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Hypertension. 2007;49:268-269
Published online before print January 8, 2007, doi: 10.1161/01.HYP.0000255016.24162.1f
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(Hypertension. 2007;49:268.)
© 2007 American Heart Association, Inc.


Editorial Commentaries

Stopping Stress at Its Origins

Richard V. Milani; Carl J. Lavie

From the Department of Cardiology, Section of Preventive Cardiology, Ochsner Medical Foundation, New Orleans, La.

Correspondence to Richard V. Milani, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121. E-mail rmilani{at}ochsner.org

We know that the vasomotor system, which regulates the capillary circulation, is much influenced by the mind.

—Charles Darwin, Expression of the Emotions in Man and Animals

The practice of medicine today is in need of transformation. The majority of diseases plaguing modern society are initiated by unhealthy lifestyle choices or events, often taking many years to develop and mature to a stage where symptoms and signs become manifest. It is only at this typically advanced stage that the healthcare system initially becomes engaged. Although many diagnoses share a common lifestyle-related etiology, we treat the silos of diagnoses with a growing list of pharmacotherapies, each targeting a single disease process, or invasively with repeated and often palliative procedures such as stents or bypass surgeries. Verbal recommendations are generally provided to our patients to curb poor lifestyle habits, but minimal investment is put forward by the healthcare industry to create an environment where successful lifestyle change can be effected. Of the many lifestyle events that impact our patients, none is more ubiquitous than stress and stress-related conditions.

The global impact of stress-related conditions is expected to rise over this decade such that by 2020, depression and anxiety disorders, including stress-related health conditions, will be second only to ischemic heart disease in prevalence.1 Although stress can occur at home or after trauma, the most ubiquitous and studied form of stress is work related. In this context, stress has been defined as an emotional experience associated with nervousness, tension, and strain.2,3 In the workplace, stress and performance describe a U-shaped relationship such that low-to-moderate levels of stress generate a positive performance, whereas a negative performance is created at moderate-to-high levels of stress.2,4 As a result, several studies, including many funded by the National Institute of Occupational Safety and Health, have documented the negative health and financial consequences of job stress. In addition to its impact on health, job-related stress has been shown to increase the cost of doing business by as much as $150 billion per year because of higher levels of absenteeism, worker’s compensation claims, accidents, customer service problems, resistance to change, litigation, and loss of intellectual capital.2

The health consequences of job stress impact most organ systems, including musculoskeletal disorders, psychological disease (ie, depression, burnout, and suicide), workplace injury, gastrointestinal disorders including ulcers, headaches, obesity, and sleep disturbances. By far and away, however, the most common and studied linkage related to stress and health is that from cardiovascular disease, which alone accounts for an estimated $117 billion per year in lost productivity and treatment because of job-related stress.2 The INTERHEART Study evaluated cardiovascular risk factors in 29 972 people from 52 countries to investigate risk of first myocardial infarction. Nine independent risk factors, including psychosocial factors, accounted for 90% of the population-attributable risk in men and 94% in women.5 These psychosocial factors, which included depression and psychosocial stress, increased the odds of first myocardial infarction by {approx}3-fold and accounted for 33% of the population-attributable risk for the development of myocardial infarction, a magnitude similar to standard risk factors, such as smoking, diabetes, and hypertension. The mechanisms relating stress to cardiovascular disease are numerous and include alterations in the autonomic profile, enhanced platelet reactivity, hypertension, coronary vasospasm, inflammation, electrical instability, and enhanced atherosclerosis.6,7 Treatment options to reduce stress include pharmacotherapy directed toward stress relief, meditation, group therapy/counseling, relaxation techniques, and exercise training.8 In patients with manifest heart disease, exercise training via cardiac rehabilitation can effectively reduce stress and improve autonomic dysregulation, as well as blood pressure and other cardiac risk factors.9 However, therapies directed toward earlier recognition and intervention at the point of origin, most commonly the worksite, are needed if widespread preventive therapies are expected to be successful.

In this issue of Hypertension, Lucini et al10 have elegantly demonstrated the relationship between work-related stress and autonomic dysregulation, specifically, oscillatory properties of RR variability that are thought to precede the development of frank hypertension. They describe a strong correlation between autonomic markers and stress perception scores and were capable of discriminating between affected workers and control subjects with a high degree of accuracy. The study, however, took an additional important step by assessing the use and efficacy of an intervention program delivered at the worksite. Using a simple onsite stress management program given during the lunch hour, the authors evaluated the stress management program on workers with known stress and compared them with employees undergoing a sham intervention. Workers participating in the stress management program demonstrated statistical improvements in symptoms of stress, as well as reductions in systolic arterial blood pressure and clear improvements in spectral indices of RR variability, whereas no beneficial effects were observed in sham-treated workers.

The implications of these findings are significant. First, given the widespread prevalence of job-related stress, its recognition and treatment should ideally be focused at the point of origin. As in the current study, the use of simple questionnaires can now reliably identify workers manifesting this behavior for targeted intervention. Given the high economic and health-related costs that result from this condition, both employees and employers can be motivated toward intervention provided the intervention is simple, effective, of reasonable duration, and nonobtrusive. Lucini et al10 are to be commended for designing a program that meets these issues yet remains quantifiable and highly effective. Further studies demonstrating the downstream health and economic benefits of this intervention are needed.

Lucini et al10 have taken us in the direction where health care must move if we are to be successful in combating heart disease and other chronic conditions. Future work in prevention must include intervention aimed at the origin of disease.

A man who suffers or stresses before it is necessary, suffers more than necessary.

—Seneca


*    Acknowledgments
 
Disclosures

None.


*    Footnotes
 
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.


*    References
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*References
 

  1. World Health Organization. The global burden of disease. In: Murray CJL, Lopez AD, eds. The Global Burden of Disease. A Comprehensive Assessment of Mortality and Disability From Diseases, Injuries and Risk Factors in 1990 and Projected to 2020. Cambridge, MA: Harvard School of Public Health; 1996: 247–293.
  2. Kalia M. Assessing the economic impact of stress-the modern day hidden epidemic. Metabolism. 2002; 51 (6 suppl 1): 49–53.[CrossRef][Medline] [Order article via Infotrieve]
  3. Cooke RA, Rousseau DM. Stress and strain from family roles and work-role expectations. J Appl Psychol. 1984; 69: 252–260.[CrossRef][Medline] [Order article via Infotrieve]
  4. Cohen S. Aftereffects of stress on human performance and social behavior: a review of research and theory. Psychol Bull. 1980; 88: 82–108.[CrossRef][Medline] [Order article via Infotrieve]
  5. Rosengren A, Hawken S, Ounpuu S, Sliwa K, Zubaid M, Almahmeed WA, Blackett KN, Sitthi-amorn C, Sato H, Yusuf S. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study. Lancet. 2004; 364: 953–962.[CrossRef][Medline] [Order article via Infotrieve]
  6. Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation. 1999; 99: 2192–2217.[Abstract/Free Full Text]
  7. Rozanski A, Blumenthal JA, Davidson KW, Saab PG, Kubzansky L. The epidemiology, pathophysiology, and management of psychosocial risk factors in cardiac practice: the emerging field of behavioral cardiology. J Am Coll Cardiol. 2005; 45: 637–651.[Abstract/Free Full Text]
  8. Lavie CJ, Milani RV. Adverse psychological and coronary risk profiles in young patients with coronary artery disease and benefits of formal cardiac rehabilitation. Arch Intern Med. 2006; 166: 1878–1883.[Abstract/Free Full Text]
  9. Lucini D, Milani RV, Costantino G, Lavie CJ, Porta A, Pagani M. Effects of cardiac rehabilitation and exercise training on autonomic regulation in patients with coronary artery disease. Am Heart J. 2002; 143: 977–983.[CrossRef][Medline] [Order article via Infotrieve]
  10. Lucini D, Riva S, Pizzinelli P, Pagani M. Stress management at the worksite: reversal of symptoms profile and cardiovascular dysregulation. Hypertension. 2007; 49: 291–297.[Abstract/Free Full Text]

Related Article:

Stress Management at the Worksite: Reversal of Symptoms Profile and Cardiovascular Dysregulation
Daniela Lucini, Silvano Riva, Paolo Pizzinelli, and Massimo Pagani
Hypertension 2007 49: 291-297. [Abstract] [Full Text] [PDF]



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Stopping Stress at Its Origins: Addressing Working Conditions
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