Unipolar Depression and the Progression of Coronary Artery Disease: Toward an Integrative Model

被引:51
作者
Ormel, Johan [1 ]
de Jonge, Peter [1 ,2 ,3 ]
机构
[1] Univ Groningen, Dept Psychiat, ICPE, Univ Med Ctr Groningen, NL-9700 RB Groningen, Netherlands
[2] Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, NL-9700 RB Groningen, Netherlands
[3] Tilburg Univ, Dept Med Psychol, Ctr Res Psychol & Somat Dis CoRPS, NL-5000 LE Tilburg, Netherlands
关键词
Depression; symptom dimensions; Coronary artery disease; Myocardial infarction; Atherosclerosis; POSTMYOCARDIAL INFARCTION DEPRESSION; ACUTE MYOCARDIAL-INFARCTION; CHRONIC MEDICAL CONDITIONS; HEART-RATE-VARIABILITY; C-REACTIVE PROTEIN; MAJOR DEPRESSION; CARDIOVASCULAR PROGNOSIS; SYMPTOM DIMENSIONS; VITAL EXHAUSTION; CARDIAC EVENTS;
D O I
10.1159/000323165
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Background: Despite extensive research on the relationship between depression and coronary artery disease (CAD) after an acute coronary syndrome (ACS), causal interpretations are still difficult. This uncertainty has led to much confusion regarding screening and treatment for depression in CAD patients. Method: A critical and conceptual analysis of the pertinent literature, which elaborates the implications of the heterogeneity in symptom pattern, etiology, and course of depression in CAD patients. Results: We propose an integrative dynamic model of the depression-CAD relationship. The model rests on three core hypotheses: (1) Depression in CAD patients consists of mixtures of two types of depression, denoted as 'cognitive/affective' and 'somatic' depression, each having a somewhat characteristic symptom expression and etiology. (2) Effects of depression on CAD depend on the type and duration of depression. The dynamic aspect of the model indicates that post-ACS depression shifts, when it persists, from a marker of the severity (somatic type) and meaning (cognitive/affective type) of the ACS to a largely indirect causal factor in the progression of CAD. (3) The most plausible pathways mediating the effects of persistent/recurrent depression, irrespective of type, on cardiac prognosis are behavioral and act by making depressed CAD patients more susceptible to other CAD risks. The model offers testable predictions and explanations for a variety of apparently unrelated or inconsistent findings. Conclusion: The proposed model may have potential for integrating findings regarding the depression-CAD relationship, contributing to the clarification of discords on screening and treatment of depression, and guiding future research. Copyright (C) 2011 S. Karger AG, Basel
引用
收藏
页码:264 / 274
页数:11
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