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 implications 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 renders of atherosclerosis. Hence, CVR may contribute to earlier stages of the myocardium electrically unstable, promoting disturbances in initiation and progression of CAD. Alternatively, this association heart rhythm (i.e., arrhythmia). In the most severe (i.e., ventricular could reflect the fact that CVR and early, subclinical CAD reflect a fibrillation), myocardial contractions become chaotic, and cessa- common etiology (e.g., autonomic or neuroendocrine responsiveness) tion of circulation may cause sudden cardiac death (SCD). that marks or confers vulnerability to CAD and CHD. Statistical associations between psychosocial risk factors and Animal research provides converging evidence regarding CVR CHD endpoints (e.g., MI, SCD) could reflect an effect on initial and CAD, as well as other psychophysiological mechanisms. In stages of CAD, pace of progression, precipitation of manifesta- nonhuman primates, the magnitude of stress-induced increases in tions of CHD (i.e., triggers) among individuals with advanced or heart rate is associated with the severity of coronary atherosclero- unstable CAD lesions, or some combination (Cohen, Kaplan, & sis (Manuck, Kaplan, Adams, & Clarkson, 1989). In this model, Manuck, 1994). As we discuss later, the disease stage affected by pharmacological blockade of sympathetically mediated CVR elim- psychosocial risk factors has implications for research and prac- inates the effects of chronic stress on initial endothelial injury and tice. As for specific mechanisms through which psychosocial advanced lesions (J. R. Kaplan, Manuck, Adams, Weingand, & factors affect the development of CAD and manifestations of Clarkson, 1987; Skantze et al., 1998). These findings constitute CHD, a growing body of research suggests that stress and negative strong evidence that physiological stress responses mediate the emotions—the primary psychological pathway hypothesized in effect of psychosocial stress on CAD. Stress-induced changes in current models—alter several physiological processes relevant to circulating concentrations of cortisol, other neuroendocrine fac- this complex pathophysiology (see Kop, 1999; Rozanski, Blumen- tors, and lipids are also associated with atherosclerosis in human thal, & Kaplan, 1999, for reviews). Of course, psychosocial risk and animal models (for a review, see Kop, 1999). factors (e.g., hostility, depression, social isolation) might also contribute to CAD and CHD through behavioral pathways (Smith & Gallo, 2001), such as health habits (e.g., smoking, inactivity) Psychophysiological Triggers of CHD and behavioral components of standard care (e.g., adherence to medication regimens, diet restrictions). Cardiologic assessments can be used to test the effects of stress on later manifestations of CHD (Rozanski, 1998). In both labora- Effects of Psychophysiological Reactivity on CAD tory and ambulatory paradigms, these techniques provide evidence that stress can evoke myocardial ischemia and that such changes Cardiovascular reactivity (CVR) has been extensively studied as predict important clinical outcomes (Kop, Gottdiener, & Krantz, a mechanism linking psychosocial risk factors and CAD (Manuck, 2001; Rozanski et al., 1999). Parallel research in humans and 1994). Briefly, more frequent, pronounced, and prolonged in- animals has elucidated mechanisms underlying these acute effects. 550 SMITH AND RUIZ

In an early study using positron emission tomography, Dean- myocardium, a condition that increases susceptibility to arrhyth- field et al. (1984) found that a stressful mental arithmetic task mia (Kovach, Nearing, & Verrier, 2001). decreased myocardial perfusion in 75% of CHD patients. Rozanski Stress also affects a variety of factors related to the readiness et al. (1988) used radionuclide ventriculography to demonstrate with which blood coagulates and clots (Von Kanel, Mills, that a stressful speech task produced transient defects in ventric- Fainman, & Dimsdale, 2001), perhaps promoting thrombolytic ular wall motion, an indicator of ischemia, and this result was events. Further, acute stress increases the viscosity of blood recently replicated by Stone et al. (1999). Related diagnostic through decreases in plasma volume (Allen & Patterson, 1995). techniques and stressors have been used to demonstrate that mental Increased viscosity, in turn, is associated with greater risk of MI, stress evokes ischemia (Burg, Jain, Soufer, Kerns, & Zaret, 1993; perhaps through increased coagulation or the oxygen demands of Goldberg et al., 1996; Gottdiener et al., 1994; Legault, Langer, circulating more viscous blood (Lowe, Lee, Rumley, Price, & Armstrong, & Freeman, 1995), including anger-arousing events Fowkes, 1997). Stress can also increase the susceptibility of pa- (Ironson et al., 1992). Several studies using ambulatory electro- tients with advanced CAD to the development of arrhythmias cardiogram recording (i.e., Holter monitoring) demonstrated that (Verrier & Lown, 1984). stress and negative emotions during daily activities are associated Regardless of its origins in oxygen demand and supply, isch- with ischemia (Barry et al., 1988; Gabbay et al., 1996; Gullette et emia induced during mental stress is potentially quite important. In al., 1997; Krantz et al., 1996), including anger (Gabbay et al., recent studies, patients who displayed ischemia during laboratory 1996), tension, and sadness (Gullette et al., 1997). It is important mental stress testing were at increased risk of recurrent coronary to note that many of the studies on mental stress and ischemia were events and death (e.g., MI, SCD, bypass graft surgery, or angio- based on relatively small and select samples of patients (e.g., those plasty; Jiang et al., 1996; Krantz et al., 1999; Sheps et al., 2002). with exercise-induced ischemia). Hence, although there are many However, some of these studies have involved relatively small and positive findings, the generalizability of this association to a select samples. Hence, the prognostic importance of mental-stress- broader range of CHD patients requires additional research. induced ischemia should be examined in additional research. As discussed above, ischemia results when myocardial oxygen These effects of acute stress on ischemia among persons with demand outstrips supply. Stress and negative emotions increase advanced CAD may contribute to the noticeable increase in acute heart rate and contractile force in both healthy and CHD popula- coronary events following dramatic stressors (e.g., earthquakes, tions (Brownley, Hurwitz, & Schneiderman, 2000; Goldberg et al., missile attacks; Dobson, Alexander, Malcolm, Steele, & Miles, 1996), thereby increasing oxygen demand. CHD patients with 1991; Meisel et al., 1991). greater CVR to laboratory mental stressors are more likely to display ischemia during exercise testing (Kral et al., 1997), labo- Conclusions Regarding Effects of Stress on CAD ratory mental stressors (Goldberg et al., 1996; Krantz et al., 1991), and CHD and ambulatory monitoring (Blumenthal, Jiang, et al., 1995). Of interest, CVR to mental stress has also been found to predict Pathways linking psychological stress and negative emotions recurrent events in post-MI patients (Manuck, Olsson, Hjemdahl, with CHD are summarized in Figure 1. From even this brief & Renqvist, 1992). However, ischemia occurs in response to review, several conclusions are warranted. First, there are several mental stressors at lower heart rates than in response to physical plausible mechanisms linking stress and negative emotions to the stressors (Kop et al., 2001). If heart rate provides an index of initiation and progression of CAD and to the subsequent emer- oxygen demand, then effects of mental stress on ischemia occur gence and course of CHD. Second, associations between psycho- during relatively low demand. This suggests that mental stress may social risk factors and CHD endpoints (i.e., MI, SCD) examined in also reduce cardiac oxygen supply. epidemiological studies of initially healthy populations could re- Both human and animal investigations have demonstrated flect an effect at one or more places during its decades-long mechanisms involving reduced supply. In these studies, CAD and development. That is, such associations could indicate that these psychological stress combine to reduce blood flow, primarily characteristics initiate or hasten the progression of CAD or pre- through coronary artery spasm or constriction due to endothelial cipitate manifestations of CHD after the development of severe dysfunction. For example, in patients undergoing coronary angiog- CAD. Of course, risk factors could have both types of effects. raphy, Yeung et al. (1991) found that mental stress decreased the Finally, in studies of the incidence and course of CHD, effects of diameter of coronary arteries. This decrease did not occur in risk factors could reflect one or more specific psychophysiological nondiseased sections, was significant at sites of mild lesions, and mechanisms. Hence, the current literature on mechanisms repre- was pronounced at more severe lesions. Other studies have repli- sents a maturing scientific base, but it also poses important ques- cated this effect (Boltwood, Taylor, Burke, Grogin, & Giacomini, tions for future research. 1993; Lacy et al., 1995). Ischemia induced by mental stress in Two of these issues are likely to receive increasing attention patients with CAD might also be due to failure of coronary vessels over the next decade. First, traditional models of these psychoso- to dilate in response to stress (Dakak, Quyyumi, Eisenhofer, Gold- matic effects emphasize the sympathetic branch of the autonomic stein, & Cannon, 1995). Dilation in response to mental stress does nervous system. However, more recent research has implicated occur in persons without CAD, reflecting an appropriate reaction parasympathetic mechanisms as well. Higher levels of parasym- to increased myocardial oxygen demand. In a canine model, in- pathetically mediated heart rate variability (vagal tone, respiratory duction of an angerlike state (i.e., access to food threatened by a sinus arrhythmia, etc.) confer reduced risk of CHD morbidity and second dog) evoked a large decrease in coronary artery blood flow mortality (Bigger et al., 1992). As we discuss later in the article, in animals with a partially occluded coronary artery (Verrier, these parasympathetic mechanisms have been linked to several Hagestad, & Lown, 1987) and promoted electrical instability of the psychosocial risk factors. Second, an intriguing body of research SPECIAL ISSUE: CORONARY HEART DISEASE 551

Figure 1. Psychophysiological influences on coronary artery disease and coronary heart disease. From “Chronic and Acute Psychological Risk Factors for Clinical Manifestations of Coronary Artery Disease,” by W. J. Kop, 1999, Psychosomatic Medicine, 61, p. 477. Copyright 1999 by the American Psychosomatic Society. Adapted with permission. HR ϭ heart rate; BP ϭ blood pressure; Sympatho/vagal ϭ sympathetic/vagal imbalance; SES ϭ socioeconomic status.

has indicated that infectious and inflammatory mechanisms con- which psychosocial characteristics were correlated with the sever- tribute to CAD and the course of CHD (Anderson et al., 1998; ity of CAD among patients referred for angiography. However, Mueller et al., 2002; Muhlestein et al., 1999; Zhu et al., 2001; for differences between CHD and control groups in cross-sectional reviews, see Becker, de Boer, & van der Wal, 2001; Libby, Ridker, studies may reflect psychosocial consequences of CHD rather than & Maseri, 2002). This suggests a point of integration of research causes (Cohen & Rodriguez, 1995). Further, selection into angiog- on psychosocial mechanisms in CHD with studies of psychosocial raphy samples and the inherent restriction in range of predictors influences on the immune system (Kiecolt-Glaser, McGuire, Rob- and outcomes may produce invalid estimates of associations be- les, & Glaser, 2002; Kop & Cohen, 2001). That is, effects of stress tween psychosocial characteristics and CAD (T. Q. Miller, Turner, and negative emotion on immune responses and inflammation may Tindale, Posavac, & Dugoni, 1991). Studies of psychosocial risk also contribute to the associations of psychological and social factors increasingly rely on more definitive methods. Well- characteristics with CAD and CHD. controlled, prospective studies of initially healthy populations or groups with carefully documented CHD are now much more Recent Research on Psychosocial Risk Factors common. Further, well-validated assessments of psychosocial pre- In prior decades, cross-sectional comparisons between CHD dictors and reliable classification of coronary outcomes are more groups and controls on personality traits, emotional disorders, and routine, as are appropriate statistical controls for possible con- aspects of the social environment were common, as were studies in founds. Hence, this literature has grown in quality as well as size. 552 SMITH AND RUIZ

Hostility as the Toxic Component of the Type A Pattern or sympathetically mediated mechanisms may be involved in the effects of anger arousal on acute MI. Hence, although the prospec- Historically, the Type A coronary-prone behavior pattern has tive evidence suggests that trait anger and hostility are more been the best known psychosocial risk factor. Despite quantitative consistent predictors of initial CHD than of its course, clinical reviews indicating that the Type A pattern (as defined by behav- studies do suggest that they could contribute to acute events. The ioral assessment) is a significant risk factor for CHD in initially more consistent association of hostility with CHD incidence and healthy populations (Matthews, 1988; T. Q. Miller et al., 1991), mortality than with the course of established disease could reflect inconsistencies in research findings led investigators to examine a selection process; hostile persons who survive initial events to be individual components of the multifaceted pattern. This research included in studies of CHD course may be at lower risk or more has identified individual differences in hostility as an important resilient for other reasons and may therefore be less likely to suffer predictor of CHD, as well as all cause mortality (T. Q. Miller, recurrent or fatal disease (R. B. Williams, 2000). Smith, Turner, Guijarro, & Hallet, 1996). As typically used in this A substantial body of research supports the prevailing view that research, the term hostility itself refers to a multidimensional psychophysiological correlates of stress and negative emotion construct (Smith, 1994). The emotional component involves anger compose the mechanism linking hostility and CHD (R. B. Wil- but also includes contempt and scorn. The behavioral component liams, Barefoot, & Shekelle, 1985). Hostility is associated with refers to verbal and physical aggression, which share an intent to heightened cardiovascular and neuroendocrine reactivity to stress- inflict harm. Finally, the term hostility most accurately describes ful social situations in the laboratory involving strangers (Chris- cognitive factors, such as cynicism, mistrust, and the tendency to tensen & Smith, 1993; S. B. Miller et al., 1998; Powch & Houston, interpret others’ actions as reflecting aggressive intent. 1996; Suarez, Kuhn, Schanberg, Williams, & Zimmermann, 1998) A quantitative review of studies published before 1995 found and family members (Smith & Brown, 1991; Smith & Gallo, that hostility predicted CHD, though the association was stronger 1999), as well as during daily activities, as assessed by ambulatory for behavioral ratings of hostility as opposed to self-reports (T. Q. assessments of blood pressure and cortisol excretion (Benotsch, Miller et al., 1996). Subsequent studies have indicated that self- Christensen, & McKelvey, 1997; Jamner, Shapiro, Goldstein, & reports of trait hostility and anger predict new coronary events Hug, 1991; Linden, Chambers, Maurice, & Lenz, 1993; Polk, among previously healthy people (Chang, Ford, Meoni, Wang, & Kamarck, & Shiffman, 2002; Pope & Smith, 1991). When recall- Klag, 2002; Everson et al., 1997; Kawachi, Sparrow, Spiro, Voko- ing previous anger-arousing events, hostile persons display larger nas, & Weiss, 1996; J. E. Williams et al., 2000). Further, self- and more prolonged increases in blood pressure (Fredrickson et al., reports of hostility have been associated with the severity and 2000). Also, unlike their more agreeable counterparts, hostile progression of atherosclerosis (Iribarren et al., 2000; Julkunen, persons do not respond to social support with reduced CVR to Salonen, Kaplan, Chesney, & Salonen, 1994; Matthews, Owens, stressors (Lepore, 1995; Smith, Uno, Uchino, & Ruiz, 2000). In Kuller, Sutton-Tyrrell, & Jansen-McWilliams, 1998; Whiteman, addition to greater psychophysiological response to stressors, hos- Dreary, & Fowkes, 2000), although there have been negative tility is also associated with lower levels of social support and findings (O’Malley, Jones, Feuerstein, & Taylor, 2000). One study greater exposure to stress at home and work (T. Q. Miller, Mark- found that the tendency to express anger outwardly predicted the sides, Chiriboga, & Ray, 1995; Newton & Kiecolt-Glaser, 1995; progression of coronary atherosclerosis as measured by repeated Smith, Pope, Sanders, Allred, & O’Keefe, 1988). This greater angiography, but cynical hostility did not (Angerer et al., 2000). psychosocial vulnerability (Smith, 1994), in turn, may reflect a Finally, hostility also predicts more rapid restenosis of coronary transactional process in which hostile persons undermine sources arteries following angioplasty (Goodman, Quigley, Moran, Meil- of support and foster conflicts through their mistrusting thoughts man, & Sherman, 1996; Mendes De Leon, Kop, de Swart, Bar, & and antagonistic actions (Smith, 1995). Unhealthy lifestyles could Appels, 1996). These studies confirmed that hostility is a CHD risk also contribute to the CHD risk associated with hostility. However, factor and suggest that it may contribute to the development and in most studies, but not all (Everson et al., 1997), statistical course of CAD. However, it is important to note that in prospective controls for health behaviors (e.g., smoking, inactivity) do not studies of patients with established CHD, individual differences in eliminate the association between hostility and subsequent CHD. anger and hostility do not appear to be robust predictors of recurrent cardiac events or survival (Hemingway & Marmot, 1999). Dominance as a Potential Coronary-Prone Trait However, studies of ischemia and other outcomes provide evidence that anger and hostility can contribute to coronary events in In their prior review in this journal, Thoresen and Powell (1992) persons with CAD. For example, in samples with documented questioned the emerging view that hostility was the only patho- CHD, hostile persons are more susceptible to ischemia (Burg et al., genic component of the Type A pattern. Subsequent studies sug- 1993; Helmers et al., 1993), and preliminary evidence suggests gested they may have been correct. Individual differences in social that they may be more susceptible to constriction of the coronary dominance may be a second risk factor within that constellation. In arteries during mental stress (Boltwood et al., 1993). As described analyses of the original prospective study of Type A (Western above, in the context of significant CAD the arousal of anger can Collaborative Group Study; Rosenman et al., 1975), Houston and evoke ischemia (Gabbay et al., 1996; Ironson et al., 1992). Finally, his colleagues (Houston, Chesney, Black, Cates, & Hecker, 1992; in two retrospective but well-controlled studies, episodes of anger Houston, Babyak, Chesney, Black, & Ragland, 1997) found that conferred a twofold increase in the likelihood of acute MI during behavioral ratings of hostility and social dominance were indepen- the following 1–2 hr (Mittleman et al., 1995; Mo¨ller et al., 1999). dent predictors of CHD and mortality. Social dominance was the This risk was greater among persons who did not routinely take label given to a set of controlling behaviors, including the tendency aspirin or beta-blocking medication, suggesting that thrombolytic to cut off and talk over the interviewer. A cross-sectional study of SPECIAL ISSUE: CORONARY HEART DISEASE 553 patients referred for thalium exercise stress testing found that Although there have also been negative findings (Wassertheil- behavioral ratings of hostility and dominance were independently Smoller et al., 1996).2 Among patients with established CHD, related to CHD (Siegman, Townsend, Civelek, & Blumenthal, depression, anxiety, pessimism, and related characteristics have 2000). In prospective studies, self-report measures of social dom- even stronger associations with recurrent coronary events (e.g., inance predicted the development of CHD (Siegman, Kubzansky, MI, cardiac procedures) and reduced survival (Ahern et al., 1990; et al., 2000; Whiteman, Deary, Lee, & Fowkes, 1997). Allison et al., 1995; Barefoot et al., 1996, 2000; Carney, Rich, The nonhuman-primate model described above provides an in- Freedland, & Sanai, 1988; Denollet & Brutsaert, 1998; Follick et triguing parallel to this research (J. R. Kaplan & Manuck, 1998). al., 1988; Frasure-Smith, Lespe´rance, Juneau, Talajic, & Bourassa, The chronic stress of repeated social reorganization (i.e., housing 1999; Frasure-Smith, Lespe´rance, & Talajic, 1995; Irvine et al., in unstable vs. stable social groups) produced more severe CAD 1999; Lespe´rance et al., 2002; Pennix et al., 2001; Scheier et al., among male macaques, but only among those in the top half of 1999), although here too there are negative findings (Lane, Carroll, behaviorally assessed dominance hierarchies. Administration of Ring, Beevers, & Lip, 2001; Mayou et al., 2000). A characteristic beta-adrenergic blockade of sympathetic input to the heart elimi- labeled vital exhaustion—consisting of low energy, irritability, nates the susceptibility of dominant animals to the atherogenic and demoralization—has also been linked to poor prognosis in effects of stress. Hence, physiological effects of recurring efforts CHD patients (Kop, Appels, Mendes de Leon, De Swart, & Bar, to assert social dominance may promote the initiation and progres- 1994; Mendes de Leon et al., 1996). Further, the effects of depres- 1 sion of CAD (J. R. Kaplan et al., 1987; Skantze et al., 1998). In sion and other indications of distress are significant even when humans, efforts to assert social influence or interpersonal control controlling for the possible confounding effects of initial illness evoke heightened CVR (Smith, Nealey, Kircher, & Limon, 1997; severity. Smith, Ruiz, & Uchino, 2000), and persons scoring high on per- Clinical psychologists would be understandably concerned by sonality measures of dominance display greater CVR during social pooling measures of depressive symptoms, anxiety symptoms, interaction (Newton, Bane, Flores, & Greenfield, 1999). Although related personality characteristics, and diagnosable anxiety and this literature is small, the available epidemiological, animal, and affective disorders, because diagnosis and treatment are facilitated psychophysiological studies suggest that dominance may confer in their differentiation. However, questions about a graded– risk for CHD. continuous versus qualitative–discontinuous distinction between depressive symptoms and depressive disorders has been the source Depression, Anxiety, and Negative Affectivity of considerable controversy (e.g., Coyne, 1994; Flett, Vredenburg, & Krames, 1997), with recent empirical support for both views Negative emotions other than anger have been widely studied (Ruscio & Ruscio, 2000; Santor & Coyne, 2001). Further, diag- over the past decade, and the findings resolve prior debates nosable disorders, subclinical symptoms, and personality traits (Booth-Kewley & Friedman, 1987; Matthews, 1988; Stone & involving depression and anxiety are closely related (Clark, Costa, 1990). In a meta-analysis, Booth-Kewley and Friedman Watson, & Mineka, 1994; Watson, Clark, & Harkness, 1994), and (1987) concluded that symptoms of depression and anxiety predict individual differences in negative affectivity or neuroticism predict CHD. This conclusion was criticized (Matthews, 1988; Stone & future emotional disorders (Zonderman, Herbst, Schmidt, Costa, & Costa, 1990) as based in part on “soft” or less definitive CHD McCrae, 1993). Future research may identify important differ- endpoints (e.g., chest pain). Individual differences in the tendency ences among these predictors in the levels of CHD risk they confer to experience negative emotions (i.e., neuroticism or negative (e.g., Herrmann, Brand-Driehorst, Buss, & Ruger, 2000) or their affectivity) are associated with somatic complaints in the absence underlying mechanisms, but presently these closely correlated of actual disease, including chest pain in persons with normal emotional characteristics seem to have similar and perhaps over- coronary arteries (Costa & McCrae, 1987; Watson & Pennebaker, lapping effects. 1989). Hence, the findings of Booth-Kewley and Friedman (1987) Autonomic processes have been identified as possible psycho- could have been biased by an association between individual physiological mechanisms linking this group of risk factors and differences in negative affect and symptom reporting similar to— CHD. For example, both anxiety and depression are associated but not actually reflecting—CHD. However, over the past decade, a number of methodologically with reduced heart rate variability—which can reflect either sound studies indicated that symptoms of depression and anxiety, heightened sympathetic activity or decreased parasympathetic ac- related emotional disorders, individual differences in the tendency tivity (or both)—and more specific indicators of vagal tone or to experience negative affect, and related personality traits indeed parasympathetic responsivity (Carney et al., 1995, 2001; Hughes confer increased risk of MI, SCD, and other “hard” indicators of & Stoney, 2000; Krittayaphong et al., 1997; Sheffield et al., 1998; CHD. Studies of initially healthy populations have shown that Stein et al., 2000; Watkins, Grossman, Krishnan, & Sherwood, symptoms of depression and anxiety and reports of hopelessness 1998). Other studies have found that depressive symptoms are predict future coronary events (i.e., MI, coronary death), even with statistical controls for health behavior (e.g., smoking) and other 1 It is important to note that among females in this model, subordinate potential confounding factors (Anda et al., 1993; Ariyo et al., rather than dominant social status confers risk. Subordinate females engage 2000; Aromaa et al., 1994; Barefoot & Schroll, 1996; Eaker, in less sexual intercourse. This results in lower levels of estrogen activity Pinsky, & Castelli, 1992; Everson et al., 1996; Everson, Roberts, in this species, which may account for the association between social status Goldberg, & Kaplan, 1998; Ford et al., 1998; Jonas & Mussolino, and CAD (J. R. Kaplan et al., 1996). 2000; Kawachi, Colditz, Ascherio, Rimm, & Giovannucci, 1994; 2 Wassertheil-Smoller et al. (1996) did find that increasing levels of Kubzansky et al., 1997; Penninx et al., 2001; Pratt et al., 1996). distress over time predicted CHD, although initial levels did not. 554 SMITH AND RUIZ associated with sympathetically mediated cardiovascular and neu- gesting that such measures reflect the individual’s general sense of roendocrine reactivity (Light, Kothandapani, & Allen, 1998). acceptance, the accessibility of internal representations of social Depression and individual differences in negative affect are also ties, and other personality processes to an equal or even greater associated with increased exposure to stressful social circum- extent than actual interpersonal events (Lakey & Drew, 1997; stances (Bolger & Schilling, 1991; Bolger & Zuckerman, 1995; G. R. Pierce, Lakey, Sarason, Sarason, & Joseph, 1997). For Coyne, Thompson, & Palmer, 2002; Daley & Hammen, 2002; example, individuals with low levels of social support tend to Daley et al., 1997; Davila, Bradbury, Cohan, & Tochluk, 1997; appraise potentially supportive behavior as less supportive than do Fincham, Beach, Harold, & Osborne, 1997; Harkness & Luther, individuals with high support (T. Pierce, Baldwin, & Lydon, 2001; S. L. Johnson & Jacob, 1997). Through a variety of cogni- 1997). Hence, although epidemiological studies have clearly indi- tive and interpersonal processes, emotionally distressed individu- cated that something tapped by measures of social isolation and als may experience more environmental stress, as well as respond support predicts the development and course of CHD, recent to it with greater psychophysiological reactivity and/or reduced research has raised questions about the precise nature of this parasympathetic dampening of stress responses. However, the predictive factor. This ambiguity could complicate the design of extent to which these mechanisms account for the effects of this risk-reducing interventions, despite the clear evidence of a predic- group of risk factors on CHD requires further investigation. tive association. Also, depression and other chronic negative affects are associ- Studies of stress and adaptation increasingly have recognized ated with suppressed immune function (Herbert & Cohen, 1993; that social strain and isolation are distinct concepts with potentially Irwin, 2001), and in one recent study of patients with CAD, depressive symptoms were associated with immunologic markers independent effects (Coyne & Bolger, 1990; Rook, 1990; Uchino, of chronic infection and inflammation (Appels, Bar, Bruggeman, Holt-Lunstad, Uno, & Flinders, 2001). Recent studies of patients & De Baets, 2000). Hence, effects of depression in particular—and with cardiovascular disease have suggested that conflict in per- psychosocial risk factors generally—on immunologic mechanisms sonal relationships predicts poor outcomes. Orth-Gomer et al. warrant further research (Kop & Cohen, 2001). Finally, other (2000) found that women with CHD who reported high levels of psychophysiological (e.g., coagulation) or behavioral (e.g., medi- marital conflict were nearly three times as likely to experience a cal adherence, lifestyle) mechanisms may also contribute to the recurrent coronary event as married but nondistressed women. association of negative affect with CHD (DiMatteo, Lepper, & Coyne et al. (2001) reported a similar association between marital Croghan, 2000; Von Kanel et al., 2001). conflict and death in a sample of patients with congestive heart failure, most of whom had experienced a prior MI. In a large Social Isolation and Conflict sample of initially healthy but high-risk men, Matthews and Gump (2002) found that increasing levels of marital stress were associ- Decades of research has indicated that social isolation and low ated with increased risk of death from CHD. Nonhuman-primate levels of perceived social support confer increased risk of CHD models suggest that chronic social stress involving conflict can (for reviews, see Berkman, 1995; Hazuda, 1994; Orth-Gomer, promote atherosclerosis (J. R. Kaplan et al., 1983; J. K. Williams 1994). Recent studies of CHD morbidity and mortality have con- et al., 1993), and this effect has recently been replicated in a rabbit firmed this association in initially healthy populations (e.g., G. A. model of atherosclerosis (McCabe et al., 2002). However, com- Kaplan et al., 1994; Orth-Gomer, Rosengren, & Wilhelmsen, pared with the literature on isolation, there has been limited re- 1993; Pennix et al., 1997; Seeman et al., 1993; Vogt, Mullooly, search on this potentially important risk factor. Ernst, Pope, & Hollis, 1992). Social isolation is particularly un- Psychophysiological studies have indicated that social support healthy in patients with preexisting CHD (Angerer et al., 2000; and conflict are associated with plausible mechanisms. Individual Berkman, Leo-Summers, & Horwitz, 1992; Case, Moss, Case, differences in perceived support and the experimental manipula- McDermott, & Eberly, 1992; Gorkin et al., 1993; Horsten et al., tion of support are generally associated with reduced cardiovas- 2000; Krumholz et al., 1998; Welin, Lappas, & Wilhelmsen, 2000; cular and neuroendocrine reactivity to stressors (Kamarck, Peter- R. B. Williams et al., 1992; Woloshin et al., 1997), although man, & Raynor, 1998; Lepore, 1998; Thorsteinsson & James, different indicators of support and isolation sometimes produce 2000; Uchino, Cacioppo, & Kiecolt-Glaser, 1996). For example, inconsistent effects (Irvine et al., 1999). In one recent study, in the presence of a friend attenuates CVR in response to stressful which low social support did not predict post-MI prognosis, high laboratory tasks (Christenfeld et al., 1997). Consistent with the support reduced the negative effects of depression on survival (Frasure-Smith, Lespe´rance, Gravel, Masson, Juneau, Talajic, & view that beneficial effects of social support do not require actual Bourassa., 2000). In nonhuman-primate models, social isolation supportive transactions, mental activation of supportive network (i.e., solitary vs. stable group housing) promotes CAD (Shively, ties also attenuates CVR to stressors (Smith, Ruiz, & Uchino, Clarkson, & Kaplan, 1989). 2001). Further, positive social ties may lower risk of CAD and Many indicators of social support and isolation have been used CHD not only through direct dampening of CVR and other in epidemiological studies, ranging from quantitative measures of components of the stress response but also through separate network characteristics and activities (e.g., membership in organi- physiological mechanisms (e.g., release of oxytocin) involved in zations, marital status) to more subjective measures of network attachment and affiliation (Knox & Uvnas-Moberg, 1998; Unvas- quality (e.g., perceived adequacy or satisfaction with support). For Moberg, 1997). Finally, conflictual interactions produce height- both types of measures, it is generally assumed that they reflect ened cardiovascular and neuroendocrine responses in laboratory actual network characteristics and social experiences. However, (for a review, see Kiecolt-Glaser & Newton, 2001) and ambulatory recent theory and research has challenged this assumption, sug- studies (e.g., Holt-Lunstad, Uchino, & Smith, 2000). SPECIAL ISSUE: CORONARY HEART DISEASE 555

Job Stress Although there are some inconsistencies, individual differences in negative affect and related disorders and traits confer increased Two models of job stress have been examined as CHD risk risk of initial development of CHD in initially healthy populations factors. The job strain model posits that jobs high in demand and increased risk of recurrent events and reduced survival among (mental and physical effort, etc.) but low in control increase risk patients with preexisting CHD. The effect of depression on prog- (Karasek, 1979; Theorell & Karasek, 1996). The second model nosis following MI currently appears to be a particularly important suggests that an asymmetry of effort relative to rewards confers risk factor, underscoring the importance of routine assessments of risk (Siegrist, 1996). Prospective studies have found that job strain its potentially unique presentation in cardiac populations (Lespe´r- is associated with increased risk of CHD morbidity and mortality ance & Frasure-Smith, 2000). The mechanisms underlying these (Bosma, Peter, Siegrist, & Marmot, 1998; Hall, Johnson, & Tsou, effects may involve parasympathetic components of autonomic 1993; Theorell et al., 1998), although low job control (e.g., deci- functioning, sympathetic reactivity, altered homeostasis, and sional latitude) may have more impact than job demands or the heightened exposure to stressors. Social isolation and low per- combination of these characteristics (Bosma et al., 1998; Hammar, ceived support are clearly associated with increased risk of CHD Alfredsson, & Johnson, 1998; J. V. Johnson, Stewart, Hall, Fred- and reduced survival, and considerable evidence suggests that their lund, & Theorell, 1996; Marmot, Bosma, Hemingway, Brunner, & impact on stress reactivity is a plausible mechanism. However, Stansfeld, 1997; Wamala, Mittleman, Horsten, Schenck- recent models of the nature of social support and isolation and the Gustafsson, & Orth-Gome´r, 2000). Further, some negative results meaning of related measures raise important questions about the have been reported (Hlatky et al., 1995). The effort–reward model specific psychosocial characteristic that confers risk. Social con- has been the focus of less research, although this imbalance has flict may prove to be an independent interpersonal influence on been found to predict the progression of atherosclerosis and new CHD. Finally, job stress predicts CHD, although the specific work coronary events (Lynch, Krause, Kaplan, Salonen, & Salonen, characteristics and underlying mechanisms responsible for these 1997; Peter, 1995; Siegrist, Peter, Junge, Cremer, & Seidel, 1990). effects remain to be clarified. Effort–reward imbalance is also associated with increased risk of With some notable exceptions (e.g., Iribarren et al., 2000; Lynch CHD even when variance associated with job strain is controlled et al., 1997; Matthews, Owens, Kuller, Sutton-Tyrrell, & Jansen- (Bosma et al., 1998). A recent review concluded that both types of McWilliams, 1998), most studies have examined indications of job stress confer increased risk of future CHD, independent of any CHD that reflect late stages of the disease (e.g., MI, CHD, death). associations between job stress and negative health behaviors Although these outcomes are obviously important, this approach (Peter & Siegrist, 2000). Further, Matthews and Gump (2002) obscures the point(s) in the natural history of the disease where recently found that the number of self-reported work stressors was risk factors exert their effects. Noninvasive measures of the sever- associated with increased risk of death from CHD. ity and progression of atherosclerosis (e.g., carotid artery ultra- Studies of mechanisms potentially underlying these effects gen- sound; computed tomography scans of coronary artery calcium erally indicated that job stress is associated with CVR and other deposits) in representative samples of initially asymptomatic stress responses. For example, persons with high levels of job adults can clarify the impact of psychosocial risk factors on earlier strain display higher levels of workday blood pressure, as assessed stages of disease, as can the use of still earlier indications of through ambulatory monitoring (Schnall et al., 1990; Schnall, arterial changes (e.g., endothelial dysfunction) in adolescents and Schwartz, Landsbergis, Warren, & Pickering, 1998). However, young adults. Cardiac imaging and other diagnostic procedures can other studies have not replicated this effect (Matthews et al., 2000) determine the role of psychosocial risk factors in later stages of or found inconsistent effects for men and women (Blumenthal, disease (Rozanski, 1998). Findings from these types of research Thyrum, & Siegel, 1995; Light, Turner, & Hinderliter, 1992). would not only answer basic questions about the timing of psy- Hence, the mechanisms underlying the effects of job stress on chosocial effects but also help to refine psychosocial interventions. CHD are not yet clearly established. Further, assessments of subclinical indications of atherosclerosis and ischemia provide alternatives to the less frequent occurrence Conclusions Regarding Risk Factors of clinical events. This permits studies of clinically relevant out- Over the past 10 years, evidence has expanded indicating that comes without the sample sizes and long follow-up periods neces- psychosocial characteristics predict the development and course of sitated by a focus on clinical events. CHD. Support for the effects of anger and hostility continues to Most psychosocial risk factors are clearly related to plausible mount, as does evidence of the association of these personality psychophysiological mechanisms. However, these associations are characteristics with mechanisms that potentially influence CAD best seen as consistent with—but not providing direct evidence and CHD. However, prospective studies of initially healthy per- of—their hypothesized mediational role in the psychosomatic pro- sons have produced some negative findings. Further, there is little cess. Animal models provide important evidence in this regard, but evidence that individual differences in anger and hostility are future human studies must incorporate measures of risk factors, consistent risk factors among patients with established disease, psychophysiological mechanisms, and CAD or CHD outcomes for even though some studies of persons with CAD find that episodes more definitive tests of mediational hypotheses. This is an ambi- of anger can trigger ischemia and coronary events. The evolution tious research strategy that may be difficult to implement in large of research on the Type A pattern has produced preliminary epidemiological studies, but analyses of this type are needed to evidence of another possible coronary-prone characteristic—social evaluate the mediational models currently guiding the field. dominance. Here too, human and animal studies have identified A major challenge in the coming decade will be to develop associations between this stable social behavior and plausible useful approaches for studying conceptually distinct but often pathophysiological mechanisms. highly correlated risk factors. These risk factors are typically 556 SMITH AND RUIZ studied separately, despite their intercorrelation. When multiple Recent Studies psychosocial characteristics are studied, usually their independent statistical effects are tested in multivariate analyses or, in rare Intervention trials designed to modify psychosocial risk factors occasions, interactive effects (i.e., moderation) are tested. Future among CHD patients have produced mixed results over the past research should determine if the overlapping aspect of correlated decade. It is important to distinguish between interventions where risk factors (e.g., social conflict, anger, and depression) is the most stress reduction, modification of coronary-prone behavior, or related risk factors are the primary focus and those focusing on robust predictor of initial and/or recurrent events to examine modification of traditional behavioral risks (e.g., smoking, exer- possible core dimensions of psychosocial risk. Alternatively, cor- cise, diet; Blumenthal & Emery, 1988). As we discuss later in the relations among risk factors may indicate distinct processes article, the latter type of intervention has been found to have through which characteristics of individuals and their social con- beneficial effects, some of which include reductions in stress and texts jointly influence the development of CAD and CHD. For related psychological risk factors. However, specific comparisons example, hostile persons experience increased exposure to stress- of stress management and similar interventions with appropriate ful interpersonal events as well as low levels of social support control conditions permit clear evaluations of the effects of psy- (Smith, 1995), and similar patterns have been found in persons chosocial risk interventions. with depression (Joiner & Coyne, 1999). Hence, rather than a core In a large and well-controlled replication of the IHDLSM inter- dimension of psychosocial risk, these aggregations of risk factors vention, Frasure-Smith et al. (1997) did not find significant inter- could reflect transactional processes in which people both influ- vention effects. A second large and well-controlled trial of stress ence and are influenced by their social networks in such a way as management for post-MI patients also found no effects on cardiac to increase or reduce cardiovascular risk. The interpersonal and recurrences (Jones & West, 1996). However, Blumenthal et al. cognitive–social traditions in personality psychology (Kiesler, (1997) did find that a stress management intervention reduced 1996; Mischel & Shoda, 1999) provide concepts and methods for clinical cardiac events. The intervention also reduced the amount studying connections between the personality traits and social of ischemia evident during ambulatory (i.e., Holter) monitoring, contexts that predict CHD. Further, they can be adapted to research particularly among patients with high initial levels of daily isch- on both risk factors (Gallo & Smith, 1999) and underlying mech- emia. It is important to note, however, that although controls were anisms (Smith, Gallo, & Ruiz, in press). Such approaches to well matched to intervention participants on important medical and correlated risk factors could help construct a more accurate “psy- demographic risk factors, the study relied on a nonrandomized chosocial epidemiology of everyday life”3 and a social psycho- no-treatment comparison group. physiology of the underlying mechanisms. Of the behavioral interventions in CHD, a multicomponent program developed by Ornish et al. (1990) has received the most attention. Stress management through meditation and other tech- Psychosocial Interventions for CHD niques is combined with aerobic exercise, a very-low-fat diet, and group support. In recent tests, the approach produced clear reduc- At the time of the review by Thoresen and Powell (1992), the tions in recurrent events, CAD severity, and evidence of improved Recurrent Coronary Prevention Project (Friedman et al., 1986) coronary circulation compared with standard care (Gould et al., represented the most compelling evidence that psychosocial risk 1995; Ornish et al., 1998). However, it is not clear which feature factors for CHD could be modified through psychological inter- of the multicomponent intervention is most responsible for its ventions, with beneficial effects on medical outcomes. Patients effects, and the extent of behavior change required has raised randomized to a control condition received counseling about ap- concerns about its usefulness in general patient populations (Bill- propriate lifestyle changes following MI, whereas patients ran- ings, 2000). In a small study, Gidron, Davidson, and Bata (1999) domized to the active intervention received group therapy consist- found that a cognitive–behavioral intervention specifically tar- ing of relaxation training, self-monitoring of stress and Type A geted at modifying hostility was effective in reducing hostility and blood pressure in CHD patients. Preliminary results also indicate behavior, cognitive restructuring, and other cognitive–behavioral that treated patients in this trial experienced fewer and briefer techniques. The intervention reduced nonfatal recurrent cardiac rehospitalizations, with significantly lower associated medical events by 44% (Friedman et al., 1986). Among patients with less costs (Davidson, 2000). In a study of high-risk persons before the severe initial disease, the intervention also significantly reduced onset of CHD, Castillo-Richmond et al. (2000) randomized hyper- cardiac deaths (Powell & Thoresen, 1988). Internal analyses sug- tensive African American participants to receive a stress manage- gested that larger reductions in Type A behavior were related to ment intervention or usual care. Relative to control participants, reduced risk of recurrent events. In a second influential study from those receiving the intervention were found to have a reduction in that period, Frasure-Smith and Prince (1985) found that an inter- carotid atherosclerosis. vention in which nurses monitored stress levels of post-MI patients and provided supportive counseling when needed (i.e., the Isch- emic Heart Disease Life Stress Monitoring Program, IHDLSM) Findings From Quantitative Reviews produced a significant reduction in cardiac deaths, relative to This diverse literature has been evaluated in several quantitative randomized controls. At the time of the previous special issue, reviews (e.g., Linden, Stossel, & Maurice, 1996). The most recent these studies and a number of smaller controlled trials suggested that such interventions were useful additions to CHD care (Thore- sen & Powell, 1992). 3 We are indebted to George A. Kaplan for this descriptive phrase. SPECIAL ISSUE: CORONARY HEART DISEASE 557 and complete of these (Dusseldorp, van Elderen, Maes, Meulman, efficacy of medical therapies has generally come from larger and & Kraaij, 1999) found evidence of beneficial effects and provided better controlled trials and that this comparison is somewhat dated. a potential explanation for inconsistent findings. Health education The specific medical therapies and protocols continue to be re- (e.g., targeted toward behavioral risk reduction) and stress man- fined. Nonetheless, this literature indicates that interventions in- agement had equivalent significant effects on cardiac recurrences, tended to reduce psychosocial risk in established CHD may im- producing on average a 34% reduction in cardiac mortality and a prove medical outcomes. 29% reduction in recurrent MI. However, small sample sizes in However, a careful examination of the relevant studies suggests many of the treatment studies, limitations in randomization and the that these conclusions are quite tentative, and many questions documentation of clinical events, and other methodological issues remain for future research. Of most importance, many of the may have resulted in inflated estimates of treatment effects. available studies were small and/or contained methodological lim- Of importance, Dusseldorp et al. (1999) found that intervention itations (i.e., nonrandomized designs). Hence, large, well- effects were moderated by effects on intermediate targets, such as controlled replications are needed. Many of the psychosocial in- change in behavioral risk factors, reductions in blood pressure, and tervention studies included in recent reviews are 10 and even 20 reductions in emotional distress. Overall treatment effects on car- years old. The medical management of CHD has changed signif- diac outcomes were significantly greater in studies where positive icantly during this period, raising two important concerns. First, it results were found for proximal intervention targets—especially is not clear that results of older psychosocial treatment studies proximal psychological outcomes. Also of interest, the large recent generalize to the context of current cardiologic care that involves studies that failed to replicate beneficial effects of psychosocial treatments (e.g., greater use of beta-blockers, aspirin and anti- interventions (i.e., Frasure-Smith et al., 1997; Jones & West, coagulants, lipid lowering agents) that impact several of the path- 1996)—included in the analyses of Dusseldorp and colleagues ways through which psychosocial risk factors may affect the (1999)—did not find significant treatment effects on emotional pathophysiology of CHD. Second, the changes in standard care distress. In contrast, the positive findings for cardiac events and have resulted in improved prognosis for CHD, and the reduced ambulatory ischemia reported by Blumenthal et al. (1997)—not variance in morbidity and mortality may make it more difficult to included in this meta-analysis—were accompanied by significant detect the incremental beneficial effects of psychosocial reductions in reported stress and hostility. Also consistent with the treatments. potential importance of intervention effects on emotional out- At a minimum, the improved prognosis for CHD resulting from comes, in a nonrandomized trial Denollet and Brutsaert (2001) refinements in routine care increases the sample size requirements found that participation in a multicomponent cardiac rehabilitation for trials intended to evaluate the effects of psychosocial interven- program (i.e., exercise, stress management, individual counseling) tions on cardiac recurrences and mortality. Blumenthal et al. as opposed to standard medical care was associated with less (1997) recently illustrated the intermediate strategy of using am- negative affect over the 3-month intervention period and improved bulatory ischemia as an outcome variable. Ambulatory ischemia is survival over the subsequent 9 years. a robust predictor of subsequent cardiac events (Kop et al., 2001). Further, ambulatory ischemia is much more common than recur- Conclusions Regarding Intervention Research rent events and therefore can provide a sensitive, clinically relevant index of intervention outcomes. Smaller studies that demon- The results of the quantitative review discussed previously strate positive results on this measure could then be replicated in suggest that interventions intended to prevent recurrent cardiac larger trials with adequate power and longer follow-ups required to events through the reduction of stress and modification of related detect effects on morbidity and mortality. psychosocial risk factors are clearly promising, and there is con- The focus on cardiac recurrences and mortality may actually siderable evidence in support of their efficacy (Kendall, Flannery- underestimate intervention effects. Psychosocial interventions also Schroeder, & Ford, 1999). Were it not for the heterogenous treat- improve emotional adjustment and functional status or activity ments evaluated, the intervention literature would seem to satisfy levels (e.g., Johnston, Foulkes, Johnston, Pollard, & Gudmunds- recently proposed criteria for empirically supported psychological dottir, 1999; Trzcieniecka-Green & Steptoe, 1996). These are therapies (i.e., internally valid evidence of treatment effects; important consequences of CHD (Swenson & Clinch, 2000) and Chambless & Hollon, 1998). This research has included variations integral components of comprehensive evaluations of health care in treating personnel, modes of delivery, and settings, though interventions (R. M. Kaplan, 1994). The use of standardized out- perhaps not in a sufficiently systematic or extensive manner as to come units, such as quality of life adjusted years (QALYs; R. M. support firm conclusions about effectiveness (i.e., external validity Kaplan, 1994), in future studies of psychosocial risk reduction or generalizability to typical clinical settings; Kendall et al., 1999). would not only capture these additional benefits but also facilitate The clinical significance (Kendall, 1999) of these intervention comparisons with a variety of other treatments including standard effects (e.g., reductions in cardiac mortality of 30%) seems obvi- medical therapies (Kaplan & Groessl, 2002). It may be that stress ous, but comparisons with other standard interventions provide management and related interventions produce improvements in further evidence. For example, widely utilized medical treatments QALYs that match or exceed some medical or surgical approaches (e.g., beta-adrenergic blocking medications, anticoagulants) re- and do so at less cost. Further, emotional distress is associated with duce mortality on average by 20% (Lau et al., 1992). In a quan- significant health care expenditures in CHD patients, primarily titative comparison across types of studies, Ketterer (1993) con- because of greater rates of rehospitalization and related procedures cluded that psychosocial interventions produced reductions in (Allison et al., 1995; Frasure-Smith, Lespe´rance, Gravel, Masson, mortality at least as large as those observed for medical and Juneau, & Talajic, 2000). Hence, effective treatments could re- surgical interventions. It is important to note that evidence of the duce these costs (e.g., Davidson, 2000). Cost-utility and cost- 558 SMITH AND RUIZ effectiveness analyses in future intervention studies have obvious sis. In each topic, as we have outlined previously, there are also importance in the current climate of health care financing and important limitations of this research and many equally important related policy debates. issues for future investigations. In studies with null results for cardiac outcomes (Frasure-Smith et al., 1997; Jones & West, 1996), it is not clear whether the failure to find significant reductions in psychosocial risk factors reflects Implications for Patient Care ineffective interventions provided to appropriate patients or use of Although acceptance of the potential role psychosocial factors otherwise-effective treatments with patients who did not need in the development and management of CHD is growing among them (Linden, 2000). For example, in Jones and West’s (1996) study, stress management was provided to an unselected sample of medical professionals (Rozanski et al., 1999), it has not become a consecutive patients, who reported generally low levels of psycho- standard component of care for most patients. Additional evidence logical distress. Future research should examine the efficacy of the reliability and predictive utility of psychosocial and psycho- of these interventions in patients selected for higher levels of physiological assessments in clinical cardiologic settings would psychosocial risk and, perhaps, examine interventions targeted likely prompt further progress in this regard. Of even more im- to patients’ predominant problem (i.e., general stress, anger, portance, additional supportive evidence of effective interventions depression). from large and well-controlled randomized trials is needed to Despite mounting evidence of their status as risk factors, only guide current care, as are criteria for the identification of patients recently have social isolation and depression been specific targets likely to benefit from specific psychosocial interventions. in controlled intervention trials. They were addressed in a recently Given the incidence and typical course of CHD and the sup- completed, multicenter trial—Enhancing Recovery in Coronary portive evidence regarding psychosocial factors available to date, Heart Disease (ENRICHD; ENRICHD Investigators, 2000). Ap- many health care professionals understandably believe they cannot proximately 3,000 acute-MI patients who met criteria for depres- wait for these remaining issues to be resolved definitively before sion or social isolation (or both) were randomized to either stan- implementing these variables in risk stratification and intervention dard care or a psychosocial intervention on the basis of cognitive strategies. Although more detailed discussions are available else- therapy techniques. Depressed patients received cognitive therapy where (Allan & Scheidt, 1996; Bellg, 1998; Smith & Ruiz, in for depression, and isolated patients received treatment to increase press), we can draw some implications from the research over the support using similar techniques. Preliminary evidence suggested past decade for current clinical practice. Psychosocial risk factors that the psychosocial intervention reduced depression and im- certainly should be included in the evaluation of CHD patients, and proved social functioning, but it had no overall effect on cardiac following such assessments, adjunctive psychosocial interventions events (recurrent MI or death; National Heart, Lung, and Blood should be considered. The efficacy findings generally support their Institute, 2001).4 However, the potential importance of effective use. However, an excessive set of behavior change requirements treatments for depression in CHD is evident in its multiple effects. would likely discourage or overwhelm patients. Hence, interven- Depression is itself a major threat to quality of life, predicts poor tions should be prioritized and approaches with multiple benefits medical outcome, and can undermine adherence to other compo- given particular consideration. nents of care (DiMatteo et al., 2000; Ziegelstein et al., 2000). For example, smoking cessation among CHD patients is asso- In addition to evaluating the usefulness of adjunctive treatments, ciated with a 40% or larger reduction in mortality (Wilson, Gibson, intervention studies also provide opportunities to test the relatively Willan, & Cook, 2000), and its cost effectiveness compares favor- well-developed mediational models of psychosocial risk. Interven- ably with standard medical treatments (e.g., thrombolytic therapy, ing psychophysiological or transactional–stress exposure mecha- cholesterol lowering medication) and behavioral approaches to nisms could be assessed in intervention studies and used in formal rehabilitation (e.g., exercise; Ades, Pashkow, & Nestor, 1997). mediational analyses. Such studies are valuable in theory testing Hence, these interventions should be a priority among smokers and could also suggest directions for refining interventions. with CHD. Exercise interventions reduce cardiac recurrences and death, and they also compare favorably to medical approaches in cost-effectiveness analyses (Ades et al., 1997). Further, exercise General Conclusions, Implications, and Future Directions interventions can reduce hypertension (Blumenthal et al., 2000; Over the past decade, evidence regarding the role of psychoso- 2002) and depressive symptoms (Babyak et al., 2000; Blumenthal cial risk factors in the development of CHD has grown consider- et al., 1999) and have been found to increase heart rate variability ably. Pathways through which stress and negative emotions influ- among CHD patients (Stahle, Nordlander, & Bergfeldt, 1999). ence the development of CAD and CHD have been identified in an Hence, unless medically contraindicated, the broad psychological extensive body of human and animal research. Epidemiological and physiological benefits of exercise (Dubbert, 2002; Salmon, studies have demonstrated generally consistent and substantial prospective effects of hostility, depression, related individual dif- 4 ferences in negative affect, and social isolation on CHD. Smaller It is important to note that this pattern of outcomes is inconsistent with the meta-analytic finding of Dusseldorp et al. (1999) in which interventions but potentially important literatures suggest similar roles for job that improved psychosocial functioning were more likely to have beneficial stress, social dominance, and social conflict. In each case, these effects of morbidity and mortality. However, additional—albeit prelimi- risk factors are associated with psychophysiological mechanisms nary—analyses from the ENRICHD trial indicate that the psychosocial through which stress and emotions could influence CAD and intervention significantly reduced recurrent CHD events among White men CHD. Finally, a small and methodologically varied literature sug- (Schniederman, 2002). Hence, it may be that the treatment was effective gests that psychosocial interventions may improve CHD progno- for subgroups of patients. SPECIAL ISSUE: CORONARY HEART DISEASE 559

2001) make this a reasonable selection as a central element of grams for physically healthy but hostile, depressed, or socially intervention plans. isolated adults approaching the age of onset for CHD. Rather, If depression or hostility are selected for more direct interven- partnerships with developmental and prevention scientists could tions, there are several empirically supported interventions (Beck identify new directions and applications for psychosocial research & Fernandez, 1998; Deffenbacher, Dahlen, Lynch, Morris, & on CHD to younger populations (R. B. Williams, 1998). Gowensmith, 2000; DeRubeis & Crits-Christoph, 1998). Certainly most psychosocial treatments contain an element of social support, Emerging Issues but more focused interventions for social isolation or low support have not undergone a similar degree of controlled evaluation Future studies of psychosocial influences on CHD should attend (Cutrona & Cole, 2000; Helgeson & Gottlieb, 2000). In the context to the generalizability of results across sociodemographic charac- of close relationships, several interventions are available for con- teristics, particularly gender, ethnicity, and SES. These character- flict (Baucom, Shoham, Mueser, Daiuto, & Stickle, 1998; Chris- istics are themselves related to CHD risk, perhaps in part through tensen & Heavey, 1999), but there is only limited evidence of their mechanisms involving the psychosocial risk factors reviewed here. usefulness in treating cardiovascular disease (Ewart, Taylor, Krae- Further, these sociodemographic variables may moderate effects of mer, & Agras, 1984). It is important to note that many stress risk factors on mechanisms or CHD outcomes, as well as the management approaches used with CHD patients have broad ap- effectiveness of interventions. For example, whether defined as a plicability to these psychosocial risk factors (e.g., Blumenthal et characteristic of individuals (e.g., income, occupational status; al., 1997). Finally, some evidence suggests that specific pharma- Gonzalez, Rodriguez, & Calero, 1998) or the neighborhoods where cologic approaches may be safe and effective in reducing symp- they live (Yen & Kaplan, 1999), low SES confers increased risk of toms of depression and hostility (Lespe´rance & Frasure-Smith, CHD morbidity and mortality. Further, at least some of this risk is 2000; Strik et al., 2000), and correlational evidence suggests that attributable to psychosocial risk factors (Lynch, Kaplan, Cohen, they may be associated with reduced coronary risk (Sauer, Berlin, Tuomilehto, & Salonen, 1996). Some ethnic minorities are at & Kimmel, 2001). However, until ongoing randomized trials are increased risk, and again, this effect may be attributable at least in completed (Shapiro et al., 1999), their impact on CHD recurrence part to psychosocial factors such as discrimination and stressful and mortality is not clearly established. living circumstances (Anderson & Armstead, 1995; D. R. Wil- liams & Collins, 1995). In both human and animal models, there Implications for Prevention are gender differences in the association between psychosocial risk factors and CHD, as well as in the likely underlying mechanisms Decades of research on behavioral risk factors has shaped agen- (J. R. Kaplan et al., 1996; Kiecolt-Glaser & Newton, 2001). das for CHD prevention. Smoking cessation, reductions in dietary Ultimately, interventions should be evaluated in specific underrep- fat and excess weight, and increases in physical activity among the resented sociodemographic groups (cf. Castillo-Richmond et al., sedentary are important public health goals and the focus of 2000) to determine their generalizability. evolving behavior change technologies. Further, the prevention of Developments in medical science will also shape the psychos- smoking, high-fat diets and obesity, and inactivity before these ocial research agenda in CHD. Advances in noninvasive assess- risks are established relatively early in life are potentially even ment methods have permitted more informative tests of the influ- more useful strategies. Preventing costly disease through behavior ence of psychosocial factors on asymptomatic atherosclerosis. change in childhood and adolescence has an obvious appeal, Other noninvasive procedures have provided clear evidence that especially given that early indications of CAD appear in these age psychological stress and related variables can evoke myocardial groups. ischemia (Rozanski, 1998). These same procedures have been used In light of these increasingly accepted preventive approaches to to evaluate the outcomes of psychosocial interventions (Blumen- the public health challenges posed by CHD, the literature on thal et al., 1997; Castillo-Richmond et al., 2000; Gould et al., psychosocial risks and related interventions suggests additional 1995). Continuing refinements of cardiologic assessments and avenues for research and application. There is limited evidence related procedures will encourage even more compelling tests of regarding the developmental origins of specific psychosocial risk psychosomatic hypotheses and more sensitive and persuasive ev- factors as measured in studies of adults. However, there is a vast idence of intervention effects. As in all areas of biomedical sci- literature on related concepts in emotional and social development ence, developments in the genetics of CAD and CHD will pose (Caspi, 1998; Coie & Dodge, 1998; Rubin, Bukowski, & Parker, new questions for psychosocial research. Genes implicated in 1998). This field has guided the development of effective inter- atherosclerotic processes (e.g., Anderson et al., 2000) or in psy- ventions for other prevention goals (e.g., reducing emotional dis- chophysiological individual differences (R. B. Williams et al., tress and aggressiveness, increasing social and emotional compe- 2001) could identify higher and lower risk groups, and this genetic tence) in children and adolescents (e.g., Blechman, 1996; status could moderate the effects of psychosocial risk factors Greenberg, Kusche, Cook, & Quamma, 1995; Tolan, Guerra, & or identify groups most likely to benefit from psychosocial Kendall, 1995), and they could be adapted to examine their effects intervention. on early indications of psychosocial risk for CHD and early Finally, future research will addresses new versions of classic indications of cardiovascular disease (e.g., blood pressure, endo- psychological questions. The interplay of early experience and thelial dysfunction) among vulnerable children and adolescents. biology in social and emotional development will inform CHD Certainly, the traditional psychosocial research agenda in CHD is prevention research and, perhaps, suggest additional psychoso- rather full. 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