We aimed to evaluate the hypothesis that chronic stress, as assessed by hair cortisol content, is associated with the development of AMI. A prospective case–control study included 56 patients admitted to hospital with AMI and 56 control patients, admitted to internal medicine wards for other indications. An enzyme immunoassay technique was used to measure cortisol in the most proximal 3 cm of hair, considered to represent the most recent 3 months of exposure. Median hair cortisol contents (range) were 295.3 (105.4–809.3)ng/g in AMI patients and 224.9 (76.58–949.9)ng/g in controls (p = 0.006, Mann–Whitney U-test). After controlling for other risk factors for AMI using multiple logistic regression, log-transformed hair cortisol content remained the strongest predictor (OR 17.4, 95% CI 2.15–140.5; p = 0.007). We demonstrated elevated hair cortisol concentrations in patients with AMI. This suggests that chronic stress, as assessed by increased hair cortisol in the 3 months prior to the event, may be a contributing factor for AMI.
Short term stress in the form of extreme fright or acute emotional upheaval has been well established as a cause of acute cardiac disease mediated by catecholamine myocardial injury, manifested clinically as sudden cardiac death and Takotsubo cardiomyopathy, and histopathologically as contraction band necrosis. Suspected but less well established is the role of short term stress in acute myocardial infarction.
Even more speculative has been the role of chronic stress, which may take such forms as vigilance, depression or chronic anxiety, in myocardial infarction. The suspected role of cortisol was based on sound pathophysiologic rationale but direct evidence to support such a role was lacking. This study makes an important contribution. I'll have more to say about this in future posts about stress and cardiovascular disease in connection with my recent attendance at this meeting.