Tuesday, October 21, 2008

Stress and Coronary Heart Disease

As with cigarette smoking, the effects of exposure to severe stress cannot be ethically evaluated in experimental human studies. However, several observational studies provide evidence associating stress with the precipitation of coronary events. In experimental animal studies, cynomolgus monkeys were exposed to stress by having their normal social housing patterns disrupted. Monkeys exposed to this stress had significantly more atherosclerosis compared with monkeys without this stress. Further studies elucidated that social status, as determined by dominance, was also a major predictor of atherosclerotic development; dominant males and females had less atherosclerosis than their subordinate counterparts. Some have suggested that these findings support the association of lower socioeconomic status and increased incidence of CHD observed in human population studies. Although it can be argued that lower social class reflects less dominance and control over the environment, other factors, such as lack of access to medical care or engaging in unhealthy lifestyle behaviors, may partially account for these findings. Perhaps the strongest support for the association of socioeconomic status and the development of CHD is found in a study of more than 1,100 Finish men, in which socioeconomic status was related to the degree of carotid artery stenosis after accounting for traditional coronary risk factors

Acute stress is considered a trigger for ischemia. Evaluation of angina includes determining if the event was triggered by physical exertion, eating, exposure to cold, or emotion. Among coronary patients, the physiologic effects of mental stress have also been studied by correlating cardiac ischemia, measured by ambulatory electrocardiographic monitoring, with daily life experiences. Carefully recorded diaries were used to identify ischemia triggered by physical activity and by specific emotions. Both moderate and intense physical and mental activities were associated with ischemic episodes. Estimates suggest that in the hour after high levels of negative emotions, the risk for ischemia doubles. The effects of mental stress have also been evaluated during angiography. Using arithmetic as an acute mental stressor, Yeung and colleagues found that stenosed coronary artery segments responded to mental stress by constricting, whereas normal segments typically responded by dilating. Studies using challenging, timed video games have demonstrated similar results. Comparisons of mental and physical activity stress tests found that mental stress produces higher diastolic blood pressure, similar systolic blood pressure, and lower heart rate responses than physical activity. These studies suggest that ischemia occurring in response to mental stress might be accounted for by inappropriate vasoconstrictor responses.

Observational studies have also examined the incidence of cardiac events and exposure to sudden stresses such as natural disasters. The incidence of fatal and nonfatal myocardial infarction (MI) in Los Angeles County significantly increased on the day of the Northridge earthquake compared with rates before and after the earthquake. In contrast, mortality rates for other types of heart disease, such as cardiomyopathy or cerebrovascular disease, were not increased. Similar increases were observed after major Japanese earthquakes and the 1991 Gulf War missile attacks in Israel. It should be noted that these studies are not able to exclude the effects of increased physical stress brought on by exertion. Interestingly, data from both the Israel missile attacks and from Japanese earthquakes suggest that the incidence of MI and CHD mortality was greater in women than in men. Post-traumatic stress scores were also higher in Japanese women than in men, suggesting that mental stress could be a trigger of these coronary events