The more anxious a person is, the greater the chances of an incident stroke, results from a prospective analysis demonstrated. The association was independent of other known risk factors including depression, researchers reported.
“Results indicated a dose-response relation between anxiety and stroke,” according to a cardiovascular behavioral medicine researcher in the department of psychiatry at the University of Pittsburgh and her associates. “Exploratory analyses suggest that behavioral factors, particularly smoking and physical activity may be important pathways to consider.”
Over a period of 22 years, the researchers studied a nationally representative sample of 6,019 people aged 25-74 years from the first National Health and Nutrition Examination Survey which was conducted from 1971 to 1975. At baseline, all study participants underwent an in-person structured interview, physical exam, and blood draw, and they completed psychological questionnaires including the General Well-Being Schedule, a four-item tool that asks respondents to rate the severity of their anxiety-related symptoms during the past month.
Strokes were identified through hospital or nursing home reports and death certificates. Numerous covariates were accounted for, including use of blood medications, diagnosis of diabetes by a physician, total serum cholesterol, body mass index, and depressive symptoms as measured by the GWB’s depressed mood subscale and by the Center for Epidemiologic Studies of depression scale.
During a mean 16-year follow-up, the researchers identified 419 cases of incident strokes (221 in men and 198 in women). They observed that every one standard deviation increase in anxiety was associated with a 17% increase in stroke risk following adjustment for demographic factors. Men and women in the highest tertile of anxiety symptoms had a 33% higher risk of stroke, compared with those in the lowest tertile following adjustment for other cardiovascular risk factors.
Poor health behaviors may be one pathway linking anxiety with stroke risk, the researchers wrote. In the present study, behaviors (particularly smoking and physical activity) had the most sizeable attenuating effect on the relationship between anxiety and incident stroke. However, since these behaviors did not account fully for the association between anxiety and incident stroke, direct biologic effects of anxiety should also be considered. Chronic anxiety could lead to excess activation of hypothalamic-pituitary-adrenal axis and sympathetic nervous system, which may increase the risk for stroke. Anxiety could also contribute to stroke or other cardiovascular diseases by lowering the threshold for arrhythmia or by reducing heart rate variability.
The researchers acknowledged certain limitations of the study, including the fact that baseline history of stroke and coronary heart disease were self-reported and that bias may have occurred due to excluding individuals lost to follow-up or missing data. We could not formally test mediation due to insufficiencies in temporal ordering of data collection. Stroke cases were identified based on discharge reports/death certificates and were not confirmed by imaging or a neurologist. Additionally, we may not have accurately captured silent strokes (resulting in an underestimate of cases in the population), although such misclassification would likely bias results toward the null.