Increased Coronary Events in Depressed Cardiovascular Patients: 5-HT2A Receptor as Missing Link?

Schins, Annique; Honig, Adriaan; Crijns, H.J.G.M.; Baur, L.H.B.; Hamulyák, Karly

doi:10.1097/01.psy.0000088596.42029.10

Cited by 84 publications

(60 citation statements)

References 93 publications

(97 reference statements)

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“…Furthermore, even subclinical levels of depression severity are associated with changes in sympathetic and parasympathetic nervous system activity and alterations in platelet responsiveness (32)(33)(34), providing support for plausible biological pathways.…”

Section: Discussionmentioning

confidence: 99%

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

et al. 2009

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Abstract. Cardiovascular disease (CVD) and depression are two of the most common human health problems. Patients with depression have an increased risk of developing cardiovascular disease and mortality after experiencing a cardiac event. Both diseases are complex disorders that are influenced by genetic and environmental factors. Brain-derived neurotrophic factor (BDNF) plays a critical role in regulating both vascular development and response to injury, and promotes survival, differentiation, and maintenance of neurons in the peripheral and nervous system. Evidence suggests that BDNF can enhance serotoninergic transmission. Serotonin modulates different brain functions and is known to regulate sleep, appetite, pain and inflammation. The aims of the present casecontrol study were to investigate the possible role of BDNF Val66Met, 5-HTTLPR and -1438 G/A polymorphisms in the development of coronary artery disease (CAD) in patients with and without depression. Regarding BDNF, our data suggest an involvement of the AA genotype in the pathogenesis of CAD in females and in the predisposition to CAD associated with depression. Furthermore, it could be argued that the GG genotype is protective against CAD in the female population and against CAD associated with depression. In our CAD population we also observed a significant increase in the L/L genotype and a decrease in the S/L genotype with respect to the controls. A higher frequency of the L allele, responsible for enhancing the efficiency of transcription, was found in CAD patients. These findings may be responsible for the increased capacity of platelet serotonin uptake previously observed in patients with CAD. Although no differences were found for genotype and allelic frequencies of the -1438 G/A polymorphism between the CAD patients and controls, we cannot exclude the possible role of this receptor in coronary artery disease.

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Section: Discussionmentioning

confidence: 99%

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

et al. 2009

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“…These effects may be associated with increased platelet reactivity observed in subjects with MDD (106-108), as well as activation of inflammatory pathways in the disease (109). The association between depressive symptoms and increased platelet activity (106,110) involves the metabolism of catecholamines in platelets (106,108,111). Similarly, CVD has also been associated with increased platelet reactivity (112), inflammation and endothelial dysfunction (105), thus supporting a potential common etiological role for immuneinflammatory dysfunction in MDD and CVD.…”

Section: Increased Mao-a Activity As a Factor Linking Depression Withmentioning

confidence: 99%

Abnormal function of monoamine oxidase-A in comorbid major depressive disorder and cardiovascular disease: Pathophysiological and therapeutic implications (Review)

Machado‐Vieira

Mallinger

2012

Mol Med Report

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Abstract. The association between major depressive disorder (MDD) and cardiovascular disease (CVD) is among the best described medical comorbidities. The presence of MDD increases the risk of cardiac admissions and mortality and increases healthcare costs in patients with CVD, and similarly, CVD affects the course and outcome of MDD. The potential shared biological mechanisms involved in these comorbid conditions are not well known. However, the enzyme monoamine oxidase-A (MAO-A), which has a key role in the degradation of catecholamines, has been associated with the pathophysiology and therapeutics of both MDD and CVD. Increased MAO-A activity results in the dysregulation of downstream targets of this enzyme and thus affects the pathophysiology of the two diseases. These deleterious effects include altered noradrenaline turnover, with a direct elevation in oxidative stress parameters, as well as increased platelet activity and cytokine levels. These effects were shown to be reversed by MAO inhibitors. Here, a model describing a key role for the MAO-A in comorbid MDD and CVD is proposed, with focus on the shared pathophysiological mechanisms and the potential therapeutic relevance of agents targeting this enzyme.

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“…e monoamine theory of depression may help to account for certain comorbidities seen with depression; for example, common pathophysiology involving the serotonergic system may explain the link with migraine headaches [69] and cardiovascular disease [70][71][72]. Furthermore, many of the nutritional risk factors for depression appear to involve monoamines; deciencies in nutrients such as folate, vitamin B12, zinc, iron, vitamin B6, omega-3 polyunsaturated fatty acids, vitamin C and carbohydrates may contribute to depressive disorders through Roy & Campbell.…”

Section: E Monoamine Eory Of Depressionmentioning

confidence: 99%

A unifying framework for depression: Bridging the major biological and psychosocial theories through stress

Roy¹,

Campbell²

2013

CIM

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A unifying framework for depression: Bridging the major biological and psychosocial theories through stress AbstractSeveral mechanisms for the development of depression have been proposed, and a comparative examination reveals considerable overlap. is paper begins by summarizing the conclusions drawn in the literature on the major biological theories: HPA-axis hyperactivity, the monoamine theory, the cytokine hypothesis/ macrophage theory, and structural changes to relevant brain regions and neurons. It then discusses the role of psychosocial stress as a bridge between the pathophysiology of depression and its predominantly psychosocial risk factors, touching upon theories o ered in psychology and in population health. is paper further proposes a unifying framework which integrates the major theories. e multiple systems involved, and the directional complexity among them, likely help to explain the wide-ranging symptoms associated with depression, and the wide variety of comorbid medical conditions. ey may also contribute to challenges in treatment, the diversity in symptoms and treatment outcomes among individuals, and the high rates of symptom persistence and relapse. e apparent bi-directionality of associations may suggest the existence of positive-feedback loops which aggravate symptoms; however, further bench research is required to con rm such phenomena. A better understanding of these interweaving associations is warranted. Additionally, given the signi cant in uence of socioeconomic and psychosocial factors on the aetiology of depression, population-level interventions that address the social determinants of health are required. Current individual-level pharmacologic approaches are designed to treat pathophysiology once it is underway, and current individual-level non-pharmacologic interventions (such as talk therapy) are designed to moderate the relationship between psychosocial stress and pathophysiology. In contrast, a key strategy for primary prevention lies in population-level interventions that address the predominantly social causes of one of depression's most notable risk factors: chronic psychosocial stress.

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Increased Coronary Events in Depressed Cardiovascular Patients: 5-HT2A Receptor as Missing Link?

Cited by 84 publications

References 93 publications

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

Abnormal function of monoamine oxidase-A in comorbid major depressive disorder and cardiovascular disease: Pathophysiological and therapeutic implications (Review)

A unifying framework for depression: Bridging the major biological and psychosocial theories through stress

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