Many individuals with a severe cardiovascular impairment, such as heart failure, coronary artery disease, or peripheral vascular disease, have chronic comorbid conditions, such as depression or diabetes, that further reduce their capacity to work. It would be efficient for the Social Security Administration (SSA), and beneficial for claimants with chronic comorbidities, to recognize claimants whose cardiovascular impairment is not severe enough to meet a listing, but who are unable to work because of the combined effect of their impairments, and to allow them at Step 3.
This chapter reviews the current state of knowledge about the extent of cardiovascular comorbidities and their effects on functional capacity. It also reviews SSA policies and procedures for evaluating claimants with multiple impairments at Step 3. The committee has no recommendations on revising these policies and procedures. Evaluating the effect of comorbidities in applying the Listings cannot be reduced to a predetermined formula and therefore should be determined by the judgment of the adjudicators. The committee intends the information in this chapter to better inform those decisions.
EXTENT OF COMORBIDITIES
Multiple morbidities are common and, generally, the more morbidities, the greater the likelihood of disability. An analysis of data from the 2005 Behavioral Risk Factor Surveillance System found that the prevalence of disability among U.S. adults ages 50 to 64 was 26.3 percent. It was much higher among those with chronic conditions, however—between 1.9 and
4.5 times higher depending on the condition. Adults with multiple chronic conditions were 42.9 times more likely to have a disability than those without comorbidities (Zhao et al., 2009).1
Depression and Anxiety
Depression and anxiety can cause profound functional impairment. Major depressive disorder produces impairment in functioning as severe as other chronic medical illnesses, including cardiovascular disease (Hays et al., 1995; Kessler et al., 2003; Ormel et al., 2008; Papakostas, 2009). The World Health Organization reports that depression is the leading cause of years lost due to disability for both men and women worldwide, and projects that depression and heart disease will be the two leading causes of disability in developed countries in the next decade (WHO, 2008). When major psychiatric and medical disorders co-occur, the proportion of disability attributable to psychiatric comorbidity is often greater than that attributable to the medical illness (Kessler et al., 2003).
Having even a few depression symptoms can contribute significantly to functional impairment and disability, although the level of impairment increases with the severity of depression (Papakostas, 2009; Spertus et al., 2000). Mild levels of anxiety may actually encourage adherence to the cardiac treatment regimen and more attentiveness to potentially fatal symptoms of heart disease; whereas moderate to severe anxiety is likely to contribute to cardiac disability, excessive medical service use, and an increased risk of further cardiac morbidity and even mortality (Frasure-Smith and Lespérance, 2008; Shen et al., 2008; Shibeshi et al., 2007). Of the two, depression is more difficult to detect, and therefore less likely to be treated or even documented in medical records. Also, substantially more research has been done on depression than anxiety or other mental disorders. Therefore, depression will be considered here in some detail, followed by a short review of research on anxiety and coronary heart disease (CHD).
Epidemiology of Depression
Depression is common in patients with cardiovascular disease. For example, at any point in time about 15 to 20 percent of patients with docu-
mented CHD have major depression, and another 20 percent have at least a few symptoms of depression (Carney and Freedland, 2008). The prevalence rates are similarly high in patients with heart failure (Jiang et al., 2007; Norra et al., 2008), peripheral artery disease (McDermott et al., 2003; Ruo et al., 2007; Smolderen et al., 2008), and other forms of cardiovascular disease (Goodwin et al., 2009). Depressed patients with cardiovascular disease have a higher rate of hospitalization, experience more frequent cardiac symptoms, have more physical impairment and functional decline, are less likely to attend cardiac rehabilitation, are slower in returning to work following a myocardial infarction, and are twice as likely to suffer a second heart attack or to die, compared with those without depression symptoms (Beck et al., 2001; Carney and Freedland, 2008; deJonge et al., 2006; Frasure-Smith and Lespérance, 2006, 2008; Ladwig et al., 1994; Lane et al., 2001; McDermott et al., 2003; Ruo et al., 2007; Soderman et al., 2003; Spertus et al., 2000).
Despite its prevalence, associated functional impairment, and risk for morbidity and mortality, depression often goes undetected. In some cases this occurs because patients consider depression to be a normal part of having heart disease and they do not report it to their physician. Others may be too embarrassed to admit to feeling depressed, especially if they were not depressed before developing heart disease. In addition, many physicians do not ask about symptoms of depression. Consequently, depression status may not be known or mentioned in a patient’s medical record.
The standard criteria for diagnosing depression are included in the Diagnostic and Statistical Manual (DSM-IV-TR) of the American Psychiatric Association (APA, 2000). A major depressive episode requires the presence of five or more depressive symptoms. These symptoms must persist for at least 2 weeks and cause clinically significant distress or functional impairment to meet the diagnostic criteria. Symptoms of depression include dysphoric mood, loss of interest in usual activities, poor concentration, difficulty in falling asleep or sleeping too much, poor appetite or overeating, feeling tired or fatigued, feeling like a failure, moving or speaking very slowly or feeling restless, and thoughts of death or suicide.
Dysthymia is a less symptomatic but chronic form of depression that is often associated with low self-esteem. Dysthymia is not diagnosed unless dysphoric mood and two or more additional depressive symptoms have been present for at least 2 years. In some cases, a major depressive episode is superimposed on dysthymia, a condition known as “double depression.”
Treatment of Depression
A variety of medications and other methods may be used to treat depression when it is identified. None of these treatment options has been shown to be more effective than the others. Patients whose depression fails to respond to one type of antidepressant, for example, may improve with another, or with a combination of drugs or other treatments. Roughly half of all patients with major depression, with or without cardiovascular disease, show at least some improvement in depression symptoms with treatment, and remission is achieved in about 20 to 30 percent of cases (Rush et al., 2008).
In addition to antidepressants, specific forms of evidence-based psychotherapy, including cognitive behavior therapy and interpersonal psychotherapy, have been shown to be as effective as medications, especially for patients with mild to moderate depression. Psychotherapy can also be helpful for severe depression, but usually in combination with antidepressant medications. For more severe depression that does not respond to medications, electroconvulsive therapy may be considered with proper precautions. In addition, experimental treatments for depression may be available in some communities.
Although about half of patients treated for depression will show significant improvement; if residual symptoms remain after the patient has been treated for depression, functional impairment is likely to persist (Papakostas, 2009). Furthermore, even after remission of depression, a complete functional recovery may take months to occur, and some patients may be unable to function outside of a highly supportive environment during that time.
Generalized Anxiety Disorder
Approximately 24 to 31 percent of patients with CHD exhibit symptoms of anxiety. A recent cohort analysis from the Heart and Soul Study found that patients with stable CHD and generalized anxiety disorder had a 62 percent higher risk of cardiovascular events such as myocardial infarction, stroke, or death than CHD patients without anxiety symptoms, after controlling for factors such as demographics, major depressive disorder, other comorbid conditions, cardiac disease severity, and medication use (Martens et al., 2010).
The prevalence of diabetes mellitus (DM) increases with age. Of U.S. adults ages 45 to 64, 11.6 percent have DM, as do 2.9 percent of those
ages 20 to 44 and 0.4 percent of those ages 0 to 19. Some individuals with a cardiovascular disease have comorbid DM, which is often associated with worse cardiovascular outcomes. For example, National Health and Nutrition Examination Survey (NHANES) data for the years 1999 to 2004 on adults ages 40 and older show that 24 percent of those who had peripheral artery disease (PAD) also had CHD, and 18 percent who had CHD also had PAD. NHANES data also show that adults ages 40 to 59 with lower extremity disease (LED) who also have DM are much more likely to have mobility limitations. Specifically, 15.6 percent of those with LED, but not DM, had mobility limitations, 29.6 percent with both LED and DM had mobility limitations, while 6 percent of those with neither LED nor DM had mobility limitations (Eberhardt et al., 2005).2 A study of a cohort of PAD patients found that PAD progressed significantly on average during 4.6 years of follow-up and that progression was independently associated with DM, among other factors (Bird et al., 1999).
A study of residents of Olmstead County, Minnesota, who experienced a validated incident of myocardial infarction (MI) from 1979 to 1989 found that 19 percent of those whose MI occurred during the period 1994 to 1998 had DM (compared with 15 percent during the period 1979 to 1983), and those with diabetes had a lower survival rate 5 years post-MI (Gandhi et al., 2006). An earlier Minnesota Heart Survey study found that 26 percent of women and 17 percent of men hospitalized for an MI in 1985 had comorbid DM (Sprafka et al., 1991).
Franklin et al. (2004) compared patients who had suffered an acute coronary event who had DM with those who did not. Approximately 25 percent of the patients with ST-segment elevation myocardial infarction, non-ST-segment elevation myocardial infarction, and unstable angina (21, 26, and 25 percent, respectively) had DM. Compared with patients without DM, they had more coronary risk factors and comorbidities, and they were more likely to experience heart failure, renal failure, cardiogenic shock, or death in the hospital.
Chronic Obstructive Pulmonary Disease and Other Respiratory Diseases
Chronic obstructive pulmonary disease (COPD) is a progressive disease that contributes to significant morbidity and mortality in the United States. Cigarette smoking is the leading cause of COPD. As the prevalence of individuals who smoke declines due to public health initiatives, incidence of COPD is expected to similarly decline over time.
Symptoms of the disease include cough with mucus, shortness of breath, fatigue, frequent respiratory infections, and wheezing. Patients may be prescribed steroid inhalers to treat associated symptoms; however, there is no curative treatment for COPD, and, therefore, the combined effects of a comorbid cardiovascular disease may lead to disability. One of the leading causes of death among patients with COPD is comorbid heart failure. In a cohort study of 1,927 patients, patients with COPD had a 194 percent increase in the risk of heart failure after adjustment for age and sex, and a 194 percent increase in the risk of death after adjustment for age and sex, compared with patients without COPD (García Rodríguez et al., 2010).
Obesity is an increasingly prevalent metabolic disorder in the United States. Heredity and environment both contribute to the development of obesity. Genes are thought to explain obesity in 30 to 70 percent of cases. High-fat diets and low levels of physical exercise are likely the conditions that most lead to overweight and eventual obesity. Overweight and obesity contribute to comorbidities, including a number of cardiovascular conditions such as arrhythmia, coronary heart disease, and heart failure (Eckel, 1997).
Defining obesity continues to be controversial, and ultimately depends on the individual. Body mass index (BMI) is the most common measurement for determining overweight and obesity, and is defined as weight (kilograms) divided by height in meters squared (kg/m2). However, a BMI-based definition of obesity does not consider the distribution of body fat across the body frame. Substantial evidence now indicates that an increased waist circumference, or waist-to-hip ratio, predicts comorbidities and mortality from obesity (Eckel, 1997).
Obesity and Ischemic Heart Disease
The relationship between obesity and ischemic heart disease has been viewed as indirect, or through channels related to both diseases, such as hypertension, dyslipidemia, or non-insulin-dependent diabetes mellitus. Insulin resistance and accompanying hyperinsulinemia are typically associated with these comorbidities (Reaven, 1988). Although most of the comorbidities associating obesity and ischemia increase in a positive relationship with BMI, they also relate to body fat distribution. However, long-term longitudinal studies indicate that obesity also predicts coronary atherosclerosis independently (Garrison and Castelli, 1985; Manson et al., 1995; Rabkin et al., 1977).
Obesity and Heart Failure
Diastolic dysfunction is common in obese individuals. When obesity is present, but systemic hypertension is absent, left ventricular volume is often increased, but wall stress usually remains normal. However, in obese patients without hypertension, increases in stroke volume and cardiac output, as well as diastolic dysfunction, are seen. These changes in the left ventricle are related to sudden death in obese patients. Increased left ventricular volume and wall stress, increased stroke volume, and cardiac output are seen as commonly in systemic hypertension as in patients with obesity (Alpert and Hashimi, 1993; Messerli and Aepfelbacher, 1995).
A study examined 22 patients with severe obesity postmortem and reported dilated cardiomyopathy as the most frequent condition associated with sudden death (Duflou et al., 1995). Dilated cardiomyopathies, presumably with concomitant cardiac arrhythmias, may be the most common cause of sudden death in patients with severe obesity. The prolonged QT interval3 also seen in obesity may predispose patients to such arrhythmias (Frank et al., 1986).
Obesity may also lead to changes in the right heart, eventually leading to right heart failure. The pathophysiology is related to sleep apnea or the obesity hypoventilation syndrome, both of which produce pulmonary hypertension and right ventricular hypertrophy, dilatation, and progressive dysfunction. All these conditions may lead to right heart failure (Menashe et al., 1965).
EVALUATING COMORBIDITIES AT THE LISTINGS STEP
Current Policies and Procedures
According to current SSA policy, claimants may be allowed at Step 3 of the sequential evaluation process on the basis that their impairment medically equals a listing if they have “a combination of impairments, no one of which meets a listing, but the findings related to these impairments are at least of equal medical significance to those of a listed impairment.” SSA also may find medical equivalence in two other ways:
The claimant’s impairment is described in a listing, but it does not exhibit one or more of the findings specified in the particular listing, or it exhibits all of the findings, but one or more of them is not as severe as specified in the listing, and there are other findings
The QT interval is the time from the electrocardiogram Q wave to the end of the T wave corresponding to electrical systole. http://www.medilexicon.com/medicaldistionary.php?t=45242 (accessed July 16, 2010).
related to the impairment that are at least of equal medical significance to the required criteria.
The claimant’s impairment is not described in a listing, but it exhibits findings that are closely analogous to a listed impairment, and these findings are at least of equal medical significance to that listed impairment.
In 2008, more than one-third of the adult cardiovascular Step 3 allowances were based on medical equivalence rather than meeting a listing.4 Medical equivalency accounted for 30 to 50 percent of the listing-based allowances, with the exception of heart transplant.5 More than 90 percent of heart transplantation Step 3 allowances were based on meeting the heart transplantation listing, probably because it is easy to ascertain objectively that a heart transplant occurred.
For children under age 18 who have a severe impairment or impairments that do not meet or medically equal a listing, SSA will determine whether the impairment or impairments functionally equal the Listings. This functional equivalence process, which applies to children only, is described in Chapter 2 of this report. For adults who have a severe impairment or impairments that do not meet or medically equal a listing, SSA will evaluate the functional limitations resulting from their impairments at Step 4 and, if necessary, Step 5 of the disability decision process, which is also described in Chapter 2.
The current procedure to determine if one or more comorbidities combine with a severe cardiovascular impairment to produce a case equaling or exceeding a listing-level impairment relies on the judgment of a medical or psychological consultant or other adjudicator. If the criteria for meeting a listing are complex and technical, as are the criteria for cardiovascular listings, an adjudicator may decide to forgo Step 3 and proceed to Steps 4 and 5, relying on the residual functional capacity evaluation to decide the claim, a process that requires more time and resources.
The committee considered whether to recommend a more objective decision-making procedure, such as adopting criteria for meeting the heart failure listing that included (1) an ejection fraction between 30 and 35 per-
cent and (2) a diagnosis of severe depression, but could find no evidence that this combination invariably results in inability to work. However, SSA is in a good position to ascertain the impact of comorbidities by analyzing patterns in cases it has decided. Taking the example above, SSA could analyze a sample of disability claims with heart failure as the primary impairment to examine the relationship with comorbidities, such as depression. If, for example, 95 percent or more of claims with a diagnosis of major depression and certain ejection fraction values are allowed at Step 5, SSA could consider creating a listing criterion for major depression in combination with those ejection fraction values. Alternatively, SSA could provide more focused training to adjudicators on how to evaluate equivalency at Step 3 in such cases. These points are addressed further in the Chapter 16 discussion of research opportunities for improving the Listings.
Alpert, M. A., and M. W. Hashimi. 1993. Obesity and the heart. American Journal of the Medical Sciences 306(2):117–123.
APA (American Psychiatric Association). 2000. Diagnostic and statistical manual of mental disorders, 4th ed., text revision (DSM-IV-TR). Washington, DC: American Psychiatric Association.
Beck, C. A., L. Joseph, P. Belisle, and L. Pilote. 2001. Predictors of quality of life 6 months and 1 year after acute myocardial infarction. American Heart Journal 142(2):271–279.
Bird, C. E., M. H. Criqui, A. Fronek, J. O. Denenberg, M. R. Klauber, and R. D. Langer. 1999. Quantitative and qualitative progression of peripheral arterial disease by non-invasive testing. Vascular Medicine 4(1):15–21.
Carney, R. M., and K. E. Freedland. 2008. Depression in patients with coronary heart disease. American Journal of Medicine 121(11 Suppl 2):S20–S27.
CDC (Centers for Disease Control and Prevention). 2010. Behavioral Risk Factor Surveillance System 2010 Questionnaire. http://www.cdc.gov/brfss/questionnaires/pdf-ques/2010brfss.pdf (accessed August 23, 2010).
deJonge, P., T. A. Spijkerman, R. H. van den Brink, and J. Ormel. 2006. Depression after myocardial infarction is a risk factor for declining health related quality of life and increased disability and cardiac complaints at 12 months. Heart 92(1):32–39.
Duflou, J., R. Virmani, I. Rabin, A. Burke, A. Farb, and J. Smialek. 1995. Sudden death as a result of heart disease in morbid obesity. American Heart Journal 130(2):306–313.
Eberhardt, M. S., S. Saydah, R. Paulose-Ram, and M. Tao. 2005. Mobility limitation among persons aged ≥ 40 years with and without diagnosed diabetes and lower extremity disease—United States, 1999–2002. Morbidity and Mortality Weekly Report 54(46):1183–1186. http://www.cdc.gov/mmwr/PDF/wk/mm5446.pdf (accessed July 16, 2010).
Eckel, R. H. 1997. Obesity and heart disease: A statement for healthcare professionals from the nutrition committee, American Heart Association. Circulation 96(9):3248–3250. http://circ.ahajournals.org/cgi/content/full/96/9/3248 (accessed August 4, 2010).
Frank, S., J. A. Colliver, and A. Frank. 1986. The electrocardiogram in obesity: Statistical analysis of 1,029 patients. Journal of the American College of Cardiology 7(2):295–299.
Franklin, K., R. J. Goldberg, F. Spencer, W. Klein, A. Budaj, D. Brieger, M. Marre, P. G. Steg, N. Gowda, J. M. Gore, and GRACE Investigators. 2004. Implications of diabetes in patients with acute coronary syndromes. The Global Registry of Acute Coronary Events.
Archives of Internal Medicine 164(13):1457–1463. http://archinte.ama-assn.org/cgi/reprint/164/13/1457 (accessed July 16, 2010).
Frasure-Smith, N., and F. Lespérance. 2006. Recent evidence linking coronary heart disease and depression. Canadian Journal of Psychiatry 51:730–737.
Frasure-Smith, N., and F. Lespérance. 2008. Depression and anxiety as predictors of 2-year cardiac events in patients with stable coronary artery disease. Archives of General Psychiatry 65(1):62–71. http://archpsyc.ama-assn.org/cgi/reprint/65/1/62 (accessed October 8, 2010).
Gandhi, G. Y., V. L. Roger, K. R. Bailey, P. J. Palumbo, J. E. Ransom, and C. L. Leibson. 2006. Temporal trends in prevalence of diabetes mellitus in a population-based cohort of incident myocardial infarction and impact of diabetes on survival. Mayo Clinic Proceedings 81(8):1034–1040. http://www.mayoclinicproceedings.com/content/81/8/1034.full.pdf+html (accessed July 16, 2010).
García Rodríguez, L. A., M. A. Wallander, E. Martín-Merino, and S. Johansson. 2010. Heart failure, myocardial infarction, lung cancer and death in COPD patients: A UK primary care study. Respiratory Medicine, May 17. Epub ahead of print. http://www.ncbi.nlm.nih.gov/pubmed/20483577 (accessed July 12, 2010).
Garrison, R. J., and W. P. Castelli. 1985. Weight and thirty-year mortality of men in the Framingham Study. Annals of Internal Medicine 103(6 Pt 2):1006–1009.
Goodwin, R. D., K. W. Davidson, and K. Keyes. 2009. Mental disorders and cardiovascular disease among adults in the United States. Journal of Psychiatric Research 43(3):239–246.
Hays, R. D., K. B. Wells, C. D. Sherbourne, W. Rogers, and K. Spritzer. 1995. Functioning and well-being outcomes of patients with depression compared with chronic general medical illnesses. Archives of General Psychiatry 52(1):11–19.
Jiang, W., M. Kuchibhatla, G. L. Clary, M. S. Cuffe, E. J. Christopher, J. D. Alexander, R. M. Califf, R. R. Krishnan, and C. M. O’Connor. 2007. Relationship between depressive symptoms and long-term mortality in patients with heart failure. American Heart Journal 154(1):102–108.
Kessler, R. C., J. Ormel, O. Demler, and P. E. Stang. 2003. Comorbid mental disorders account for the role impairment of commonly occurring chronic physical disorders: Results from the National Comorbidity Survey. Journal of Occupational and Environmental Medicine 45(12):1257–1266.
Ladwig, K. H., G. Roll, G. Breithardt, T. Budde, and M. Borggrefe. 1994. Post-infarction depression and incomplete recovery 6 months after acute myocardial infarction. Lancet 343(8888):20–23.
Lane, D., D. Carroll, C. Ring, D. G. Beevers, and G. Y. Lip. 2001. Predictors of attendance at cardiac rehabilitation after myocardial infarction. Journal of Psychosomatic Research 51(3):497–501.
Manson, J. E., W. C. Willett, M. J. Stampfer, G. A. Colditz, D. J. Hunter, S. E. Hankinson, C. H. Hennekens, and F. E. Speizer. 1995. Body weight and mortality among women. New England Journal of Medicine 333(11):677–685.
Martens, E. J., P. de Jonge, B. Na, B. E. Cohen, H. Lett, and M. A. Whooley. 2010. Scared to death? Generalized anxiety disorder and cardiovascular events in patients with stable coronary heart disease: The Heart and Soul Study. Archives of General Psychiatry 67(7):750–758.
McDermott, M. M., P. Greenland, J. M. Guralnik, K. Liu, M. H. Criqui, W. H. Pearce, C. Chan, J. Schneider, L. Sharma, L. M. Taylor, A. Arseven, M. Quann, and L. Celic. 2003. Depressive symptoms and lower extremity functioning in men and women with peripheral arterial disease. Journal of General Internal Medicine 18(6):461–467.
Menashe, V. D., C. Farrehi, and M. Miller. 1965. Hypoventilation and cor pulmonale due to chronic upper airway obstruction. Journal of Pediatrics 67:198–203.
Messerli, F. H., and F. C. Aepfelbacher. 1995. Hypertension and left-ventricular hypertrophy. Cardiology Clinics 13(4):549–557.
Norra, C., E. C. Skobel, M. Arndt, and P. Schauerte. 2008. High impact of depression in heart failure: Early diagnosis and treatment options. International Journal of Cardiology 125(2):220–231.
Ormel, J., M. Petukhova, S. Chatterji, S. Aguilar-Gaxiola, J. Alonso, M. C. Angermeyer, E. J. Bromet, H. Burger, K. Demyttenaere, G. de Girolamo, J. M. Haro, I. Hwang, E. Karam, N. Kawakami, J. P. Lépine, M. E. Medina-Mora, J. Posada-Villa, N. Sampson, K. Scott, T. B. Ustun, M. Von Korff, D. R. Williams, M. Zhang, and R. C. Kessler. 2008. Disability and treatment of specific mental and physical disorders across the world. British Journal of Psychiatry 192(5):368–375.
Papakostas, G. I. 2009. Major depressive disorder: Psychosocial impairment and key considerations in functional improvement. American Journal of Managed Care 15(11 Suppl): S316–S321. http://www.ajmc.com/media/pdf/A269_09decPapakostasS316to321.pdf (accessed August 23, 2010).
Rabkin, S. W., F. A. Mathewson, and P. H. Hsu. 1977. Relation of body weight to development of ischemic heart disease in a cohort of young North American men after a 26 year observation period: The Manitoba Study. American Journal of Cardiology 39(3):452–458.
Reaven, G. M. 1988. Banting lecture: Role of insulin resistance in human disease. Diabetes 37(12):1595–1607.
Ruo, B., K. Liu, L. Tian, J. Tan, L. Ferrucci, J. M. Guralnik, and M. M. McDermott. 2007. Persistent depressive symptoms and functional decline among patients with peripheral arterial disease. Psychosomatic Medicine 69(5):415–424.
Rush, A. J., J. Kilner, M. Fava, S. R. Wisniewski, D. Warden, A. A. Nierenberg, and M. H. Trivedi. 2008. Clinically relevant findings from STAR*D. Psychiatric Annals 38(3): 188–193.
Shen, B. J., Y. E. Avivi, J. F. Todaro, A. Spiro III, J. P. Laurenceau, K. D. Ward, and R. Niaura. 2008. Anxiety characteristics independently and prospectively predict myocardial infarction in men: The unique contribution of anxiety among psychologic factors. Journal of the American College of Cardiology 51(2):113–119.
Shibeshi, W. A., Y. Young-Xu, and C. M. Blatt. 2007. Anxiety worsens prognosis in patients with coronary artery disease. Journal of the American College of Cardiology 49(20):2021–2027.
Smolderen, K. G., A. E. Aquarius, J. de Vries, O. R. Smith, J. F. Hamming, and J. Denollet. 2008. Depressive symptoms in peripheral arterial disease: A follow-up study on prevalence, stability, and risk factors. Journal of Affective Disorders 110(1–2):27–35.
Soderman, E., J. Lisspers, and O. Sundin. 2003. Depression as a predictor of return to work in patients with coronary artery disease. Social Science & Medicine 56(1):193–202.
Spertus, J. A., M. McDonnell, C. L. Woodman, and S. D. Fihu. 2000. Association between depression and worse disease-specific functional status in outpatients with coronary artery disease. American Heart Journal 140(1):105–110.
Sprafka, J. M., G. L. Burke, A. R. Folsom, P. G. McGovern, and L. P. Hahn. 1991. Trends in prevalence of diabetes mellitus in patients with myocardial infarction and effect of diabetes on survival: The Minnesota Heart Survey. Diabetes Care 14(7):537–543.
WHO (World Health Organization). 2008. The global burden of disease: 2004 update. Geneva, Switzerland: WHO Press. http://www.who.int/healthinfo/global_burden_disease/2004_report_update/en/index.html (accessed August 3, 2010).
Zhao, G., E. S. Ford, C. Li, J. E. Crews, and A. H. Mokdad. 2009. Disability and its correlates with chronic morbidities among U.S. adults aged 50 ≤ 65 years. Preventive Medicine 48(2):117–121.