel and Calhoun. J
Human Hypertension 2012
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Primary Aldosteronism in Indonesian moderate to
severe OSA patients
Table 1. Characteristics of OSA subjects with primary aldosteronism (PA) and nonPA
Characteristics PA Non PA p
N 16 24
Age (years) 53 (37-63) 52.5 (30-65) 0.658a
Gender male 13 13 0.079b
BMI (kg/m2) 27.33 (23.87-32.69) 27.87 (21.30-34.93) 0.847a
AHI
(times/hour) 41.45 (16.6-99.1) 38.85 (20.7-83.6) 0.934a
O2 nadir (%) 81 (54-90) 82.5 (20-93) 1.0a
Renin (pg/mL) 299.84 (14.85-5140.58) 369.23 (9.97-5250.74) 0.6a
Aldosteron 7488.56 (4217.86- 4687.38(2834.77- <0.05a
(pg/mL) 16367.97) 15878.67) *
ARR 35.64 (25.46-532.31) 6.18 (0.80-19.51) -

Note: values in median (minimum-maximum), a Mann Whitney U test, b Chi square test,
*statistically significant, ARR= Aldosterone Renin Ratio, Cry1= Cryptochrome1, Cry2=
Cryptochrome2 Tedjasukmana et al. Unpublished data
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Primary Aldosteronism in Indonesian
moderate to severe OSA patients
40% moderate to severe OSA patients with hypertension suffer
from primary aldosteronism (Aldosterone Renin Ratio/ARR >20).
Primary aldosteronism in OSA is not related to gender (p= 0.07),
OSA severity (p= 0.3)
Primary aldosteronism in OSA is correlated with BMI (Spearman’s
rho= 0.583, p= 0.09).

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Conclusion
Nocturnal dipping

• BP decreases during sleep


• Reduced dipping of BP during sleep increases CV risk.

Sleep duration

• Habitual short sleep duration is associated with hypertension, especially during


middle age.

Insomnia

• Insomnia with short sleep duration is associated with increased hypertension risk.
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Conclusion
RLS/PLMD

• RLS has a weak association with hypertension


• PLMD increases BP, especially when associated with arousals.

OSA

• Moderate to severe OSA is associated with prevalent hypertension; however, there


are conflicting results examining incident hypertension
• CPAP use reduces systolic and diastolic BP only modestly
• OSA is present in up to 90% of patients with resistant hypertension that may be
linked to hyperaldosteronism.

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