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Psychosocial Influences on the Development and Course of Coronary Heart Disease: Current Status and Implications for Research and Practice

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Psychosocial Influences on the Development and Course of Coronary Heart Disease: Current Status and Implications for Research and Practice Journal of Consulting and Clinical Psychology Copyright 2002 by the American Psychological Association, Inc. 2002, Vol. 70, No. 3, 548–568 0022-006X/02/$5.00 DOI: 10.1037//0022-006X.70.3.548 Psychosocial Influences on the Development and Course of Coronary Heart Disease: Current Status and Implications for Research and Practice Timothy W. Smith and John M. Ruiz University of Utah Psychosocial characteristics predict the development and course of coronary heart disease (CHD). In this review, the authors discussed human and animal research on psychophysiological mechanisms influenc- ing coronary artery disease and its progression to CHD. They then reviewed literature on personality and characteristics of the social environment as risk factors for CHD. Hostility confers increased risk, and a group of risk factors involving depression and anxiety may be especially important following myocardial infarction. Social isolation, interpersonal conflict, and job stress confer increased risk. Psychosocial interventions may have beneficial effects on CHD morbidity and mortality, although inconsistent results and a variety of methodological limitations preclude firm conclusions. Finally, they discussed implica- tions for clinical care and the agenda for future research. Coronary heart disease (CHD) is the leading cause of death in the Like the article on CHD in the previous special issue on behav- United States; each year about 450,000 people die from CHD, ioral medicine in this journal (Thoresen & Powell, 1992), we and 1,000,000 experience an initial or recurrent coronary event focused primarily on the second major topic—psychosocial influ- (American Heart Association, 2001). Among healthy 40-year olds, ences on the development and course of CHD. We also reviewed between 40% and 50% of men and between 25% and 35% of women one aspect of the third topic—interventions targeting psychosocial will later develop CHD (Lloyd-Jones, Larson, Beiser, & Levy, 1999). risk factors and their underlying psychophysiological mechanisms. Over $100 billion is spent on CHD each year in the United States in Perhaps the most important implication of research on psychoso- direct medical costs, disability payments, and lost productivity (Amer- cial risk factors for coronary disease is that interventions targeting ican Heart Association, 2001). This disease involves the three major these factors could reduce cardiac morbidity and mortality. This is topics composing behavioral medicine and health psychology, mak- not to say that behavioral approaches to prevention of CHD (e.g., ing it a central focus throughout their 30-year history. In the first (i.e., smoking cessation) and management of other psychosocial aspects health behavior and prevention), modifiable behavioral risk factors of established CHD (i.e., adherence to medical regimens) are less (e.g., smoking, activity level, diet) are important risk factors for the important. They are essential in a comprehensive approach (Smith development of CHD (Stamler et al., 1999; Wannamethee, Shaper, & Ruiz, in press), but simply beyond our present scope. Walker, & Ebrahim, 1998), and behavior change is an essential Research on psychosocial influences on CHD and related inter- component of prevention. In the second topic (i.e., stress and disease ventions has expanded dramatically over the past decade. The or psychosomatics), other psychological and social factors have more landscape is no longer dominated by the Type A behavior pattern, direct effects on the development and course of CHD through the though research evolving from this risk factor continues. Research intervening psychobiological effects of stress and negative emotions. on the psychobiologic mechanisms linking psychosocial risk fac- In the third (i.e., psychosocial aspects of medical illness and care), tors to the course of CHD has grown in sophistication and is tied established CHD has extensive emotional and social impacts on more closely to the complex pathophysiology of coronary artery patients and their families, behavior is a key element of standard care disease (CAD) and CHD. Finally, evidence regarding the efficacy (e.g., medication adherence, dietary change, exercise), and psycho- of adjunctive psychosocial interventions has grown substantially, social interventions are useful additions to traditional medical and in its technical sophistication, in the number and scale of the trials, surgical treatment. and in the array of interventions it addresses. In this update, we review these topics and discuss emerging issues in research and practice. First, however, we review the pathophysiology of CAD Editor’s Note. Philip C. Kendall served as the action editor for this and CHD, with a specific emphasis on the potential role of stress article.—TWS and related emotions. This research provides a firm scientific foundation for the role of psychological and social influences on Timothy W. Smith and John M. Ruiz, Department of Psychology, the development and course of CHD and for related intervention University of Utah. strategies. John M. Ruiz is now in the Department of Psychiatry, University of Pittsburgh School of Medicine. Mechanisms Linking Psychosocial Characteristics and Preparation of this article was supported by National Institutes of Health Coronary Disease Grant 1 R01 AG18903-01. Correspondence concerning this article should be addressed to Timothy CHD is composed of several manifestations of one underlying W. Smith, Department of Psychology, University of Utah, 390 South 1530 condition—CAD. Initially, lipids and related cells (e.g., macro- East, Room 502, Salt Lake City, Utah 84112. E-mail: tim.smith@ phages, foam cells) accumulate in microscopic amounts in artery psych.utah.edu walls. These deposits grow into visible fatty streaks as early as 548 SPECIAL ISSUE: CORONARY HEART DISEASE 549 middle childhood and increase in prevalence with age (Strong et creases in blood pressure and heart rate, as well as related cardio- al., 1999; Tuzcu et al., 2001). Components of the inflammatory vascular changes (e.g., increased sympathetic stimulation of the and reparative response to injury (e.g., monocytes, smooth muscle myocardium, reduced parasympathetic dampening, increased car- cell proliferation) foster the deposit of lipoprotiens into cellular diac output and peripheral resistance), are hypothesized to initiate structures within artery walls (Ross, 1999). Later, extracellular and hasten the development of CAD. There are two distinct hy- accumulation of lipid deposits causes a thickening of the wall, potheses regarding CVR (Smith & Gerin, 1998). First, it is seen as extending outward. Eventually, these lesions include fibrous tis- an individual difference variable that marks or itself confers risk. sues and calcification and encroach into the artery opening (i.e., Second, CVR is seen as a mediating mechanism through which lumen) in a progressive manner (Stary et al., 1995). Advanced psychosocial risk factors (e.g., social isolation, trait hostility) af- lesions can occur in late adolescence and early adulthood and fect CAD and CHD. become increasingly common and extensive with age (McGill et Findings from several types of studies suggest that CVR pro- al., 2000). As lesions intrude into the lumen, blood flow is im- motes development of CAD. The magnitude of CVR to psycho- peded and oxygen supply reduced in the area of myocardium logical stressors is associated with severity and progression of supplied by the vessel. carotid artery atherosclerosis, assessed with ultrasound (Barnett, Clinical manifestations of CHD appear decades after the initial Spence, Manuck, & Jennings, 1997; Kamarck et al., 1997; Mat- stages and asymptomatic progression of CAD. Myocardial isch- thews, Owens, Kuller, Sutton-Tyrrell, Lassila, & Wolfson, 1998). emia occurs when oxygen demand exceeds supply. Many episodes Further, individual differences in CVR potentiate the effects of of ischemia are without symptoms or “silent,” but ischemia during other psychosocial risk factors (e.g., low socioeconomic status; physical exertion or, in some instances, emotional stress can pro- SES) on carotid atherosclerosis (Lynch, Everson, Kaplan, Salonen, duce chest pain (i.e., angina pectoris). Structural narrowing of the & Salonen, 1998). Carotid atherosclerosis contributes to stroke but lumen at lesion sites can be exacerbated temporarily by contraction is also associated with the presence and severity of CAD. Prevail- of smooth muscle within the artery wall. In advanced lesions, the ing models suggest that stress-induced increases in heart rate and calcified and fibrous cap may rupture or fragment. Exposed tissues blood pressure promote damage to the endothelium, making it promote clotting (i.e., thrombus), further impeding blood flow. more susceptible to inflammation and lipid deposition (Fuster, Portions of thrombi may be dislodged (i.e., emboli), often blocking Badimon, Badimon, & Chesebro, 1992; Manuck, 1994). In a narrower artery segments (Muller, Abela, Nesto, & Tofler, 1994). recent study of healthy adults, Sherwood, Johnson, Blumenthal, Thrombi and emboli can cause near or complete blockage of blood and Hinderliter (1999) found that an underlying determinant of flow resulting in severe ischemia. This causes rapidly worsening CVR (i.e., increased peripheral resistance) was associated with chest pain (i.e., unstable angina) or death of heart muscle (myo- endothelial dysfunction in healthy young adults, an early indication cardial infarction, MI) (Stary et al., 1995). Ischemia also
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