Depression and Medication Adherence in Outpatients With Coronary Heart Disease

Gehi, Anil K.; Haas, Donald; Pipkin, Sharon; Whooley, Mary A.

doi:10.1001/archinte.165.21.2508

Cited by 432 publications

(304 citation statements)

References 65 publications

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“…While this makes the study highly relevant to the CAD population, where subsyndromal symptoms predominate, these findings may not apply to those with MDD. Depressive symptoms and subthreshold depression in CAD have been shown to be clinically important, as they predict mortality (Barefoot et al., 2000) and adherence to treatment (Gehi, Haas, Pipkin, & Whooley, 2005; Rieckmann et al., 2006; Ziegelstein et al., 2000). As such, identifying novel treatment targets is of particular importance as milder forms of depression impact prognosis in those with CAD (Barefoot et al., 2000) and are often undertreated (Ellis, Eagle, Kline‐Rogers, & Erickson, 2005).…”

Section: Discussionmentioning

confidence: 99%

Plasma sphingolipids and depressive symptoms in coronary artery disease

et al. 2017

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BackgroundDepression is highly prevalent in individuals with coronary artery disease (CAD) and increases the risk of future cardiac events and mortality. Sphingolipids have been implicated in the pathophysiology of both CAD and depression. This study assessed the association between plasma sphingolipid concentrations and depressive symptoms in CAD subjects.MethodsDepressive symptoms were measured using the depression subscale of the self‐reported Hospital Anxiety and Depression Scale (HADS). Sphingolipid concentrations were measured from fasting plasma samples using high‐performance liquid chromatography‐coupled electrospray ionization tandem mass spectrometry (LC/MS/MS). Linear regression models were used to assess associations between log‐transformed concentrations of plasma sphingolipids and depressive symptoms.ResultsA total of 111 CAD patients (mean (SD) age = 63.6 ± 6.4, 84.7% male) were included. In linear regression analyses, higher plasma concentrations of ceramides C16:0 (β = 0.204, p = .026) and C18:0 (β = 0.209, p = .023) and sphingomyelin SM18:1 (β = 0.210, p = .024) were significantly associated with higher HADS depression subscale score after adjusting for covariates.ConclusionSphingolipids, in particular the ceramide species C16:0 and C18:0 and the sphingomyelin species SM18:1, may be implicated in the pathophysiology of depression in CAD. The association between plasma sphingolipid concentrations and depression should be further examined in CAD patients and in other populations.

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Section: Discussionmentioning

confidence: 99%

Plasma sphingolipids and depressive symptoms in coronary artery disease

et al. 2017

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“…A few studies have found a link between depression and change in platelet activation [68], and between phobic anxiety and abnormalities in the platelet serotonin transporters and intracellular calcium levels, leading to changes in the fibrinolytic system [64]. Platelets play a key role in the development of atherosclerosis, thrombosis and acute coronary syndromes [65], thereby possibly increasing the risk for cardiac mortality in ICD patients.…”

Section: Platelet Activationmentioning

confidence: 99%

Psychological vulnerability, ventricular tachyarrhythmias and mortality in implantable cardioverter defibrillator patients: is there a link?

Pedersen

Brouwers

Versteeg

2012

Expert Review of Medical Devices

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“…Alterations in cardiac autonomic tone 16 Common genetic vulnerability 17 Enhanced activity of the hypothalamic pituitary-axis 18 Greater platelet activation 19 Increased catecholamine levels 20 Increased whole blood serotonin 21 Inflammatory processes 22 Lower omega-3 fatty acid levels 23 Mental-stress induced ischemia 24 Toxicity of tricyclic antidepressants 25 Potential behavioral mechanisms Dietary factors 26 Lack of exercise 27 Medication nonadherence 28 Poor social support 29 …”

Section: Potential Biological Mechanismsmentioning

confidence: 99%

Depression and Cardiovascular Disease

Whooley¹

2006

JAMA

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Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder. CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.

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Depression and Medication Adherence in Outpatients With Coronary Heart Disease

Abstract: Depression is associated with medication nonadherence in outpatients with CHD. Medication nonadherence may contribute to adverse cardiovascular outcomes in depressed patients.

Cited by 432 publications

References 65 publications

Plasma sphingolipids and depressive symptoms in coronary artery disease

Plasma sphingolipids and depressive symptoms in coronary artery disease

Psychological vulnerability, ventricular tachyarrhythmias and mortality in implantable cardioverter defibrillator patients: is there a link?

Depression and Cardiovascular Disease

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