Older patients with coronary artery disease often experience depressive symptoms and are vulnerable to developing cognitive impairment. Whether depressive symptoms increase their risk of cognitive decline is unknown.
To examine the association between the stability of depressive symptoms and cognitive decline for 30 months among patients undergoing coronary angiography and to explore whether any observed associations were modified by the presence of the apolipoprotein E (APOE) ε4 allele.
Urban tertiary care hospital serving southern Alberta.
Three hundred fifty patients 60 years or older (73.7% male) undergoing nonemergent catheterization (October 27, 2003, through February 28, 2007) without prior revascularization. We compared a baseline measure of depressive symptoms (Geriatric Depression Scale score ≥5) with a dynamic measure capturing change from baseline to 12 months.
Mean change in domain (z scores for attention/executive function, learning/memory, and verbal fluency) and global (raw Mini-Mental State Examination) cognitive scores from baseline to 6, 12, and 30 months and from 12 to 30 months.
In adjusted models, participants with persistent depressive symptoms (at baseline and ≥1follow-up visit) showed significantly greater declines at 30 months in attention/executive function (mean z score change, -0.22), learning/memory (-0.19), verbal fluency (-0.18), and global cognition (mean Mini-Mental State Examination [MMSE] score change, -0.99) compared with participants with no or baseline-only depressive symptoms. Persistent depressive symptoms were associated with significantly greater declines in all cognitive measures from 12 to 30 months after adjusting for sociodemographic and clinical factors. For global cognition, a significantly greater decline was evident for patients with persistent depressive symptoms and the APOE ε4 allele (mean MMSE score change, -2.93 [95% CI, -4.40 to -1.45]).
Depressive symptoms persist in some patients with coronary artery disease, placing them at a greater risk for cognitive decline. Whether this decline is additionally modified by the presence of APOE ε4 requires further investigation.
"Cognitive deficits are prevalent in patients with coronary artery disease (CAD) [1-4] and, accordingly, patients with CAD are at risk of accelerative cognitive decline and transition to dementia . Major depression significantly amplifies the rate of cognitive decline in those with CAD [6,7], as well as worsening functional outcomes and increasing the risk of mortality [8,9]. The prevention of cognitive decline in patients with CAD may rely not only on adequate treatment of depressive symptoms, but also on a targeted inhibition of the mechanisms leading to cognitive decline in those with depression. "
[Show abstract][Hide abstract] ABSTRACT: Background
Patients with coronary artery disease (CAD) are at risk of accelerated cognitive decline, particularly those with major depression. Mechanisms for cognitive deficits associated with CAD, and the effects of depression, remain poorly understood. However, CAD is associated with inflammatory processes that have been linked to neurodegeneration, may contribute to cognitive decline, and are elevated in depression. Platelet-activating factors (PAFs) are emerging as key lipid mediators that may be central to those processes and highly relevant to cognitive decline in CAD.
This cross-sectional study investigated relationships between various PAFs and cognitive performance in 24 patients with CAD (age, 60.3 ± 9.4; 70.8% male). Analyses were repeated in a subgroup of 15 patients with CAD with major depression (DSM-IV). Cognitive performance was assessed using a standardized battery and summary z scores were calculated based on age, sex, and education norms. Global cognitive performance was the average of domain-specific z scores. Plasma PAF analyses were performed using electrospray ionization mass spectrometry (precursor ion scan).
A greater abundance of PAF PC(O-18:0/2:0) was associated with poorer global cognitive performance in patients with CAD (r = -0.45, P = 0.03). In the major depressed subgroup, PAF PC(O-18:0/2:0) (r = -0.59, P = 0.02) as well as PC(O-16:0/2:0) (r = -0.52, P = 0.04), and lyso-PAF PC(O-16:0/0:0) (r = -0.53, P = 0.04) were associated with poorer global cognitive performance. A greater abundance of PAF PC(O-19:5/2:0) was associated with better global cognitive performance (r = 0.55, P = 0.03), suggesting a possible compensatory species.
This study suggests that certain PAFs might be associated with global cognitive performance in patients with CAD, with stronger relationships observed in those with major depression. Confirmation of these preliminary findings is warranted.
Journal of Neuroinflammation 07/2014; 11(1):119. DOI:10.1186/1742-2094-11-119 · 5.41 Impact Factor
"Atherosclerosis plays a major role in the development of both coronary artery disease and dementia. In the Cardiovascular Health Study cohort, the incidence of dementia was higher in those with prevalent coronary artery disease,28 and several studies have confirmed that coronary artery disease is associated with cognitive impairment,29–31 reduced hippocampal volume,32 dementia due to platelet hyperactivity,33 and increased senile plaque formation in cortical areas of the brain.34 A recent study by Graban and colleagues showed that coronary artery disease was observed more frequently in VaD patients.35 "
[Show abstract][Hide abstract] ABSTRACT: As life expectancy lengthens, dementia is becoming a significant human condition in terms of its prevalence and cost to society worldwide. It is important in that context to understand the preventable and treatable causes of dementia. This article exposes the link between dementia and heart disease in all its forms, including coronary artery disease, myocardial infarction, atrial fibrillation, valvular disease, and heart failure. This article also explores the cardiovascular risk factors and emphasizes that several of them are preventable and treatable. In addition to medical therapies, the lifestyle changes that may be useful in retarding the onset of dementia are also summarized.
"Another important confounder to consider in the relationship between cognitive impairment and mortality is psychological depression. It is imperative to consider the effects of depression due to the purported microvasculature changes that in turn affect cognitive functioning  . Moreover, consistent findings show that depression increases "
[Show abstract][Hide abstract] ABSTRACT: Background:
The additive effects of cognitive impairment and depression on mortality risk after cardiac surgery are unknown.
Patients were assessed on a battery of six neurocognitive measures before cardiac surgery (N = 521) and at six month follow up (N = 377/521, 72.4%). Cognitive impairment classification was based on cognitive test scores 1 SD below age and sex matched normative data, and classified according to amnestic, non-amnestic and mixed cognitive impairment subtypes. Survival analyses entered cognitive impairment subtypes and depression interactions terms adjusted for 12 common risk factors.
There were 5407 person years for analysis (median 11.1 year survival, interquartile range of 7.9 to 13.1) and 176 deaths (33.8%) by the census date. Before cardiac surgery, patients with a mixed-cognitive impairment (adjusted hazard ratio (HR) = 2.53; 95% confidence interval (CI), 1.57-4.06, p<.001) and non-amnestic cognitive impairment (adjusted HR = 1.51; 95%, 1.00-2.32, p = .05) were at greater mortality risk. Six month analyses corroborated that the mixed-cognitive impairment group were at higher mortality risk (adjusted HR = 2.35; 95% CI, 1.30-4.25, p = .005). When change in neurocognitive functioning over time was analyzed, a higher mortality risk was evident only amongst patients with cognitive impairment evident at baseline and six months (adjusted HR = 1.83; 95% CI, 1.08-3.10, p = .03). No cognition by depression interaction term was significant.
These data suggest that a mixed cognitive impairment subtype, and continuing cognitive impairment before and six months after cardiac surgery, is associated with long term mortality, independent of depression and common risk factors.
International journal of cardiology 04/2013; 168(3). DOI:10.1016/j.ijcard.2013.03.123 · 4.04 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.