Original Research

Sleep Duration, Sleep Quality, and Markers of Subclinical

Arterial Disease in Healthy Men and Women
Chan-Won Kim,* Yoosoo Chang,* Di Zhao, Miguel Cainzos-Achirica, Seungho Ryu,
Hyun-Suk Jung, Kyung Eun Yun, Yuni Choi, Jiin Ahn, Yiyi Zhang, Sanjay Rampal, Youngji Baek,
Joao A. Lima, Hocheol Shin, Eliseo Guallar, Juhee Cho, Eunju Sung
ObjectiveShort and long sleep duration are associated with increased risk of clinical cardiovascular events, but the
association between sleep duration and subclinical cardiovascular disease is not well established. We examined the
association between sleep duration and sleep quality with coronary artery calcification (CAC) and with brachialankle
pulse wave velocity (PWV) in a large sample of young and middle-aged asymptomatic adults.
Approach and ResultsWe conducted a cross-sectional study of adult men and women who underwent a health checkup
examination, including assessment of sleep duration and quality and coupled with either CAC (n=29203) or brachial
ankle PWV (n=18106). The multivariate-adjusted CAC score ratios (95% confidence interval) comparing sleep durations
of 5, 6, 8, and 9 hours with 7 hours of sleep were 1.50 (1.171.93), 1.34 (1.101.63), 1.37 (0.991.89), and 1.72 (0.90
3.28), respectively (P for quadratic trend=0.002). The corresponding average differences in brachialankle PWV were
6.7 (0.7512.6), 2.9 (1.7 to 7.4), 10.5 (4.516.5), and 9.6 (0.7 to 19.8) cm/s, respectively (P for quadratic trend=0.019).
Poor subjective sleep quality was associated with CAC in women but not in men, whereas the association between poor
subjective sleep quality and brachialankle PWV was stronger in men than in women.
ConclusionsIn this large study of apparently healthy men and women, extreme sleep duration and poor subjective sleep
quality were associated with increased prevalence of CAC and higher PWV. Our results underscore the importance of an
adequate quantity and quality of sleep to maintain cardiovascular health.(Arterioscler Thromb Vasc Biol. 2015;35:00-00.
DOI: 10.1161/ATVBAHA.115.306110.)
Key Words: coronary calcification pulse wave velocity sleep duration
sleep quality subclinical atherosclerosis

leep of adequate duration and quality is essential to restore

functional capacity and maintain homeostasis.1,2 Adequate
sleep may also be critical for cardiovascular health,35 as several epidemiological studies have shown an increased risk
for clinical cardiovascular disease (CVD) events with both
short and long sleep duration.68 A common criticism of these
studies is that sleep disturbances may be the consequence of
comorbidities, such as obesity or depression, which confound
the associations between sleep duration and CVD.9 Thus, it is
important to evaluate the associations between sleep disturbances and subclinical measures of arterial disease in young
and apparently healthy participants who are less likely to be
affected by comorbidities or medication use.

Coronary artery calcium (CAC) and arterial stiffness are

subclinical measures of vascular disease, which predict the
development of CVD events.1012 The few studies that have evaluated the association between sleep duration and CAC reported
largely negative results1315 but were limited by insufficient sample size. A small prospective study showed a reduced incidence
of CAC with increasing sleep duration14 and 2 small cross-sectional studies showed that long sleep duration is associated with
higher brachialankle pulse wave velocity (baPWV),16,17 but the
limited sample size precluded a detailed estimate of the dose
response relationship.14 Moreover, little is known about the
association of subjective sleep quality with the risk of subclinical vascular disease. Therefore, we examined the associations

Received on: December 23, 2014; final version accepted on: July 24, 2015.
From the Center for Cohort Studies, Total Healthcare Center (C.-W.K., Y. Chang, S. Ryu, H.-S.J., K.E.Y., Y. Choi, J.A., Y.B., J.C.) and Department of
Occupational and Environmental Medicine (Y.C., S. Ryu), Kangbuk Samsung Hospital, Sungkyunkwan University, School of Medicine, Seoul, South Korea;
Departments of Epidemiology (D.Z., M.C.-A., Y.Z., S. Rampal, E.G., J.C.) and Medicine (E.G.), Welch Center for Prevention, Epidemiology, and Clinical
Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD; Department of Cardiology, Ciccarone Center for the Prevention
of Heart Disease, Johns Hopkins Medical Institutions, Baltimore, MD (M.C.-A.); Department of Social and Preventive Medicine, Julius Centre University
of Malaya, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia (S. Rampal); Division of Cardiology, Johns Hopkins University School of
Medicine, Baltimore, MD (J.A.L.); Department of Family Medicine, Kangbuk Samsung Hospital and Sungkyunkwan University School of Medicine, Seoul,
South Korea (H.S., E.S.); Department of Clinical Research Design & Evaluation, SAIHST, Sungkyunkwan University, Seoul, Korea (Y. Chang, S. Ryu, J.C.);
and Biostatistics and Clinical Epidemiology Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea (J.C.).
*Drs Kim and Chang are joint first authors.
The online-only Data Supplement is available with this article at http://atvb.ahajournals.org/lookup/suppl/doi:10.1161/ATVBAHA.115.306110/-/DC1.
Correspondence to Eunju Sung, MD, PhD, Department of Family Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University, School of Medicine, 108
Pyeong-dong, Jongno-gu, Seoul 110-746, South Korea. E-mail eju.sung@samsung.com; or Juhee Cho, PhD, Department of Clinical Research Design & Evaluation,
SAIHST, Sungkyunkwan University, Samsung Medical Center, 50, Irwon-Dong Kangnam-gu, Seoul, 135-710, South Korea. E-mail jcho@skku.edu
2015 American Heart Association, Inc.
Arterioscler Thromb Vasc Biol is available at http://atvb.ahajournals.org

DOI: 10.1161/ATVBAHA.115.306110

2 Arterioscler Thromb Vasc Biol October 2015

Nonstandard Abbreviations and Acronyms

baPWV
CAC
CVD

brachialankle pulse wave velocity

coronary artery calcification
cardiovascular disease

between sleep duration and quality with subclinical vascular

disease assessed by CAC and by baPWV in a large sample of
young and middle-aged asymptomatic men and women participating in a health screening program. Consistent with studies of
sleep and clinical CVD end points, we hypothesized that participants with short and long sleep durations, and those with poor
quality sleep, will have an increased prevalence of abnormalities
in subclinical markers of arterial disease.

Materials and Methods

Materials and Methods are available in the online-only Data
Supplement.

Results
Baseline Characteristics of Study Participants
The mean age of the participants in the CAC component of
the study (n=29203) was 41.8 years, and 81.4% of participants were men. The prevalence of CAC scores >0 was 14.2%
(n=4158), including a 12.0% prevalence of CAC scores of 1
to 100 (n=3501) and a 2.2% prevalence of CAC scores >100
(n=657). The mean (SD) sleep duration was 6.4 hours (1.1),
and 84.3% of participants reported good subjective sleep quality. Compared with participants who slept 7 hours, short (5
hours) sleepers were older, less likely to be married, and more
likely to have health-enhancing physical activity level, depression, hypertension, diabetes mellitus, and to be current smokers
and high-frequency alcohol users (Table1). Long (9 hours)
sleepers were less likely to be men, university graduates, or
current smokers, and had a lower frequency of alcohol intake,
but were more likely to have health-enhancing physical activity level, depression, hypertension, and diabetes mellitus than
those who slept 7 hours. Sleep quality increased with increasing
sleep duration. The mean age of participants in the PWV component of the study (n=18106) was 45.8 years, and 69.0% of the
participants were men. Factors related to sleep duration among
participants in the PWV component were similar to those associated with sleep duration in the CAC component (Table2).

Sleep Duration, CAC, and baPWV

The association between sleep duration and CAC was
U-shaped (Table3). The proportion of participants with a
positive CAC score among those sleeping 5, 6, 7, 8, and
9 hours was 16.2, 15.1, 12.5, 12.6, and 18.4%, respectively.
The multivariate-adjusted CAC score ratios (95% confidence
interval [CI]) comparing sleep durations of 5, 6, 8, and 9
hours with 7 hours were 1.50 (1.171.93), 1.34 (1.101.63),
1.37 (0.991.89), and 1.72 (0.903.28), respectively (P for
quadratic trend=0.002). Both short and long sleep duration
were associated with CAC even after adjustment by subjective sleep quality and by a modified Pittsburgh Sleep Quality
Index score (not shown).

The association between sleep duration and baPWV was also

U-shaped (Table4). The multivariable-adjusted average differences in baPWV (95% CI) comparing sleep durations of 5, 6,
8, and 9 hours with 7 hours were 6.7 (0.712.6), 2.9 (1.7 to
7.4), 10.5 (4.716.5), and 9.6 (0.7 to 19.8) cm/s, respectively (P
for quadratic trend=0.019). Sensitivity analyses setting baPWV
values >2000 to 2000 cm/s yielded similar findings (not shown).

Sleep Quality, CAC, and baPWV

Poor subjective sleep quality was associated with CAC in women
but not in men (P for interaction <0.001; Table3). Women
with poor subjective sleep quality had an increased prevalence
of positive CAC scores compared with those with good subjective sleep quality (8.8 versus 5.6%; P<0.001), whereas no
significant difference was observed between subjective sleep
quality and the prevalence of positive CAC scores in men (16.9
versus 15.8%; P=0.13). The CAC score ratios comparing poor
with good sleep quality were 1.10 (95% CI, 0.861.42) and
2.46 (95% CI, 1.304.65) in men and women, respectively. In
women, this association remained significant after adjusting for
potential confounders and biological mediators.
Poor subjective sleep quality was associated with higher
baPWV, but the association was stronger in men than in
women (Table4). The multivariable-adjusted average differences in baPWV (95% CI) comparing poor with good sleep
quality were 6.6 (1.611.6) and 2.7 (5.3 to 10.7) in men and
women, respectively.

Subgroup Analyses
The association between sleep duration with both CAC and
baPWV was modified by age. For CAC, a U-shaped association was evident in both young and old participants, but
the association was slightly stronger in younger participants
(Table5). For baPWV, older participants showed a U-shaped
pattern, but in younger participants, only short sleep duration
was associated with increased baPWV (Table6). Other factors
did not significantly modify the association of sleep duration
with CAC or baPWV.

Discussion
In this large study of apparently healthy men and women, sleep
duration showed a U-shaped association with coronary calcification and arterial stiffness, independent of cardiovascular
risk factors, socioeconomic characteristics, and subjective sleep
quality. Participants who reported 7 hours of sleep duration had
lower burden of CAC and lower baPWV when compared with
participants with shorter or longer sleep durations. Poor subjective sleep quality was also associated with a higher burden of
CAC and a higher baPWV, although the association with CAC
was stronger in women, whereas the association with baPWV
was stronger in men. Because of the large sample size of our
study compared with previous studies in this area, we were able
to provide detailed doseresponse analysis of the association of
sleep duration with CAC and with baPWV for a wide range of
sleep durations and observed a U-shaped relationship.
Only 3 studies have evaluated the association between
sleep duration and CAC.1315 Two small studies were essentially null.13,15 In addition to sample size, the discrepancies

Kim et al Sleep Duration and Subclinical Arterial Disease 3

Table 1. Baseline Characteristics of Participants in the Coronary Artery Calcium Component of the Study (n=29203)*
Sleep Duration, h
Overall
No. of participants
Age, y
Men, %

P for Trend

29203

4564

11819

9416

2869

535

41.8 (7.3)

42.3 (7.5)

41.9 (6.8)

41.5 (7.2)

41.6 (8.4)

41.6 (10.5)

<0.001

81.4

81.6

86.3

81.4

66.2

51.8

<0.001

Never

41.9

40.4

39.0

42.4

52.5

59.3

<0.001

Former

26.7

23.9

28.4

27.2

23.3

17.6

Current

31.4

35.7

32.6

30.4

24.2

23.1

None

12.9

12.9

10.7

12.3

19.8

32.9

Moderate

68.7

65.4

69.0

71.2

67.0

54.2

High

18.5

21.7

20.2

16.5

13.3

12.9

HEPA, %

17.8

18.5

18.0

17.4

18.3

21.7

<0.001

Married, %

90.3

87.2

90.2

91.1

92.9

90.8

<0.001

University education or higher, %

75.8

75.5

78.6

76.0

67.3

56.5

<0.001

Smoking status, %

Alcohol, %

Depression, %

1.8

2.3

4.3

<0.001

24.3 (3.1)

24.7 (3.2)

24.5 (3.0)

24.1 (3.1)

23.7 (3.2)

23.7 (3.3)

<0.001

Systolic BP, mmHg

112.9 (12.7)

113.1 (12.7)

113.4 (12.5)

112.8 (12.7)

111.5 (13.0)

111.5 (14.5)

<0.001

Diastolic BP, mmHg

73.5 (10.0)

73.5 (10.1)

73.9 (9.9)

73.4 (9.9)

72.3 (10.0)

72.3 (10.7)

<0.001

BMI, kg/m2

Hypertension, %
Fasting glucose, mg/dL
Diabetes mellitus, %
Total cholesterol, mg/dL

2.6

16.5
98.6 (16.3)
5.6
202.5 (35.3)

5.2

2.3

<0.001

18.2
99.0 (17.2)

16.7
98.8 (16.5)

6.1
203.5 (35.6)

5.7
202.9 (35.1)

15.7
98.3 (15.8)
5.1
202.3 (35.1)

15.0
97.8 (15.0)
4.9
201.0 (36.5)

21.2
97.8 (19.1)
8.8

<0.001
0.002
<0.001

201.0 (34.5)

0.001

HDL cholesterol, mg/dL

53.8 (13.5)

54.0 (13.9)

53.4 (13.3)

53.7 (13.2)

54.9 (14.1)

54.9 (15.3)

<0.001

LDL cholesterol, mg/dL

128.9 (32.2)

129.7 (32.5)

129.4 (32.1)

128.9 (32.0)

126.9 (32.3)

126.9 (32.2)

<0.001

Triglycerides, mg/dL

136.5 (90.4)

138.1 (87.2)

139.6 (91.2)

134.9 (89.5)

129.3 (96.4)

129.3 (76.6)

<0.001

hsCRP, mg/dL

0.1 (0.3)

0.1 (0.3)

0.1 (0.3)

0.1 (0.3)

0.1 (0.2)

0.1 (0.4)

0.01

HOMA-IR

1.3 (0.92.0)

1.3 (0.92.0)

1.3 (0.92.0)

1.3 (0.92.0)

1.3 (0.92.0)

1.3 (0.82.1)

0.95

84.3

64.3

84.9

90.7

91.7

87.1

<0.001

85.8

83.8

84.9

87.5

87.5

81.7

<0.001

1100

12.0

13.8

12.8

10.5

10.1

14.8

>100

2.2

2.4

2.3

2.0

2.5

3.6

20.0 (6.058.0)

25.0 (7.077.0)

23.5 (7.081.0)

Subjective good sleep quality, %

CAC score, %

Agatston units

19.0 (5.059.0)

19.0 (5.056.0)

18.0 (5.058.0)

0.01

BMI indicates body mass index; BP, blood pressure; CAC, coronary artery calcification; HDL, high-density lipoprotein; HEPA, health-enhancing physical activity;
HOMA-IR, homeostasis model assessment of insulin resistance; hsCRP, high sensitivity C-reactive protein; and LDL, low-density lipoprotein.
*Values are mean (SDs) or percentage.
Median (interquartile range).
Median (interquartile range) in participants with a CAC score >0.

with our findings may be based on the analytic approach, as

these studies estimated the average change in CAC per 1 hour
increase in sleep duration assuming a linear relationship,14,15
or compared mean sleep duration across CAC groups (0,
199, and 100).13 In the Coronary Artery Risk Development
in Young Adults (CARDIA) study, sleep duration measured
by actigraphy was related to an increased incidence of CAC
after >5 years of follow-up.14 In the CARDIA study, the small
number of events (61 incident cases of CAC) precluded a
more detailed study of the doseresponse relationship. Only
2 studies have evaluated the association between sleep duration and arterial stiffness.16,17 In a population-based study of

3508 Taiwanese adults, long sleep duration was associated

with a higher risk of increased arterial stiffness in males. Both
studies, conducted in East Asian populations, found a positive
association of long sleep duration with PWV. Our results are in
line with these findings and also showed that participants with
short sleep duration also had increased baPWV when compared with those who reported with 7 hours of sleep duration.
Our study thus provides novel evidence that the association
of sleep duration with markers of subclinical coronary atherosclerosis and of arterial stiffness is U-shaped, and provides a
pathological basis for both linking short and long sleep duration with an increased incidence of CVD events. Indeed, our

4 Arterioscler Thromb Vasc Biol October 2015

Table 2. Baseline Characteristics of Participants in the BaPWV Component of the Study (n=18106)*
Sleep Duration, h
Overall
No. of participants

18106

Age, y

45.8 (10.0)

Men, %

69.0

2536

6203

46.3 (10.1)

6151

45.5 (9.2)

65.6

72.7

45.4 (9.7)
70.7

8
2514

9
702

P for Trend

46.2 (11.1)

48.1 (13.2)

0.006

63.4

52.9

<0.001
<0.001

Smoking status, %
Never

45.1

46.6

42.5

45.3

47.7

53.7

Former

24.3

21.6

25.0

25.0

25.0

18.7

Current

30.6

31.9

32.5

29.8

27.3

27.6

Alcohol, %
None

18.7

19.9

16.1

17.2

22.4

36.6

Moderate

58.1

54.9

58.7

60.6

57.4

45.2

<0.001

High

23.2

25.2

25.2

22.2

20.3

18.4

HEPA, %

22.4

23.2

22.0

21.9

22.4

26.5

0.001

Married, %

86.9

83.9

86.8

88.7

86.9

81.4

<0.001

University education or higher, %

74.0

71.0

78.8

75.9

67.4

49.0

<0.001

5.6

<0.001

Depression, %
BMI, kg/m2

3.5

7.2

3.1

2.5

3.0

23.6 (3.0)

23.8 (3.2)

23.7 (2.9)

23.5 (3.0)

23.2 (3.0)

22.9 (3.0)

Systolic BP, mmHg

110.9 (13.4)

111.2 (13.7)

111.0 (13.2)

110.9 (13.4)

110.4 (13.4)

110.8 (14.4)

0.053

Diastolic BP, mmHg

71.6 (10.0)

71.9 (10.2)

71.7 (9.9)

71.6 (9.9)

71.1 (10.0)

71.1 (10.5)

0.001

Hypertension, %
Fasting glucose, mg/dL
Diabetes mellitus, %
Total cholesterol, mg/dL

8.7
97.2 (14.6)
3.6
200.2 (34.2)

9.9

8.7

97.8 (17.6)

97.3 (14.0)

4.5
200.9 (34.8)

3.6
201.5 (33.5)

8.4
97.1 (14.2)
3.3
199.9 (34.2)

8.0
96.5 (13.4)
3.1
197.8 (34.9)

<0.001

9.9

0.13

97.9 (15.4)

0.025

4.1
198.7 (35.3)

0.030
<0.001

HDL cholesterol, mg/dL

56.7 (14.6)

57.0 (14.6)

56.9 (14.6)

56.3 (14.6)

56.7 (14.4)

57.5 (15.6)

0.47

LDL cholesterol, mg/dL

126.2 (31.7)

126.2 (31.9)

127.1 (31.0)

126.2 (32.0)

123.9 (32.1)

124.4 (32.9)

<0.001

Triglycerides, mg/dL

120.3 (82.1)

121.4 (83.5)

120.6 (83.8)

120.4 (79.6)

118.5 (83.7)

118.4 (76.1)

0.17

hsCRP, mg/dL

0.1 (0.4)

0.1 (0.4)

0.1 (0.4)

0.1 (0.3)

0.1 (0.4)

0.2 (0.3)

0.14

HOMA-IR

1.1 (0.71.7)

1.1 (0.71.7)

1.1 (0.71.7)

1.1 (0.81.7)

1.1 (0.71.7)

1.1 (0.71.6)

Subjective good sleep quality, %

BaPWV, cm/s

81.7
1340.0 (181.2)

55.5
1345.0 (184.1)

81.2
1337.3 (170.8)

89.0
1334.1 (177.9)

90.6
1346.2 (195.5)

0.39

86.7

<0.001

1364.1 (226.0)

0.30

BaPWV indicates brachialankle pulse wave velocity; BMI, body mass index; BP, blood pressure; HDL, high-density lipoprotein; HEPA, health-enhancing physical
activity; HOMA-IR, homeostasis model assessment of insulin resistance; hsCRP, high sensitivity C-reactive protein; and LDL, low-density lipoprotein.
*Values are mean (SDs) or percentage.
Median (interquartile range).

findings are consistent with previous epidemiological studies

on the association between sleep duration and clinical CVD
events or mortality. Sleep duration showed a U-shaped association with CHD incidence and CVD mortality in several population-based cohort studies.1820 In a meta-analysis of cohort
studies, the relative risks for incident CHD in participants with
short and long sleep duration were 1.48 and 1.38, respectively.6
Several mechanisms may account for the U-shaped association of sleep duration with coronary calcification and with
arterial stiffness. Quantitatively and qualitatively insufficient
sleep is associated with many cardiometabolic abnormalities,21 including elevated blood pressure,22 impaired glucose
metabolism,23 and inflammatory markers,24 which may be
mediated by changes in cortisol levels.25,26 The association
of sleep duration with CAC and baPWV did not materially
change after adjusting for body mass index, systolic blood
pressure, fasting serum glucose, or C-reactive protein, but we

did not have measures of cortisol levels in our study. Sleep

deprivation was also associated with endothelial dysfunction27 and increased endothelin-1 leading to elevated vascular
smooth muscle tone.28 In addition, a recent study by our group
showed that short sleep duration and poor sleep quality were
associated with an increased risk of nonalcoholic fatty liver
disease, a marker of pathological ectopic fat deposition29 that
may be associated with subclinical vascular disease.30,31
With respect to the mechanisms involved in the association between long sleep duration with CAC and baPWV, long
sleep duration has been associated with increased levels of
inflammatory markers.32 Sleep fragmentation and concomitant nocturnal arousal attributed to long sleep duration33,34 may
also activate the sympathetic nervous system.35 Additional
mechanistic studies are needed to fully understand the association of both short and long duration of sleep with coronary
atherosclerosis and arterial stiffness.

Kim et al Sleep Duration and Subclinical Arterial Disease 5

Table 3. Coronary Artery Calcium Score Ratios (95% Confidence Interval) by Sleep Duration Category and Sleep Quality
(n=29203)*
Overall

Men

Women

Crude

Multivariable-Adjusted

Crude

Multivariable-Adjusted

Crude

Multivariable-Adjusted

5 h

2.24 (1.692.96)

1.50 (1.171.93)

2.03 (1.522.71)

1.48 (1.141.92)

6.10 (2.3116.13)

1.66 (0.713.84)

6h

1.76 (1.412.20)

1.34 (1.101.63)

1.53 (1.221.92)

1.33 (1.091.63)

2.25 (0.955.35)

1.29 (0.622.67)

Sleep duration category

7h

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

8h

1.07 (0.751.53)

1.37 (0.991.89)

1.40 (0.952.06)

1.24 (0.871.75)

2.75 (1.017.48)

2.22 (0.955.21)

9 h

3.77 (1.957.26)

1.72 (0.903.28)

9.27 (4.2620.18)

1.53 (0.723.23)

8.42 (1.9336.67)

2.70 (0.7110.22)

<0.001

0.19

P value for quadratic

trend

<0.001

0.002

<0.001

0.006

Subjective sleep quality

Good

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

1.00 (Reference)

Poor

1.45 (1.181.79)

1.23 (0.981.55)

1.01 (0.851.19)

1.10 (0.861.42)

2.61 (1.544.41)

2.46 (1.304.65)

CAC indicates coronary artery calcium.

*CAC score ratios derived from Tobit regression models using ln (CAC+1) as the outcome.
Adjusted for age, sex, study center, year of visit, education, marital status, depression, smoking status, alcohol consumption, physical activity, body mass index,
fasting glucose, systolic blood pressure, diastolic blood pressure, height, and heart rate.
Derived from a quadratic term to test nonlinear relationships centered at 7-h sleep duration.

The relationship between sleep duration and CAC were

statistically significantly different in younger compared with
older participants, but the overall shape and direction of the
association were similar. For baPWV, young participants with
long duration of sleep did not have increased arterial stiffness.
Some studies have shown that the adverse effects of extreme
sleep duration on health are weaker in older participants and
hypothesized that the age-related increase in comorbidities
may confound the association between sleep and cardiovascular health.22,36 This hypothesis is unlikely to explain the
differences in our study, as study participants were asymptomatic and free of clinically overt disease, but we did not have
detailed sleep questionnaires to assess the potentially different
reasons for extreme sleep durations in younger compared with
older participants.

Interestingly, the observed associations between sleep

duration and subclinical CVD were independent of subjective
sleep quality. In a recent study, subjective sleep disturbance
mediated the effect of self-reported short sleep duration on an
increased risk of obesity, which is a risk factor for coronary
atherosclerosis.37 In our study, poor subjective sleep quality
slightly attenuated the association between sleep duration and
markers of subclinical arterial disease, but the association
remained significant. Our findings suggest that extreme sleep
duration may affect cardiovascular system even in individuals
who reported subjective good sleep quality.
The association of sleep quality with CAC was stronger in
women compared with men, whereas the association of sleep
quality with baPWV was stronger in men compared with
women. There are well-known differences between men and

Table 4. Average Differences (95% Confidence Interval) in BrachialAnkle Pulse Wave Velocity (cm/s) by Sleep Duration Category
and Sleep Quality (n=18106)
Overall
Crude

Men

Multivariable-Adjusted*

Women

Crude

Multivariable-Adjusted*

Crude

Multivariable-Adjusted*

Sleep duration category

5 h

13.9 (5.5 to 22.3)

6.7 (0.7 to 12.6)

10.9 (1.2 to 20.7)

5.6 (1.9 to 13.0)

35.1 (20.5 to 49.7)

6.4 (3.4 to 16.3)

6h

3.2 (3.2 to 9.6)

2.9 (1.7 to 7.4)

1.9 (9.0 to 5.3)

1.7 (3.8 to 7.2)

8.9 (3.1 to 20.9)

5.3 (2.7 to 13.3)

7h

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

8h

12.1 (3.7 to 20.5)

10.5 (4.5 to 16.5)

23.1 (13.2 to 32.9)

12.1 (4.5 to 19.7)

13.9 (0.5 to 28.3)

9.4 (0.2 to 19.0)

9 h

30.1 (15.9 to 44.2)

9.6 (0.7 to 19.8)

68.9 (50.6 to 87.1)

20.6 (6.4 to 34.8)

26.1 (4.9 to 47.4)

2.3 (16.6 to 12.1)

<0.001

0.019

<0.001

0.029

<0.001

0.58

P value for quadratic

trend
Subjective sleep quality
Good

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

0.0 (Reference)

Poor

1.3 (5.6 to 8.1)

6.6 (1.6 to 11.6)

5.6 (2.5 to 13.7)

7.6 (1.2 to 13.9)

10.9 (0.8 to 22.7)

2.7 (5.3 to 10.7)

*Adjusted for age, sex, study center, year of visit, education, marital status, depression, smoking status, alcohol consumption, physical activity, body mass index,
fasting glucose, systolic blood pressure, diastolic blood pressure, height, and heart rate.
Derived from a quadratic term to test nonlinear relationships centered at 7-h sleep duration.

6 Arterioscler Thromb Vasc Biol October 2015

Table 5. Multivariable-Adjusted Coronary Artery Calcium Score Ratios (95% Confidence Interval) by Sleep Duration Category in
Selected Population Subgroups (n=29203)*
Sleep Duration, h
5

P for Interaction

<45 (n=20865)

1.97 (1.342.91)

1.78 (1.322.40)

1.00 (Reference)

1.41 (0.872.29)

2.38 (0.757.49)

0.001

45 (n=8338)

1.23 (0.757.49)

0.91 (0.691.22)

1.00 (Reference)

1.65 (1.042.61)

2.26 (1.074.77)

Non-current smoker (n=17499)

1.55 (1.102.20)

1.39 (1.071.81)

1.00 (Reference)

1.64 (1.082.50)

1.79 (0.654.93)

Current smoker (n=8018)

1.47 (0.962.25)

1.41 (0.991.99)

1.00 (Reference)

0.86 (0.461.60)

1.13 (0.284.47)

Non-drinker (n=3760)

0.74 (0.371.51)

0.96 (0.551.66)

1.00 (Reference)

0.77 (0.351.68)

2.67 (1.007.15)

Drinker (n=25443)

1.67 (1.282.18)

1.41 (1.141.74)

1.00 (Reference)

1.54 (1.092.19)

1.47 (0.623.51)

<25 (n=17966)

1.60 (1.122.28)

1.36 (1.041.78)

1.00 (Reference)

1.50 (0.982.27)

2.34 (0.945.78)

25 (n=11203)

1.42 (1.002.02)

1.32 (1.001.76)

1.00 (Reference)

1.19 (0.721.97)

1.22 (0.502.98)

<16 (n=24850)

1.49 (1.131.95)

1.28 (1.041.58)

1.00 (Reference)

1.28 (0.901.82)

1.83 (0.814.14)

16 (n=2411)

1.42 (0.603.34)

1.25 (0.582.71)

1.00 (Reference)

2.24 (0.687.35)

0.39 (0.052.88)

No (n=23955)

1.61 (1.212.13)

1.40 (0.682.01)

1.00 (Reference)

1.40 (0.972.02)

2.15 (1.034.50)

Yes (n=4806)

1.17 (0.682.01)

1.07 (0.701.64)

1.00 (Reference)

1.22 (0.632.38)

0.87 (0.233.29)

Age, y

Smoking status
0.85

Alcohol intake
0.21

BMI, kg/m2
0.85

CESD scores
0.49

HEPA
0.51

BMI indicates body mass index; CESD, Center for Epidemiologic Study Depression scale; and HEPA, health-enhancing physical activity.
*Adjusted for age, sex, study center, year of visit, education, marital status, depression, smoking status, alcohol consumption, physical activity, body mass index,
fasting glucose, systolic blood pressure, diastolic blood pressure, height, and heart rate.

women in terms of cardiovascular risk and the development of

atherosclerosis, which maybe mediated by hormonal differences
or difference in health behaviors.3840 Few studies have evaluated potential mechanisms for the interaction between sex and
subjective sleep quality on subclinical arterial disease. Elevated
inflammatory markers may be associated with poorer subjective
sleep quality in women but not in men,4143 but the implications
of these differences for the development of atherosclerosis and
arterial stiffness are unknown. In addition to possible biological
mechanisms, the differences between men and women that we
observed in our study could have originated because of multiple
comparisons or because the number of women that participated
in our study was smaller than the number of men, with increased
variability in the results for women. Further research is needed to
confirm these findings and to establish the role of sex in modulating the impact of sleep quality on subclinical arterial disease.
In our study, PWV was measured using the brachialankle
method. BaPWV is a convenient, relatively simple measurement, which integrates peripheral and central arterial stiffness.
Moreover, as the brachialankle method overcomes some of the
technical issues associated with carotid-femoral measurements,
it is appealing for epidemiological research and clinical practice, particularly in obese patients. To compare PWV measurements across studies, it is important to note that baPWV are
usually 1 to 2 m/s higher than carotid-femoral measurements.44
Several limitations should be considered when interpreting our findings. First, sleep duration was measured based
on self-report, and a misclassification of primary exposure
categorization may have occurred because self-reported
sleep duration is moderately associated with objective sleep

measures.45 Second, we excluded participants with a history

of sleep apnea, but we did not screen participants for the
presence of obstructive sleep apnea using an objective measure. Although poor subjective sleep quality and obesity are
strongly correlated with sleep apnea46,47 and may confound the
U-shaped relationships between sleep duration and markers
of subclinical arterial disease, we found that these potential
confounders did not change this associations, indicating that it
is unlikely that only sleep apnea could account for the higher
CAC scores or higher baPWV associated with extreme sleep
duration. Third, extreme sleep duration and poor sleep quality may simply be markers of other underlying pathologies.
Although we cannot completely rule out this possibility, our
study sample was comprised relatively young healthy adults
with a minimal number of comorbidities and no clinically evident CVD. Adjusting for depressive symptom score did not
modify the associations. Finally, our results were based on a
sample of relatively healthy young Korean men and women
and may not be generalizable to other populations.
The major strengths of our study were the large sample
size, the use of high quality data collection methods to obtain a
detailed panel of potential confounders and mediators, and the
use of a relatively healthy population without a history of sleep
disorders or CVD, in which the associations between sleep
duration and markers of subclinical arterial disease were less
likely to be confounded by comorbidities or medication use.

Conclusions
In conclusion, we found that extreme sleep duration or poor
subjective sleep quality was associated with higher CAC

Kim et al Sleep Duration and Subclinical Arterial Disease 7

Table 6. Multivariable-Adjusted Average Differences (95% Confidence Interval) in BrachialAnkle Pulse Wave Velocity (cm/s) by
Sleep Duration Category in Selected Population Subgroups (n=18106)*
Sleep Duration, h
5

P for Interaction
<0.001

Age, y
<45 (n=8996)

9.7 (2.0 to 17.4)

6.9 (1.2 to 12.6)

0.0 (Reference)

3.2 (4.2 to 10.7)

9.7 (23.8 to 4.3)

45 (n=9110)

3.9 (5.6 to 13.5)

1.7 (9.1 to 5.7)

0.0 (Reference)

22.2 (12.4 to 32.0)

22.9 (7.4 to 38.4)

Smoking status
Non-current smoker (n=10379) 2.4 (5.5 to 10.3)

1.2 (4.7 to 7.0)

0.0 (Reference)

6.6 (1.1 to 14.3)

1.0 (12.9 to 14.8)

Current smoker (n=4573)

12.4 (0.5 to 24.4)

7.5 (1.5 to 16.4)

0.0 (Reference)

17.3 (4.7 to 29.9)

9.3 (13.7 to 32.4)

Non-drinker (n=3380)

9.6 (4.7 to 23.9)

4.7 (6.9 to 16.3)

0.0 (Reference)

18.0 (4.3 to 31.8)

2.9 (15.8 to 21.6)

Drinker (n=14726)

5.9 (0.7 to 12.5)

2.6 (2.3 to 7.5)

0.0 (Reference)

8.8 (2.2 to 15.5)

12.1 (0.4 to 24.6)

<25 (n=12690)

4.6 (2.6 to 11.8)

2.6 (2.8 to 8.0)

0.0 (Reference)

9.1 (2.1 to 16.1)

5.9 (5.7 to 17.6)

25 (n=11203)

8.1 (2.9 to 19.0)

2.0 (6.5 to 10.5)

0.0 (Reference)

18.0 (6.3 to 29.7)

26.6 (5.4 to 47.9)

0.56

Alcohol intake
0.62

BMI, kg/m2
0.15

CESD scores
<16 (n=12631)
16 (n=1623)

1.8 (5.5 to 9.1)

1.6 (3.7 to 6.9)

0.0 (Reference)

8.8 (1.7 to 15.8)

3.9 (9.2 to 16.9)

4.6 (13.1 to 22.4)

11.4 (4.7 to 27.6)

0.0 (Reference)

17.6 (4.3 to 39.4)

1.6 (33.6 to 30.5)

0.13

HEPA
No (n=14059)

5.4 (1.4 to 12.1)

4.1 (0.9 to 9.2)

0.0 (Reference)

11.9 (5.2 to 18.7)

10.2 (1.5 to 21.9)

Yes (n=4047)

9.2 (3.8 to 22.2)

3.1 (13.1 to 7.0)

0.0 (Reference)

5.2 (8.0 to 18.3)

7.6 (13.4 to 28.6)

0.42

BMI indicates body mass index; CESD, Center for Epidemiologic Study Depression scale; and HEPA, health-enhancing physical activity.
*Adjusted for age, sex, study center, year of visit, education, marital status, depression, smoking status, alcohol consumption, physical activity, body mass index,
fasting glucose, systolic blood pressure, diastolic blood pressure, height, and heart rate.

score ratios and higher baPWV. Our results underscore the

importance of adequate sleep quantity and quality to maintain
cardiovascular health and support the need for considering
subjects with extreme duration or poor subjective quality of
sleep at high risk for CVD.

Acknowledgments
We are grateful to the hospital staff including physicians, nurses, and
cardiac imaging technologists for their assistance with the study.

Disclosures
None.

References
1. Saper CB, Cano G, Scammell TE. Homeostatic, circadian, and emotional regulation of sleep. J Comp Neurol. 2005;493:9298. doi: 10.1002/
cne.20770.
2. Hanlon EC, Van Cauter E. Quantification of sleep behavior and of its impact on
the cross-talk between the brain and peripheral metabolism. Proc Natl Acad
Sci U S A. 2011;108(suppl 3):1560915616. doi: 10.1073/pnas.1101338108.
3. Porkka-Heiskanen T, Zitting KM, Wigren HK. Sleep, its regulation
and possible mechanisms of sleep disturbances. Acta Physiol (Oxf).
2013;208:311328. doi: 10.1111/apha.12134.
4. Li Y, Zhang X, Winkelman JW, Redline S, Hu FB, Stampfer M, Ma J,
Gao X. Association between insomnia symptoms and mortality: a prospective study of U.S. men. Circulation. 2014;129:737746. doi: 10.1161/
CIRCULATIONAHA.113.004500.
5. Redline S, Foody J. Sleep disturbances: time to join the top 10 potentially
modifiable cardiovascular risk factors? Circulation. 2011;124:20492051.
doi: 10.1161/CIRCULATIONAHA.111.062190.
6. Cappuccio FP, Cooper D, DElia L, Strazzullo P, Miller MA. Sleep duration predicts cardiovascular outcomes: a systematic review and metaanalysis of prospective studies. Eur Heart J. 2011;32:14841492. doi:
10.1093/eurheartj/ehr007.

7. Shankar A, Charumathi S, Kalidindi S. Sleep duration and self-rated

health: the national health interview survey 2008. Sleep. 2011;34:1173
1177. doi: 10.5665/SLEEP.1232.
8. Sabanayagam C, Shankar A. Sleep duration and cardiovascular disease: results
from the National Health Interview Survey. Sleep. 2010;33:10371042.
9. Stranges S, Dorn JM, Shipley MJ, Kandala NB, Trevisan M, Miller MA,
Donahue RP, Hovey KM, Ferrie JE, Marmot MG, Cappuccio FP. Correlates
of short and long sleep duration: a cross-cultural comparison between the
United Kingdom and the United States: the Whitehall II Study and the
Western New York Health Study. Am J Epidemiol. 2008;168:13531364.
doi: 10.1093/aje/kwn337.
10. Keelan PC, Bielak LF, Ashai K, Jamjoum LS, Denktas AE, Rumberger
JA, Sheedy PF II, Peyser PA, Schwartz RS. Long-term prognostic value of
coronary calcification detected by electron-beam computed tomography
in patients undergoing coronary angiography. Circulation. 2001;104:412
417. doi: 10.1161/hc2901.093112.
11. Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and risk
of atherosclerotic events. Arterioscler Thromb Vasc Biol. 2003;23:554
566. doi: 10.1161/01.ATV.0000060460.52916.D6.
12. Ninomiya T, Kojima I, Doi Y, Fukuhara M, Hirakawa Y, Hata J, Kitazono
T, Kiyohara Y. Brachial-ankle pulse wave velocity predicts the development of cardiovascular disease in a general Japanese population: the
Hisayama Study. J Hypertens. 2013;31:47783; discussion 483. doi:
10.1097/HJH.0b013e32835c5c23.
13. Matthews KA, Strollo PJ Jr, Hall M, Mezick EJ, Kamarck TW, Owens JF,
Buysse DJ, Reis SE. Associations of Framingham risk score profile and
coronary artery calcification with sleep characteristics in middle-aged men
and women: Pittsburgh Sleep SCORE study. Sleep. 2011;34:711716. doi:
10.5665/SLEEP.1032.
14. King CR, Knutson KL, Rathouz PJ, Sidney S, Liu K, Lauderdale DS.
Short sleep duration and incident coronary artery calcification. JAMA.
2008;300:28592866. doi: 10.1001/jama.2008.867.
15. Matthews KA, Everson-Rose SA, Kravitz HM, Lee L, Janssen I, SuttonTyrrell K. Do reports of sleep disturbance relate to coronary and aortic calcification in healthy middle-aged women?: Study of womens health across
the nation. Sleep Med. 2013;14:282287. doi: 10.1016/j.sleep.2012.11.016.
16. Yoshioka E, Saijo Y, Kita T, Okada E, Satoh H, Kawaharada M, Kishi
R. Relation between self-reported sleep duration and arterial stiffness:

8 Arterioscler Thromb Vasc Biol October 2015

a cross-sectional study of middle-aged Japanese civil servants. Sleep.
2011;34:16811686. doi: 10.5665/sleep.1434.
17. Tsai TC, Wu JS, Yang YC, Huang YH, Lu FH, Chang CJ. Long sleep duration associated with a higher risk of increased arterial stiffness in males.
Sleep. 2014;37:13151320. doi: 10.5665/sleep.3920.
18. Ayas NT, White DP, Manson JE, Stampfer MJ, Speizer FE, Malhotra A,
Hu FB. A prospective study of sleep duration and coronary heart disease
in women. Arch Intern Med. 2003;163:205209.
19. Ikehara S, Iso H, Date C, Kikuchi S, Watanabe Y, Wada Y, Inaba Y,
Tamakoshi A; JACC Study Group. Association of sleep duration with mortality from cardiovascular disease and other causes for Japanese men and
women: the JACC study. Sleep. 2009;32:295301.
20. Shankar A, Koh WP, Yuan JM, Lee HP, Yu MC. Sleep duration and coronary heart disease mortality among Chinese adults in Singapore: a population-based cohort study. Am J Epidemiol. 2008;168:13671373. doi:
10.1093/aje/kwn281.
21. Knutson KL. Sleep duration and cardiometabolic risk: a review of

the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab.
2010;24:731743. doi: 10.1016/j.beem.2010.07.001.
22. Gangwisch JE, Heymsfield SB, Boden-Albala B, Buijs RM, Kreier F,
Pickering TG, Rundle AG, Zammit GK, Malaspina D. Short sleep duration as a risk factor for hypertension: analyses of the first National Health
and Nutrition Examination Survey. Hypertension. 2006;47:833839. doi:
10.1161/01.HYP.0000217362.34748.e0.
23. Tasali E, Leproult R, Spiegel K. Reduced sleep duration or quality: relationships with insulin resistance and type 2 diabetes. Prog Cardiovasc Dis.
2009;51:381391. doi: 10.1016/j.pcad.2008.10.002.
24. Vgontzas AN, Zoumakis E, Bixler EO, Lin HM, Follett H, Kales A,
Chrousos GP. Adverse effects of modest sleep restriction on sleepiness,
performance, and inflammatory cytokines. J Clin Endocrinol Metab.
2004;89:21192126. doi: 10.1210/jc.2003-031562.
25. Balbo M, Leproult R, Van Cauter E. Impact of sleep and its disturbances on hypothalamo-pituitary-adrenal axis activity. Int J Endocrinol.
2010;2010:759234. doi: 10.1155/2010/759234.
26. Rosmond R, Dallman MF, Bjrntorp P. Stress-related cortisol secretion in
men: relationships with abdominal obesity and endocrine, metabolic and
hemodynamic abnormalities. J Clin Endocrinol Metab. 1998;83:1853
1859. doi: 10.1210/jcem.83.6.4843.
27. Calvin AD, Covassin N, Kremers WK, Adachi T, Macedo P, Albuquerque
FN, Bukartyk J, Davison DE, Levine JA, Singh P, Wang S, Somers VK.
Experimental sleep restriction causes endothelial dysfunction in healthy
humans. J Am Heart Assoc. 2014;3:e001143. doi: 10.1161/JAHA.114.001143.
28. Weil BR, Mestek ML, Westby CM, Van Guilder GP, Greiner JJ, Stauffer
BL, DeSouza CA. Short sleep duration is associated with enhanced endothelin-1 vasoconstrictor tone. Can J Physiol Pharmacol. 2010;88:777
781. doi: 10.1139/Y10-046.
29. Kim CW, Yun KE, Jung HS, Chang Y, Choi ES, Kwon MJ, Lee EH, Woo
EJ, Kim NH, Shin H, Ryu S. Sleep duration and quality in relation to nonalcoholic fatty liver disease in middle-aged workers and their spouses. J
Hepatol. 2013;59:351357. doi: 10.1016/j.jhep.2013.03.035.
30. Kim D, Choi SY, Park EH, Lee W, Kang JH, Kim W, Kim YJ, Yoon
JH, Jeong SH, Lee DH, Lee HS, Larson J, Therneau TM, Kim WR.
Nonalcoholic fatty liver disease is associated with coronary artery calcification. Hepatology. 2012;56:605613. doi: 10.1002/hep.25593.
31. Salvi P, Ruffini R, Agnoletti D, Magnani E, Pagliarani G, Comandini G,
Pratic A, Borghi C, Benetos A, Pazzi P. Increased arterial stiffness in
nonalcoholic fatty liver disease: the Cardio-GOOSE study. J Hypertens.
2010;28:16991707. doi: 10.1097/HJH.0b013e32833a7de6.
32. Dowd JB, Goldman N, Weinstein M. Sleep duration, sleep quality, and
biomarkers of inflammation in a Taiwanese population. Ann Epidemiol.
2011;21:799806. doi: 10.1016/j.annepidem.2011.07.004.

33. Grandner MA, Drummond SP. Who are the long sleepers? Towards an
understanding of the mortality relationship. Sleep Med Rev. 2007;11:341
360. doi: 10.1016/j.smrv.2007.03.010.
34. Somers VK, Dyken ME, Mark AL, Abboud FM. Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med. 1993;328:303307. doi:
10.1056/NEJM199302043280502.
35. Dekker JM, Crow RS, Folsom AR, Hannan PJ, Liao D, Swenne CA, Schouten
EG. Low heart rate variability in a 2-minute rhythm strip predicts risk of
coronary heart disease and mortality from several causes: the ARIC Study.
Atherosclerosis Risk In Communities. Circulation. 2000;102:12391244.
36. Magee CA, Kritharides L, Attia J, McElduff P, Banks E. Short

and long sleep duration are associated with prevalent cardiovascular disease in Australian adults. J Sleep Res. 2012;21:441447. doi:
10.1111/j.1365-2869.2011.00993.x.
37. Vgontzas AN, Fernandez-Mendoza J, Miksiewicz T, Kritikou I, Shaffer
ML, Liao D, Basta M, Bixler EO. Unveiling the longitudinal association
between short sleep duration and the incidence of obesity: the Penn State
Cohort. Int J Obes (Lond). 2014;38:825832. doi: 10.1038/ijo.2013.172.
38. Mosca L, Barrett-Connor E, Wenger NK. Sex/gender differences in cardiovascular disease prevention: what a difference a decade makes. Circulation.
2011;124:21452154. doi: 10.1161/CIRCULATIONAHA.110.968792.
39. Rossi P, Francs Y, Kingwell BA, Ahimastos AA. Gender differences
in artery wall biomechanical properties throughout life. J Hypertens.
2011;29:10231033. doi: 10.1097/HJH.0b013e328344da5e.
40. Stranges S, Guallar E. Cardiovascular disease prevention in women: a rapidly evolving scenario. Nutr Metab Cardiovasc Dis. 2012;22:10131018.
doi: 10.1016/j.numecd.2012.10.001.
41. Prather AA, Epel ES, Cohen BE, Neylan TC, Whooley MA. Gender
differences in the prospective associations of self-reported sleep quality with biomarkers of systemic inflammation and coagulation: findings
from the Heart and Soul Study. J Psychiatr Res. 2013;47:12281235. doi:
10.1016/j.jpsychires.2013.05.004.
42. Miller MA, Kandala NB, Kivimaki M, Kumari M, Brunner EJ, Lowe
GD, Marmot MG, Cappuccio FP. Gender differences in the cross-sectional relationships between sleep duration and markers of inflammation:
Whitehall II study. Sleep. 2009;32:857864.
43. Suarez EC. Self-reported symptoms of sleep disturbance and inflammation, coagulation, insulin resistance and psychosocial distress: evidence for gender disparity. Brain Behav Immun. 2008;22:960968. doi:
10.1016/j.bbi.2008.01.011.
44. Tanaka H, Munakata M, Kawano Y, Ohishi M, Shoji T, Sugawara J,
Tomiyama H, Yamashina A, Yasuda H, Sawayama T, Ozawa T. Comparison
between carotid-femoral and brachial-ankle pulse wave velocity as measures of arterial stiffness. J Hypertens. 2009;27:20222027. doi: 10.1097/
HJH.0b013e32832e94e7.
45. Lauderdale DS, Knutson KL, Yan LL, Liu K, Rathouz PJ. Self-reported
and measured sleep duration: how similar are they? Epidemiology.
2008;19:838845. doi: 10.1097/EDE.0b013e318187a7b0.
46. Gunnarsson SI, Peppard PE, Korcarz CE, Barnet JH, Aeschlimann SE,
Hagen EW, Young T, Hla KM, Stein JH. Obstructive sleep apnea is associated with future subclinical carotid artery disease: thirteen-year followup from the Wisconsin sleep cohort. Arterioscler Thromb Vasc Biol.
2014;34:23382342. doi: 10.1161/ATVBAHA.114.303965.
47. Strohl KP, Brown DB, Collop N, George C, Grunstein R, Han F, Kline
L, Malhotra A, Pack A, Phillips B, Rodenstein D, Schwab R, Weaver
T, Wilson K; ATS Ad Hoc Committee on Sleep Apnea, Sleepiness, and
Driving Risk in Noncommercial Drivers. An official American Thoracic
Society Clinical Practice Guideline: sleep apnea, sleepiness, and driving risk in noncommercial drivers. An update of a 1994 Statement.
Am J Respir Crit Care Med. 2013;187:12591266. doi: 10.1164/
rccm.201304-0726ST.

Significance
Sleep duration showed a U-shaped association with subclinical arterial disease, independent of socioeconomic and lifestyle variables, other
cardiovascular risk factors, and subjective sleep quality. In addition, poor subjective sleep quality was associated with coronary artery calcification in women but not in men, whereas the association between poor subjective sleep quality and brachialankle pulse wave velocity was
stronger in men than in women. Our results underscore the importance of adequate sleep quantity and quality to maintain cardiovascular health
and also support the need to consider subjects with extreme duration or poor subjective quality of sleep at high risk for cardiovascular disease.