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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Sleep Med. 2012 Mar 31;13(6):728–731. doi: 10.1016/j.sleep.2012.01.015

Functional capacity is a better predictor of coronary heart disease than depression or abnormal sleep duration in Black and White Americans

Oladipupo Olafiranye a,b,*, Girardin Jean-Louis a,c, Mike Antwi a, Ferdinand Zizi a,c, Raphael Shaw a, Perry Brimah a, Gbenga Ogedegbe d
PMCID: PMC3372763  NIHMSID: NIHMS363166  PMID: 22465451

Abstract

Objective

To assess whether functional capacity is a better predictor of coronary heart disease (CHD) than depression or abnormal sleep duration.

Methods

Adult civilians in the USA (n=29,818, mean age 48 ± 18 years, range 18–85 years) were recruited by a cross-sectional household interview survey using multistage area probability sampling. Data on chronic conditions, estimated habitual sleep duration, functional capacity, depressed moods and sociodemographic characteristics were obtained.

Results

Thirty-five percent of participants reported reduced functional capacity. The CHD rates among White and Black Americans were 5.2% and 4%, respectively. Individuals with CHD were more likely to report extreme sleep durations [short sleep (≤ 5 h) or long sleep (≥ 9 h); odds ratio (OR) 1.65, 95% confidence interval (CI) 1.38–1.97; P<0.0001], less likely to be functionally active [anchored by the ability to walk one-quarter of a mile without assistance (OR 6.27, 95% CI 5.64–6.98; P<0.0001)] and more likely to be depressed (OR 1.78, 95% CI 1.60–1.99; P<0.0001) than their counterparts. On multivariate regression analysis adjusting for sociodemographic factors and health characteristics, only functional capacity remained an independent predictor of CHD (OR 1.81, 95% CI 1.42–2.31; P<0.0001).

Conclusion

Functional capacity was an independent predictor of CHD in the study population, whereas depression and sleep duration were not independent predictors.

Keywords: Functional capacity, Depression, Sleep duration, Coronary heart diseas, Physical activity, Mood

1. Introduction

Aberrant sleep duration, depression and impaired functional capacity are associated with coronary heart disease (CHD). There is a strong and consistent association between both short and long sleep durations and CHD [14]. Sleep disturbance constitutes a form of stress [5], which is directly related to the degree of objective sleep disturbance [6]. This has been shown to predict coronary events, and is linked to increased myocardial infarction (MI) [7].

An increasing body of evidence also suggests that psychological illness, such as depression, may have a negative impact on cardiovascular health [812]. Depression is associated with increased risk of adverse outcome and worse prognosis in individuals with congestive heart failure [13,14] and acute MI [1520], and in patients who have undergone coronary artery bypass surgery [11,21,22].

Converging data indicate that depression, sleep disturbance and poor functional capacity often co-exist [23,24]. As these factors cluster together in a variable fashion, it is difficult to discern the potential mechanism by which they exert their pathophysiological effects. Both physical activity and sleep disturbance constitute diagnostic indices for major depression [25]. Individuals experiencing depression or life stress are likely to be functionally limited [23,24], which is an independent risk factor for CHD [26,27]. Pathophysiological mechanisms that are potentially important in the development of CHD have been linked to physical inactivity and/or poor functional capacity [28]. Despite the growing evidence linking CHD to aberrant sleep duration, depression and poor functional capacity, independent associations between these factors and CHD have not been established. Hence, this cross-sectional study tested the hypothesis that functional capacity is a better predictor of CHD than depression or sleep duration.

2. Methods

2.1. Participants

This study was approved by the Institutional Review Board of State University of New York Downstate Medical Center. Data were obtained from 29,818 Americans (age range 18–85 years) participating in the 2005 National Health Interview Survey (NHIS). The present analysis included data from White (85%) and Black (15%) Americans of both genders (males 44%, females 56%).

2.2. Procedures

The NHIS is a cross-sectional household interview survey conducted annually by the National Center for Health Statistics of the Centers for Disease Control and Prevention. The NHIS uses a multistage area probability design that permits representative sampling of US households. Probability samples of the civilian adult population of all 50 states and the District of Columbia were obtained. It is estimated that the final sample was characterized by a response rate of 69%. No significant differences were found in the demographic characteristics between responders and non-responders. Details on sample design can be found in Design and Estimation for the National Health Interview Survey, 1995–2005 [29].

Participants provided sociodemographic data and information about physician-diagnosed chronic conditions during face-to-face interviews conducted by trained interviewers from the US Census Bureau. The chronic conditions included hypertension, heart disease, cancer, diabetes and arthritis. Participants also estimated habitual sleep duration (using full hour units, i.e. 5 h, 6 h, 7 h, etc.); no information on specific sleep disorders was elicited during the interview. Participants also reported depressed moods (i.e. feeling of sadness, hopelessness, worthlessness and poor effort) experienced in the past 30 days. The depression severity score used in this analysis represents a composite score, summing answers from the above-mentioned four items; scores ranged from 0 to 20 with low scores indicating greater depression. Functional capacity was measured by asking respondents whether they were able to walk one-quarter of a mile without assistance; respondents were classified as ‘limited’ if they answered that it would be very difficult or they would be unable to perform this activity, or ‘not limited’ if they were able to perform this activity.

Surveys were conducted using computer-assisted personal interviewing, which uses a computer program for data collection that guides the interviewer through the questionnaire. The interviewer enters survey responses directly into the computer. The program uses a computer algorithm to determine whether data entered by the user match against all possible responses to specific questions; the program also checks for consistency against other data collected during the interview, and saves the responses into a survey data file [30].

2.3. Statistical analysis

As the NHIS dataset amalgamates data from different samples using a multistage area probability sampling design, all analyses performed in this study used weighted statistics based on the final weights provided with the NHIS dataset. These weights represent a product of weights for corresponding units computed in each of the sampling stages. Frequency and measures of central tendency were used to describe the sample. In preliminary analyses, Pearson and Spearman correlations were used to explore relationships between variables of interest. Fisher’s exact test was used to assess differences in categorical variables, and analysis of variance was used for parametric variables.

Univariate logistic regression analyses were performed to assess the relationships between the three main factors: sleep duration, depression and functional capacity. Before constructing the final model assessing the best predictor of CHD, binary relationships were assessed between hypothesized predictors and the dependent variable; only predictors showing a P-value <0.05 were entered into the final model [31]. Covariates entered into the model were: sex, age, race/ethnicity, income, body mass index (BMI), and a history of hypertension, diabetes, arthritis or heart disease. All analyses were performed using Statistical Package for the Social Sciences Version 17.0 (IBM Corporation, NY, USA).

3. Results

The health characteristics of the individuals participating in the NHIS are provided in Table 1. The sample included White (85%) and Black (15%) Americans of both genders (males 44%, females 56%). Thirty-five percent of participants reported functional limitation due to chronic conditions: hypertension (28%), heart disease (8%), diabetes (9%) and arthritis (23%). The CHD rates among White and Black Americans were 5.2% and 4%, respectively.

Table 1.

Comparison of sociodemographic and health data of Black and White Americans participating in the 2005 National Health Interview Survey.

Variable Black
Americans
(15%)
White
Americans
(85%)
F2 P-value
Age (mean ± SD) 45.56 ±16.91 48.02 ± 18.02 72 0.0001
Female sex (%) 61 56 52 0.0001
Income >$35,000 (%) 16 24 140 0.0001
Body mass index (%
obese)
52 38 193 0.0001
Hypertension (%) 36 27 133 0.0001
Diabetes (%) 12 8 62 0.0001
Heart disease (%) 6 8 29 0.0001
Arthritis (%) 22 24 11 0.0001

SD, standard deviation.

Results of univariate regression analysis showed that individuals with CHD were more likely to report short (≤5 h) or long (≥9 h) sleep durations [odds ratio (OR) 1.65, 95% confidence interval (CI) 1.38–1.97; P<0.0001] than their counterparts. Results also showed that individuals with CHD were less likely to be functionally active [anchored by the ability to walk one-quarter of a mile (OR 6.27, 95% CI 5.64–6.98; P<0.0001)], and were more likely to be depressed [OR 1.78, 95% CI 1.60–1.99; P<0.0001] than their counterparts. Functional capacity was directly correlated with both short and long sleep durations [r=0.23 (P<0.0001) and r=0.25 (P<0.0001), respectively], and inversely correlated with depression [r=−0.27 (P<0.0001)].

Results of multivariate logistic regression analysis indicated that functional capacity remained a significant independent predictor of CHD (OR 1.81, 95% CI 1.42–2.31; P<0.0001). As shown in Table 2, adjusting for the effects of age, gender, race/ethnicity, income, BMI, and a history of hypertension, diabetes and arthritis demonstrated that extreme sleep duration and depressed mood were not significant independent predictors of CHD. However, in subgroup analysis, depression was an independent predictor of CHD in White Americans but not in Black Americans (Table 3).

Table 2.

Regression coefficients for coronary heart disease with sleep, depression, medical and sociodemographic factors, and functional capacity of the participants in the 2005 National Health Interview Survey.

Variables Odds ratio 95% Confidence interval
Lower Upper P-value
Age 1.058 1.049 1.067 0.000
Gender 0.486 0.392 0.603 0.000
Race/ethnicity 0.674 0.489 0.930 0.016
Income 0.701 0.497 0.988 0.043
Hypertension 2.564 2.005 3.279 0.000
Diabetes 1.795 1.390 2.319 0.000
Arthritis 1.246 0.987 1.574 0.064
Body mass index 1.275 1.006 1.616 0.045
Sleep 1.083 0.830 1.412 0.557
Depression 1.236 0.988 1.546 0.064
Functional capacity 1.811 1.417 2.314 0.000

Table 3.

Regression coefficients for coronary heart disease with sleep, depression, medical and sociodemographic factors, and functional capacity of Black and White Americans in the 2005 National Health Interview Survey.

Race Variable Odds ratio 95% Confidence interval P-value
Lower Upper
White Age 1.055 1.048 1.062 0.000
Gender 0.405 0.449 0.483 0.000
Income 0.665 0.509 0.870 0.000
Hypertension 2.644 2.179 3.209 0.000
Diabetes 1.504 1.205 1.877 0.000
Arthritis 1.360 1.128 1.641 0.001
Body mass index 1.112 0.990 1.249 0.074
Sleep 1.160 0.930 1.447 0.187
Depression 1.289 1.070 1.552 0.008
Functional capacity 1.731 1.418 2.112 0.000
Black Age 1.034 1.013 1.056 0.001
Gender 0.719 0.418 1.237 0.234
Income 0.239 0.056 1.025 0.054
Hypertension 7.330 2.955 18.181 0.000
Diabetes 4.010 2.341 6.867 0.000
Arthritis 1.074 0.593 1.943 0.814
Body mass index 0.926 0.641 1.336 0.681
Sleep 0.676 0.359 1.273 0.225
Depression 1.555 0.915 2.641 0.103
Functional capacity 2.407 1.305 4.439 0.005

4. Discussion

This study found that depression, sleep duration and poor functional capacity are associated with CHD. Interestingly, functional capacity remained an independent predictor of CHD after adjusting for sociodemographic factors and health characteristics, whereas depression and sleep duration did not remain independent predictors. This finding is consistent with data suggesting that physical activity predicts the likelihood of cardiovascular disease beyond that explained by commonly measured cardiometabolic risk factors [32]. Although the mechanism of this association is not entirely clear, research has shown that exercise improves coronary artery flow reserves in patients with CHD [33]. Among patients with congestive heart failure, research indicates that exercise increases the anaerobic threshold [34], and improves ventilator response and heart rate variability [35]. This evidence provide justification for the integration of regular exercise into the management of CHD and psychosocial disorders.

The present finding of a positive association between depression and CHD is consistent with prior reports [812]. In the subgroup analysis, depression was found to be an independent predictor of CHD in White Americans but not in Black Americans. This may be related to differences in population size and the limited power of subgroup analysis. In a meta-analysis involving healthy volunteers, the presence of major depression was associated with increased risk of adverse coronary events [12]. In patients who had undergone coronary artery bypass surgery, the occurrence of depressive symptoms was associated with a greater risk of graft disease progression [11]. Although the mechanism is unclear, poor psychosocial functioning may impact on cardiovascular health via biological mechanisms such as cortisol hypersecretion, disturbed hypothalamic–pituitary–adrenal axis function, elaboration of pro-inflammatory cytokines, endothelial dysfunction, atherogenic lipid profile and development of metabolic syndrome [8,10]. Unhealthy lifestyle changes (smoking, unhealthy diet, sendentary lifestyle, non-compliance with medication) have also been suggested as a possible explanation for the association between psychosocial factors and CHD [8,3639]. Consistent with the present finding, a recent study involving 49,321 young Swedish men who were followed for 37 years showed that early-onset depression is not an independent predictor of CHD after adjusting for well-established vascular risk factors [40]. These observations raise concerns about the true association between depression and CHD.

In agreement with previous studies, the present study found a strong association between abnormal sleep duration and CHD [14]. Although the mechanism underlying the observed association is not well understood, it may relate to adverse physiological changes relating to CHD risk that are associated with sleep disturbance [41,42]. Both long and short sleep durations are associated with elevated markers of inflammation, abnormal lipid profile, insulin resistance, increased BMI, diabetes mellitus and hypertension [4346], all of which are independent predictors of CHD [47]. Sleep disturbance in itself can constitute a form of stress [5], which is directly related to the degree of objective sleep disturbance [6]. This has been shown to predict coronary events, possibly mediated through increased sympathetic nervous system activity [7,8]. Investigators have observed that sympathetic arousal and early-morning insomnia were associated with cardiac disease in a sample of 4041 patients [48]. Among older adults, the severity of insomnia was directly related to use of cardiovascular drugs, general fatigue, exhaustion, angina pectoris, cardiac insufficiency, worsened objective and subjective health, presence of negative T waves on electrocardiogram, and lower survival rates [49]. However, in the present study, abnormal sleep duration was not an independent predictor of CHD after controlling for other sociodemographic factors and health characteristics.

This study has some limitations. First, the findings may not be generalized to Black and White individuals across the lifespan, as the majority of the study population were White Americans aged <65 years. Also, research has shown clear evidence of race/ethnicity-based neurobiological differences in sleep regulation, depression and CHD risk [50]. Second, this analysis was based on subjective reports of depression, functional capacity and sleep duration. Future studies should examine associations between these factors using objective data.

In conclusion, this study found that functional capacity was an independent predictor of CHD after adjusting for sociodemographic factors and health characteristics, whereas depression and sleep duration were not independent predictors.

Acknowledgments

Funding source

This research was supported by funding from the NIH (R01MD004113, R25HL105444 and P20MD005092).

Footnotes

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References

  • 1.Ayas NT, White DP, Manson JE, Stampfer MJ, Speizer FE, Malhotra A, et al. A prospective study of sleep duration and coronary heart disease in women. Arch Intern Med. 2003;163:205–209. doi: 10.1001/archinte.163.2.205. [DOI] [PubMed] [Google Scholar]
  • 2.Tamakoshi A, Ohno Y. Self-reported sleep duration as a predictor of all-cause mortality: results from the JACC Study, Japan. Sleep. 2004;27:51–54. [PubMed] [Google Scholar]
  • 3.Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, et al. A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort. Sleep. 2007;30:1659–1666. doi: 10.1093/sleep/30.12.1659. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Sabanayagam C, Shankar A. Sleep duration and cardiovascular disease: results from the National Health Interview Survey. Sleep. 2010;33:1037–1042. doi: 10.1093/sleep/33.8.1037. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Van Diest R, Appels WP. Sleep physiological characteristics of exhausted men. Psychosom Med. 1994;56:28–35. doi: 10.1097/00006842-199401000-00004. [DOI] [PubMed] [Google Scholar]
  • 6.Vgontzas AN, Tsigos C, Bixler EO, Stratakis CA, Zachman K, Kales A, et al. Chronic insomnia and activity of the stress system: a preliminary study. J Psychosom Res. 1998;45:21–31. doi: 10.1016/s0022-3999(97)00302-4. [DOI] [PubMed] [Google Scholar]
  • 7.Schwartz SW, Cornoni-Huntley J, Cole SR, Hays JC, Blazer DG, Schocken DD. Are sleep complaints an independent risk factor for myocardial infarction? Ann Epidemiol. 1998;8:384–392. doi: 10.1016/s1047-2797(97)00238-x. [DOI] [PubMed] [Google Scholar]
  • 8.Rozanski A, Blumenthal J, Kaplan J. Impact of psychosocial factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation. 1999;99:2192–2217. doi: 10.1161/01.cir.99.16.2192. [DOI] [PubMed] [Google Scholar]
  • 9.Kubzansky LD, Kawachi I. Going to the heart of the matter: do negative emotions cause coronary heart disease. J Psychosom Res. 2000;48:323–337. doi: 10.1016/s0022-3999(99)00091-4. [DOI] [PubMed] [Google Scholar]
  • 10.Strike P, Steptoe A. Psychosocial factors in the development of coronary artery disease. Prog Cardiovasc Dis. 2004;46:337–347. doi: 10.1016/j.pcad.2003.09.001. [DOI] [PubMed] [Google Scholar]
  • 11.Wellenius GA, Mukamal KJ, Kulshreshtha A, Asonganyi S, Mittleman MA. Depressive symptoms and the risk of atherosclerotic progression among patients with coronary artery bypass grafts. Circulation. 2008;117:2313–2319. doi: 10.1161/CIRCULATIONAHA.107.741058. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Rugulies R. Depression as a predictor for coronary heart disease. a review and meta-analysis. Am J Prev Med. 2002;23:51–61. doi: 10.1016/s0749-3797(02)00439-7. [DOI] [PubMed] [Google Scholar]
  • 13.Jiang W, Alexander J, Christopher E, Kuchibhatla M, Gaulden LH, Cuffe MS, et al. Relationship of depression to increased risk of mortality and rehospitalization in patients with congestive heart failure. Arch Intern Med. 2001;161:1849–1856. doi: 10.1001/archinte.161.15.1849. [DOI] [PubMed] [Google Scholar]
  • 14.Murberg TA, Bru E, Svebak S, Tveteras R, Aarsland T. Depressed mood and subjective health symptoms as predictors of mortality in patients with congestive heart failure: a two-year follow-up study. Int J Psychiatry Med. 1999;29:311–326. doi: 10.2190/0C1C-A63U-V5XQ-1DAL. [DOI] [PubMed] [Google Scholar]
  • 15.Frasure-Smith N, Lesperance F, Talajic M. Depression and 18-month prognosis after myocardial infarction. Circulation. 1995;91:999–1005. doi: 10.1161/01.cir.91.4.999. [DOI] [PubMed] [Google Scholar]
  • 16.Lesperance F, Frasure-Smith N, Talajic M, Bourassa MG. Five-year risk of cardiac mortality in relation to initial severity and one-year changes in depression symptoms after myocardial infarction. Circulation. 2002;105:1049–1053. doi: 10.1161/hc0902.104707. [DOI] [PubMed] [Google Scholar]
  • 17.Ahern DK, Gorkin L, Anderson JL, Tierney C, Hallstrom A, Ewart C, et al. Biobehavioral variables and mortality or cardiac arrest in the Cardiac Arrhythmia Pilot Study (CAPS) Am J Cardiol. 1990;66:59–62. doi: 10.1016/0002-9149(90)90736-k. [DOI] [PubMed] [Google Scholar]
  • 18.Welin C, Lappas G, Wilhelmsen L. Independent importance of psychosocial factors for prognosis after myocardial infarction. J Intern Med. 2000;247:629–639. doi: 10.1046/j.1365-2796.2000.00694.x. [DOI] [PubMed] [Google Scholar]
  • 19.Bush DE, Ziegelstein RC, Tayback M, Richter D, Stevens S, Zahalsky H, et al. Even minimal symptoms of depression increase mortality risk after acute myocardial infarction. Am J Cardiol. 2001;88:337–341. doi: 10.1016/s0002-9149(01)01675-7. [DOI] [PubMed] [Google Scholar]
  • 20.Horsten M, Mittleman MA, Wamala SP, Schenck-Gustafsson K, Orth-Gomer K. Depressive symptoms and lack of social integration in relation to prognosis of CHD in middle-aged women. The Stockholm Female Coronary Risk Study. Eur Heart J. 2000;21:1072–1080. doi: 10.1053/euhj.1999.2012. [DOI] [PubMed] [Google Scholar]
  • 21.Connerney I, Shapiro PA, McLaughlin JS, Bagiella E, Sloan RP. Relation between depression after coronary artery bypass surgery and 12-month outcome: a prospective study. Lancet. 2001;358:1766–1771. doi: 10.1016/S0140-6736(01)06803-9. [DOI] [PubMed] [Google Scholar]
  • 22.Blumenthal JA, Lett H, Babyak M, White W, Smith P, Mark D, et al. Depression as a risk factor for mortality following coronary artery bypass surgery. Lancet. 2003;362:604–609. doi: 10.1016/S0140-6736(03)14190-6. [DOI] [PubMed] [Google Scholar]
  • 23.Fox K. The influence of physical activity on mental well being. Public Health Nutr. 1999;2:411–418. doi: 10.1017/s1368980099000567. [DOI] [PubMed] [Google Scholar]
  • 24.Paluska SA, Schwenk TL. Physical activity and mental health: current concepts. Sports Med. 2000;29:167–180. doi: 10.2165/00007256-200029030-00003. [DOI] [PubMed] [Google Scholar]
  • 25.World Health Organization. The ICD-10 classification of mental and behavioural disorders: clinical descriptions and diagnostic guidelines. Geneva: World Health Organization; 1992. [Google Scholar]
  • 26.Blair SN, Morris JN. Healthy hearts and the universal benefits of being physically active: Physical activity and health. Ann Epidemiol. 2009;19:253–256. doi: 10.1016/j.annepidem.2009.01.019. [DOI] [PubMed] [Google Scholar]
  • 27.Wannamethee S, Shaper A. Physical activity and cardiovascular disease. Semin Cardiovasc Med. 2002;2:257–266. doi: 10.1055/s-2002-35400. [DOI] [PubMed] [Google Scholar]
  • 28.Bauman AE. Updating the evidence that physical activity is good for health: an epidemiological review 2000–2003. J Sci Med Sport. 2004;7:6–19. doi: 10.1016/s1440-2440(04)80273-1. [DOI] [PubMed] [Google Scholar]
  • 29.Botman SL, Moore TF, Moriarity CL, Parsons VL. Design and estimation for the National Health Interview Survey, 1995–2004. National Center for Health Statistics. Vital Health Stat 2. 2000;130:1–31. [PubMed] [Google Scholar]
  • 30.National Center for Health Statistics. [last accessed 07/02/2010];National Health Interview Survey: questionnaires, datasets, and related documentation. Available at: http://www.cdc.gov/nchs/nhis/about_nhis.htm.
  • 31.Hosmer DW, Taber S, Lemeshow S. The importance of assessing the fit of logistic regression models: a case study. Am J Public Health. 1991;81:1630–1635. doi: 10.2105/ajph.81.12.1630. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.McGuire KA, Janssen I, Ross R. Ability of physical activity to predict cardiovascular disease beyond commonly evaluated cardiometabolic risk factors. Am J Cardiol. 2009;104:1522–1526. doi: 10.1016/j.amjcard.2009.07.023. [DOI] [PubMed] [Google Scholar]
  • 33.Hambrecht R, Wolf A, Gielen S, Linke A, Hofer J, Erbs S, et al. Effect of exercise on coronary endothelial function in patients with coronary artery disease. N Engl J Med. 2000;342:454–460. doi: 10.1056/NEJM200002173420702. [DOI] [PubMed] [Google Scholar]
  • 34.McKelvie RS, Teo KK, Roberts R, McCartney N, Humen D, Montague T, et al. Effects of exercise training in patients with heart failure: the Exercise Rehabilitation Trial (EXERT) Am Heart J. 2002;144:23–30. doi: 10.1067/mhj.2002.123310. [DOI] [PubMed] [Google Scholar]
  • 35.Piña IL, Apstein CS, Balady GJ, Belardinelli R, Chaitman BR, Duscha BD, et al. Exercise and heart failure: a statement from the American Heart Association Committee on Exercise, Rehabilitation, and Prevention. Circulation. 2003;107:1210–1225. doi: 10.1161/01.cir.0000055013.92097.40. [DOI] [PubMed] [Google Scholar]
  • 36.Yusuf S, Hawkin S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case–control study. Lancet. 2004;364:937–952. doi: 10.1016/S0140-6736(04)17018-9. [DOI] [PubMed] [Google Scholar]
  • 37.Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation. 1998;97:1837–1847. doi: 10.1161/01.cir.97.18.1837. [DOI] [PubMed] [Google Scholar]
  • 38.Kubzansky LD, Cole SR, Kawachi I, Vokonas PS, Sparrow D. Shared and unique contributions of anger, anxiety, and depression to coronary heart disease: a prospective study in the Normative Aging Study. Ann Behav Med. 2006;31:21–29. doi: 10.1207/s15324796abm3101_5. [DOI] [PubMed] [Google Scholar]
  • 39.DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk factor for noncompliance with medical treatment: Meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med. 2000;160:2101–2107. doi: 10.1001/archinte.160.14.2101. [DOI] [PubMed] [Google Scholar]
  • 40.Janszky I, Ahnve S, Lundberg I, Hemmingsson T. Early-onset depression, anxiety, and risk of subsequent coronary heart disease: 37-year follow-up of 49,321 young Swedish men. J Am Coll Cardiol. 2010;56:31–37. doi: 10.1016/j.jacc.2010.03.033. [DOI] [PubMed] [Google Scholar]
  • 41.Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354:1435–1439. doi: 10.1016/S0140-6736(99)01376-8. [DOI] [PubMed] [Google Scholar]
  • 42.Meier-Ewert HK, Ridker PM, Rifai N. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol. 2004;43:678–683. doi: 10.1016/j.jacc.2003.07.050. [DOI] [PubMed] [Google Scholar]
  • 43.Spiegel K, Leproult R, L'Hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004;89:5762–5771. doi: 10.1210/jc.2004-1003. [DOI] [PubMed] [Google Scholar]
  • 44.Stranges S, Cappuccio FP, Kandala NB, Miller MA, Taggart FM, Kumari M, et al. Cross-sectional versus prospective associations of sleep duration with changes in relative weight and body fat distribution: the Whitehall II study. Am J Epidemiol. 2008;167:321–329. doi: 10.1093/aje/kwm302. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45.Gangwisch JE, Heymsfield SB, Boden-Albala B, Buijs RM, Kreier F, Pickering TG, et al. Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey. Hypertension. 2006;47:833–839. doi: 10.1161/01.HYP.0000217362.34748.e0. [DOI] [PubMed] [Google Scholar]
  • 46.Gottlieb DJ, Redline S, Nieto FJ, Baldwin CM, Newman AB, Resnick HE, et al. Association of usual sleep duration with hypertension: the Sleep Heart Health Study. Sleep. 2006;29:1009–1014. doi: 10.1093/sleep/29.8.1009. [DOI] [PubMed] [Google Scholar]
  • 47.Greenland P, Knoll MD, Stamler J, Neaton JD, Dyer AR, Garside DB, et al. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA. 2003;290:891–897. doi: 10.1001/jama.290.7.891. [DOI] [PubMed] [Google Scholar]
  • 48.Fraguas RJ, Iosifescu DV, Alpert J, Wisniewski SR, Barkin JL, Trivedi MH, et al. Major depressive disorder and comorbid cardiac disease: is there a depressive subtype with greater cardiovascular morbidity? Results from the STAR*D study. Psychosomatics. 2007;48:418–425. doi: 10.1176/appi.psy.48.5.418. [DOI] [PubMed] [Google Scholar]
  • 49.Jensen E, Dehlin O, Hagberg B, Samuelsson G, Svensson T. Insomnia in an 80-year-old-population: relationship to medical, psychological and social factors. J Sleep Res. 1998;7:183–189. doi: 10.1046/j.1365-2869.1998.00118.x. [DOI] [PubMed] [Google Scholar]
  • 50.Armitage R, Hoffmann RF. Sleep EEG, depression and gender. Sleep Med Rev. 2001;5:237–246. doi: 10.1053/smrv.2000.0144. [DOI] [PubMed] [Google Scholar]

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