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Background and Purpose: Major depression is an independent risk factor for increased morbidity and mortality in patients with coronary artery disease (CAD). Increased platelet activity and vascular endothelial dysfunction are possible pathways through which depression may increase cardiovascular risk. Citalopram exhibits strong selective inhibition of human platelet activation, but little is known about its effects on vascular endothelium. We assessed whether treatment of depressed CAD patients with citalopram alters platelet/endothelial biomarkers. The study was performed within the framework of the CREATE trial., Methods: We assessed the effect of citalopram on P-selectin, beta-thromboglobulin (betaTG), soluble intercellular cell adhesion molecule-1 (sICAM-1), and total nitric oxide (tNO). Plasma samples were obtained at baseline and week 12 from subjects randomized to citalopram 20-40 mg daily (n = 36), or placebo (n = 21). Anticoagulants, aspirin, and clopidogrel were permitted., Results: Treatment with citalopram was associated with greater increase in tNO over 12 weeks compared to placebo (P = 0.005). There were no differences for the other biomarkers such as P-selectin (P = 0.70), betaTG (P = 0.46) and ICAM (P = 0.59)., Conclusion: Treatment with citalopram for 12 weeks in depressed CAD patients is associated with enhanced production of nitric oxide despite the co-administration of commonly prescribed anti-platelet regimens including aspirin and clopidogrel. Clinical implications of these findings are unclear, but improved endothelial function is implied by the increased NO production, suggesting that citalopram may be of particular benefit for patients with comorbid depression and vascular disease including CAD, stroke, peripheral artery disease, and diabetes.

Depression is commonly present in patients with coronary heart disease (CHD) and is independently associated with increased cardiovascular morbidity and mortality. Screening tests for depressive symptoms should be applied to identify patients who may require further assessment and treatment. This multispecialty consensus document reviews the evidence linking depression with CHD and provides recommendations for healthcare providers for the assessment, referral, and treatment of depression.

Objectives: We tested whether improvements in depressive symptoms precede improved adherence to aspirin in patients with acute coronary syndromes (ACS)., Background: Depression is associated with medication nonadherence in patients with ACS, but it is unclear whether changes in depression impact on adherence., Methods: Electronic medication monitoring was used to measure adherence to aspirin during a 3-month period in a consecutive cohort of 172 patients (25 to 85 years) recruited within 1 week of hospitalization for ACS. Depressive symptom severity was assessed using the Beck Depression Inventory (BDI) during hospitalization and at 1 and 3 months after hospitalization. Adherence was defined as the percentage of days aspirin was taken as prescribed., Results: Depression severity in hospital was associated with nonadherence in a gradient fashion: 15% of non-depressed patients (BDI score 0 to 4), 29% of mildly depressed patients (BDI score 10 to 16), and 37% of patients with moderately-to-severely depressive symptoms (BDI score >16) took aspirin less than 80% of the time (p = 0.03). A cross-lagged path analytic model revealed that improvements in depressive symptoms in the first month after the ACS were associated with improvements in adherence rates in the subsequent 2 months (standardized direct effect -0.32, p = 0.016)., Conclusions: Diagnosis and treatment of depressive symptoms may improve medication adherence in patients after ACS.

Objectives: To review the recent literature on the relation between depression and coronary heart disease (CHD), including both etiologic studies (that is, depression preceding development of CHD) and prognostic studies (that is, depression predicting prognosis in established CHD), and to assess the degree to which the literature supports a causal interpretation of the link between depression and CHD., Method: We searched the MEDLINE, Current Contents, and PsycINFO databases for articles published between December 15, 2003, and December 15, 2005, containing combinations of several key words related to CHD, prognosis, and depression. We reviewed papers for evidence of 6 rule-of-thumb criteria for making causal inferences: objective CHD outcome measures, prospective designs, results showing consistent and strong dose-response relations, adequate covariate adjustment, biological plausibility, and evidence from clinical trials that changing depression alters CHD risk., Results: We found 8 recent etiologic studies, 16 prognostic studies, 2 publications with both types of data, and 23 review papers. Although there was much methodological variability concerning measurement of depression and assessment of cardiac outcomes, the recent etiologic studies increase the evidence of a role for depression. Recent prognostic data are less consistent. Small studies showing no link between depression and CHD prognosis continue to appear, despite lack of adequate statistical power., Conclusions: The recent literature continues to support both an etiologic and a prognostic role for depression in CHD. Despite this evidence, there have been few clinical trials of depression treatment in CHD patients and no clinical trials of depression prevention. Additional trials are needed.

Panic disorder (PD) and panic-like anxiety have been associated with an increased risk of cardiovascular death. No study has specifically examined the association between panic attacks and ischemia in patients who have coronary artery disease (CAD). We hypothesized that panic attacks would induce myocardial perfusion defects in patients who have CAD and PD. Sixty-five patients who had CAD and positive results with nuclear exercise stress testing (35 with PD and 30 without PD served as controls) underwent a well-established panic challenge test (1 vital capacity inhalation of a gas mixture containing 35% carbon dioxide and 65% oxygen) and were injected with technetium-99m sestamibi at inhalation. Single-photon emission computed tomography was used to assess per-panic challenge perfusion defects, and heart rate, blood pressure, and 12-lead electrocardiogram were continuously measured during the procedure. Patients were not withdrawn from their cardiac medications. Patients who had PD were significantly younger than the controls; otherwise groups did not differ with respect to gender, cardiac medications, nuclear exercise test results, and baseline heart rate and blood pressure. Seventy-four percent of patients (26 of 35) who had PD had a panic attack at inhalation versus 6.7% of controls (2 of 30, p <0.001). As hypothesized, patients who had PD and demonstrated a panic attack were more likely to develop a reversible myocardial perfusion defect than were controls who did not have an attack (80.9% vs 46.4% p = 0.009). Thus, despite being on their cardiac medications, panic attacks preferentially induced significant perfusion defects in patients who had CAD and PD. In conclusion, panic attacks in patients who have CAD appear to be bad for the heart.

Objective: Major North American cardiology organizations do not currently list depression among the officially recognized cardiac risk factors, yet many behavioral medicine specialists believe depression to be an important risk. We wondered what was missing from the available data., Methods: The Medline, Current Contents, and PsychInfo databases were used to perform a systematic review of the literature linking depression and depressive symptoms with cardiac disease outcomes. Because of previous reviews, we paid particular attention to publications from 2001 to 2003., Results: We identified 21 etiologic and 43 prognostic publications that had prospective designs, used recognized measures of depression, and included objective outcome measures. We also identified 79 review articles. In addition to issues of sample size, sample characteristics, and timing of measures, we noted heterogeneity in the definitions of depression, frequent repeat publications from the same data sets, heterogeneity of outcome measures, a variety of approaches for covariate selection, and a preponderance of review articles, all factors that cannot help to convince skeptics., Conclusions: Despite these issues, the bulk of the data from prospective studies with recognized indices of depression and objective outcome measures is supportive of depression as a cardiac risk factor.

High rates of depression have been reported in patients with coronary artery disease, and depression has been repeatedly shown to adversely affect cardiac morbidity and mortality. Despite these findings, little work has been devoted to evaluating effective antidepressant treatments for this subpopulation. This open-label trial assessed the efficacy and acceptability of interpersonal psychotherapy in depressed patients with stable coronary artery disease. Seventeen patients with coronary artery disease who met DSM-IV criteria for major depression received 12 weekly sessions of interpersonal psychotherapy. Outcome was assessed with the 17-item Hamilton Depression Rating Scale and the Beck Depression Inventory II. Ten patients received medication during the trial, and seven patients received interpersonal psychotherapy alone. The patients showed a significant reduction in scores on both the Hamilton depression scale and the Beck Depression Inventory II from baseline, with 53% of the patients meeting criteria for remission, as defined by scores of < or =7 and < or =14 on the Hamilton depression scale and the Beck Depression Inventory II, respectively. Medicated and unmedicated patients responded similarly to interpersonal psychotherapy. These data provide support for the potential use of interpersonal psychotherapy in depressed patients with coronary artery disease. The therapy was well tolerated and accepted by patients, with a high proportion achieving remission. Future randomized clinical trials are needed to establish its efficacy.

Objective: The natural course of elevated depressive symptoms or subthreshold depression in patients with an acute coronary syndrome (ACS) is presented, as is the prognostic impact. Safe and effective psychological treatment options are desirable for subthreshold depression in patients with ACS, should they prove tolerable, efficacious, and cost-effective to cardiologists and their patients. To achieve this long-term goal, we propose focusing on 3 intermediate goals. First, we need to understand which symptoms or patterns of symptoms (eg, fatigue, anhedonia, guilt feelings) are specifically predictive of ACS recurrence. Second, the prevalence of known psychosocial vulnerabilities (proximal causes) of depressive disorders should be assessed in patients with ACS, to understand better the etiology of these symptoms in these patients. Third, randomized controlled trials of vulnerability-related, evidence-based psychological depression interventions in cardiac patients are needed. The ways in which psychological proximal cause theories are relevant--or irrelevant--for both the treatment of depressive symptoms in post-ACS patients and the prevention of ACS recurrence are discussed.

Objective: This study was conducted to determine whether or not depression is associated with higher levels of inflammatory markers in patients recovering from acute coronary syndromes., Method: Plasma levels of soluble intercellular adhesion molecule 1 (sICAM-1) and interleukin-6 (IL-6) and the serum level of C-reactive protein were measured in 481 patients 2 months after hospitalization for acute coronary syndromes. Diagnosis of major depression was based on the Structured Clinical Interview for DSM-IV., Results: Depressed patients showed significantly higher sICAM-1 levels, a difference that remained significant after adjustment for potential confounders (gender, smoking, presence of metabolic syndrome). Although there was no significant association between depression and IL-6, there was an interaction between depression and statin therapy for levels of C-reactive protein. Depressed patients not taking statins had markedly higher C-reactive protein levels than did nondepressed patients. There was no relationship with depression in those receiving statins., Conclusions: These results suggest chronic endothelial activation among depressed patients after acute coronary syndromes. Further research is needed to determine whether or not higher levels of sICAM-1 may identify a subgroup of depressed patients at particularly high risk for cardiac events among patients with established coronary artery disease or among those without previous coronary artery disease.

Some degree of depression affects at least 30% of hospitalized patients with coronary artery disease (CAD), and is associated with increased risks of mortality and continuing depression over at least the first year following hospital discharge. Despite its consequences for prognosis and quality of life, depression is underrecognized and undertreated in cardiac patients. The diagnosis of depression is complicated in patients with medical illness. Their symptoms can reflect physical as well as psychological complaints. Many CAD patients resist the idea of additional medications, and drug interactions can be problematic for those willing to accept antidepressant treatment. Finally, depression tends to recur. Its successful treatment requires a long-term commitment from both physician and patient. This article examines the special challenges involved in diagnosing depression in patients with CAD, outlines available psychotherapeutic and pharmacological treatments, and considers the issues involved in deciding which patients to treat, with what approach, and for how long.

The article presents a study on the effectivity of citalopram and interpersonal psychotherapy in reducing depressive symptoms. Results revealed that citalopram improves the Hamilton Depression Rating Scale and Beck Depression Inventory II scores more than the placebo. It also indicated greater improvement in scores in Inventory of Depressive Severity and Interpersonal Relationships Inventory. It is concluded that citalopram reduces depressive symptoms more than the placebo.