The interaction between anxiety and CHD is less studied compared to that of depression and CHD. Kawachi and colleagues reported that a short phobic anxiety measure predicted nonfatal MI and fatal CHD over two years in men.23 One study found that high levels of worry were associated with nonfatal MI and fatal CHD over 20 years.24 In addition, several studies suggest that anxiety might contribute to the development of CHD in initially healthy individuals and also linked anxiety to cardiac death and MI.23,24,25 Other studies on the other hand found no association.26,27
Analysis from Normative Aging Study which included 735 men (mean age 60), found that anxiety characteristics independently and prospectively predicted MI incidence after controlling for age, education, marital status, fasting glucose, body mass index, high-density lipoprotein cholesterol, and systolic blood pressure in proportional hazards models. Phobia was associated with 1.36 relative risk for AMI while manifest anxiety increased AMI risk by 1.43 folds. These relationships remained significant after further adjusting for health behaviors (drinking, smoking, and caloric intake), medications for hypertension, high cholesterol, and diabetes during follow-up and additional psychological variables (depression, type A behavior, hostility, anger, and negative emotion). The authors concluded that anxiety-prone dispositions appear to be a robust and independent risk factor of MI among older men.28
Recently Roest and colleagues published a large meta-analysis which included twenty studies comprised of 249,846 persons. The analysis revealed that anxious persons were at risk of CHD (HR 1.26; 95% CI 1.15 to 1.38) and cardiac death (HR: 1.48; 95% CI: 1.14 to 1.92), independent of demographic variables, biological risk factors, and health behaviors. This suggests that anxiety seemingly is an independent risk factor for CHD.29
Post-traumatic stress disorder (PTSD) is one form of anxiety disorders that drew special attention in the last few years as a potential contributor to development of CHD. PTSD affects those exposed to traumatic events and is associated with re-experiencing, avoidance, and hyperarousal symptoms related to such events. Since the disorder reflects dysregulation of the stress-response system, which is associated with potentially atherogenic processes, a link between PTSD and CHD has long been speculated.
Boscarino performed a prospective study random sample of 4,328 male Vietnam veterans, who did not have heart disease at baseline. After controlling for known coronary risk factors, study found that a diagnosis of PTSD more than doubled the risk for early-age heart disease mortality (hazard ratio= 2.25; 95% CI, 1.02–4.95).30
Adults with PTSD exhibit neuroendocrine alterations characterized by enhanced negative feedback sensitivity of glucocorticoid receptors in the stress-response system and lower than normal urinary and plasma cortisol levels. Exaggerated catecholamine responses to trauma-related stimuli have also been found in adults diagnosed with PTSD. Higher concentrations of circulating catecholamines and increased total body sympathetic activity may eventually lead to autonomic nervous system dysfunction, including diminished heart rate variability, baroreflex dysfunction, and increased QT interval variability. Chronic stress and emotional arousal may also lead to or exacerbate endothelial damage and promote the development of atherosclerosis.31,32,33
Hostility is a personality and character trait with attitudinal (cynicism and mistrust of others), emotional (anger), and behavioral (overt and repressed aggression) components.34 Similar to the above conditions, the interaction between hostility and coronary heart disease is a matter of debate.
High hostility level has been shown to be related to increased risk of angiographically documented coronary atherosclerosis, essential hypertension, CHD incidence, and all-cause mortality. This, however, has been attributed to unhealthy lifestyle associated with this personality trait. Everson and colleagues have shown that the association between cynical distrust and cardiovascular outcomes was explained by simultaneous adjustment for smoking, alcohol consumption, physical activity, and body mass index.35 A post hoc analysis from CARDIA trial found that high hostility level may predispose young adults to coronary artery calcification independent of traditional risk factors.36 In a recent large meta-analysis which included 25 studies, anger and hostility were associated with increased CHD events in the healthy population studies (combined hazard ratio [HR]: 1.19; 95% confidence interval [CI]: 1.05 to 1.35, p =0.008) and with poor prognosis in the CHD population studies (HR: 1.24; 95% CI: 1.08 to 1.42, p =0.002). Interestingly, in this analysis the harmful effect of anger and hostility on CHD events in the healthy populations was greater in men than women.37 In the same analysis the apparently harmful effects of anger and hostility on CHD were no longer significant in either the healthy or disease populations after fully controlling for behavioral covariates such as smoking, physical activity or body mass index, and socioeconomic status. This supports the notion that if anger and hostility do influence CHD risk, effects might be primarily mediated via behavioral pathways.
Recently however, Newman and colleagues examined the relation between hostility and incident ischemic heart disease (IHD) and evaluated whether observed hostility is superior to patient-reported hostility for the prediction of IHD in a large, prospective observational study. They found that participants with any observed hostility had a greater risk of incident IHD than those without. No such relation was found for patient-reported hostility. Those with any observed hostility had a significantly greater risk of incident IHD (HR: 2.06, 95% confidence interval: 1.04 to 4.08), after adjusting for cardiovascular (age, sex, Framingham Risk Score) and psychosocial (depression, positive affect, patient-reported hostility, and anger) risk factors. The analysis demonstrated that compared with patient-reported measures, observed hostility is a superior predictor of IHD. In addition, the presence of any observed hostility at baseline was associated with a two-fold increased risk of incident IHD over 10 years of follow-up.38