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PITTSBURGH -- Common symptoms of depression such as fatigue, sleep disturbances, and anhedonia may trigger initima-media thickness changes associated with subclinical atherosclerosis, researchers here reported.
PITTSBURGH, Feb. 7 -- Common symptoms of depression such as fatigue, sleep disturbances, and anhedonia may trigger initima-media thickness changes associated with subclinical atherosclerosis, researchers here reported.
In a study of 324 healthy older adults, higher depressive symptoms at baseline were significantly associated with greater three-year change in intima-media thickness (?R2 =0.026, P=0.002), found Jesse C. Stewart, Ph.D. of the University of Pittsburgh, and colleagues.
Thickening of the carotid arterial wall was specifically related to somatic-vegetative symptoms (?R2 =0.027, P=0.002), but was not related to anger, hostility, anxiety and other cognitive-affective symptoms, they reported in the February issue of Archives of General Psychiatry.
Those findings emerged from analysis of data from the Pittsburgh Healthy Heart Project, an ongoing prospective cohort study of 464 healthy older men and women.
At baseline 324 participants completed standard questionnaires (Beck Depression Inventory II, Beck Anxiety Inventory, and Cook-Medley Hostility Scale) that assessed depressive symptoms, anxiety symptoms, hostility, anger experience, and anger expression.
Mean carotid intima-media thickness was assessed by B-mode ultrasonography at baseline and at three-year follow-up.
Dr. Stewart said the results were "consistent with the findings of past investigations examining the effect of depression-related factors on subclinical atherosclerotic progression."
The earlier studies linked cognitive-affective symptoms with intima-media changes. Dr. Stewart said the earlier studies did not examine somatic-vegetative aspects of depression, so "it is not possible to determine whether the observed relationships were specific to the cognitive-affective aspects."
Dr. Stewart said the study was limited by an "oversight" in the computer-based depression questionnaires that asked patients to list symptoms during the past week rather than the previous two weeks, which was the correct time frame for the standardized instrument used. He said, however, that while this error caused "minor interpretation problems" the net result was most likely an underestimation that may have weakened the relationship between symptoms and changes in the arterial wall.
Another potential limitation was the failure to detect a relationship between traditional risk factors such as hypertension and carotid intima-media thickening. But in this case Dr. Stewart said this may reflect a beneficial effect of antidepressants, particularly treatment selective serotonin reuptake inhibitors as well as a relatively brief follow-up period and the overall good health of the sample.
The authors also pointed out that "because this study included only healthy, older individuals, our findings may not be generalizable to younger populations or to older populations in which chronic medical disorders are prevalent. Therefore, it is necessary that our results be replicated in population-based studies with less stringent inclusion criteria."
Finally, Dr. Stewart concluded that identifying potentially harmful depressive symptoms might "facilitate the development of focused interventions designed to reduce the coronary artery disease risk of individuals prone to experience negative emotions."