New Postoperative Depressive Symptoms and Long-Term Cardiac Outcomes After Coronary Artery Bypass Surgery

Department of Medicine, Cardiothoracic Surgery, Weill Medical College, Cornell University, New York, NY 10021, USA.
American Journal of Geriatric Psychiatry (Impact Factor: 4.24). 03/2002; 10(2):192-8. DOI: 10.1097/00019442-200203000-00010
Source: PubMed


The authors evaluated the impact of an increase in depressive symptoms at 6 months after elective coronary artery bypass graft surgery on long-term cardiac morbidity and mortality between 6 and 36 months postoperatively. Patients who had low scores for depressive symptomatology pre-operatively and who completed follow-up at 6 months were contacted again 36 months after surgery to assess cardiac and neurologic morbidity and mortality. At 36 months after surgery, an interval history was completed, and baseline questionnaires were readministered. Follow-up was obtained on 123/124 patients (99%). The rate of combined new cardiac morbidity/mortality between 6 and 36 months was 13.6% among those with newly increased depressive symptoms at 6 months vs. 3.0% in the patients without new depressive symptoms at 6 months. Only an increase in depressive symptoms at 6 months was related to the occurrence of subsequent cardiac complications between 6 and 36 months. In this small sample of patients, increased depressive symptoms at 6 months after surgery appear to be associated with the occurrence of subsequent major cardiac morbidity/ mortality.

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    • "Depression or depressive symptoms are a prevalent and debilitating form of maladaptive neuroplasticity affecting approximately 20–40% of people with CHD [88–90]. Depression and cardiovascular events have been widely studied in CHD; depressed people are more likely to develop CHD (meta-analytic effect size, 1.5–2.7) "
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    ABSTRACT: Physical activity is a seemingly simple and clinically potent method to decrease morbidity and mortality in people with coronary heart disease (CHD). Nonetheless, long-term maintenance of physical activity remains a frustratingly elusive goal for patients and practitioners alike. In this paper, we posit that among older adults with CHD, recidivism after the initiation of physical activity reflects maladaptive neuroplasticity of malleable neural networks, and people will revert back to learned and habitual physical inactivity patterns, particularly in the setting of stress or depression. We hypothesize that behavioral interventions that successfully promote physical activity may also enhance adaptive neuroplasticity and play a key role in the maintenance of physical activity through the development of new neuronal pathways that enhance functional ability in older adults. Conversely, without such adaptive neuroplastic changes, ingrained maladaptive neuroplasticity will prevail and long-term maintenance of physical activity will fail. In this paper we will: (1) describe the enormous potential for neuroplasticity in older adults; (2) review stress and depression as examples of maladaptive neuroplasticity; (3) describe an example of adaptive neuroplasticity achieved with a behavioral intervention that induced positive affect in people with CHD; and (4) discuss implications for future work in bench to bedside translational research.
    Neural Plasticity 10/2012; 2012(1):516364. DOI:10.1155/2012/516364 · 3.58 Impact Factor
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    • "McKhann et al.[15] showed between 13% and 9% of 124 CABG patients at one month and twelve month follow up, respectively, reported clinically relevant depressive symptoms not evident at the time of surgery. Peterson et al.[16] explain newly developed depressive symptoms resulting from the stressors of surgery that can produce an adjustment response, or reactive type depression. In any case, as described below, identifying depression in the CABG surgery patient is complicated by the somatic symptoms experienced in CAD and the physical stressors of surgery. "
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    • "It is well established that depression adversely affects outcomes from chronic medical conditions. Patients with coronary artery disease and comorbid depression have functional disability [6], poorer outcomes following coronary artery bypass surgery [7], a worse prognosis following an episode of unstable angina [8] and increased mortality [9] as compared to those without depression. The biologic rationale for increased vulnerability of depressed patients with coronary artery disease is thought to be a manifestation of hypothalalmic–pituitary–adrenocortical axis hyperactivity, decreased heart rate variability and changes in platelet receptor function [10]. "
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