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The mechanisms by which antidepressants may reduce coronary heart disease risk.

Mathews MJ, Mathews EH, Liebenberg L - BMC Cardiovasc Disord (2015)

Bottom Line: Using biomarker relative risk data the pathogenetic effects are representable as measurable effects based on changes in biomarkers.The use of selective serotonin reuptake inhibitors (SSRIs) is postulated to have potential to decrease CHD risk.These effects might be mediated with the use of SSRI's.

View Article: PubMed Central - PubMed

Affiliation: CRCED Pretoria, North-West University, P.O. Box 11207, Silver Lakes, 0054, South Africa. mjmathews@rems2.com.

ABSTRACT

Background: Depression is known to increase the risk for coronary heart disease (CHD) likely through various pathogenetic actions. Understanding the links between depression and CHD and the effects of mediating these links may prove beneficial in CHD prevention.

Methods: An integrated model of CHD was used to elucidate pathogenetic pathways of importance between depression and CHD. Using biomarker relative risk data the pathogenetic effects are representable as measurable effects based on changes in biomarkers.

Results: A 'connection graph' presents interactions by illustrating the relationship between depression and the biomarkers of CHD. The use of selective serotonin reuptake inhibitors (SSRIs) is postulated to have potential to decrease CHD risk. Comparing the 'connection graph' of SSRI's to that of depression elucidates the possible actions through which risk reduction may occur.

Conclusions: The CHD effects of depression appear to be driven by increased inflammation and altered metabolism. These effects might be mediated with the use of SSRI's.

No MeSH data available.


Related in: MedlinePlus

Conceptual model of general health factors, salient CHD pathogenetic pathways and CHD hallmarks. Note. From “How do high glycemic load diets influence coronary heart disease?” by Mathews M, Liebenberg L, Mathews EH Nutr Metab 2015;12:6 [9]. The affective pathway of pharmacotherapeutics, boxes, is shown in Fig. 1, and salient serological biomarkers are indicated by tags (). The blunted arrows denote antagonize or inhibit and pointed arrows denote up-regulate or facilitate. ACE denotes angiotensin-converting-enzyme; BDNF, brain-derived neurotrophic factor; β-blocker, beta-adrenergic antagonists; BNP, B-type natriuretic peptide; COX, cyclooxygenase; CRP, C-reactive protein; D-dimer, fibrin degradation product D; FFA, free fatty acids; GCF, gingival crevicular fluid; HDL, high-density lipoprotein; HbA1c, glycated hemoglobin A1c; Hs, homocysteine; ICAM, intracellular adhesion molecule; IGF-1, insulin-like growth factor-1; IL, interleukin; LDL, low-density lipoprotein; MAPK, mitogen-activated protein (MAP) kinase; MCP, monocyte chemoattractant protein; MIF, macrophage migration inhibitory factor; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NFκβ, nuclear factor-κβ; NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; OPG, osteoprotegerin; oxLDL, oxidized LDL; P. gingivalis, Porphyromonas gingivalis; PAI, plasminogen activator inhibitor; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; ROS, reactive oxygen species; SCD-40, recombinant human sCD40 ligand; SMC, smooth muscle cell; SSRI, serotonin reuptake inhibitors; TF, tissue factor; TMAO, an oxidation product of trimethylamine (TMA); TNF-α , tumor necrosis factor-α; vWF, von Willebrand factor; VCAM, vascular cell adhesion molecule
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Fig1: Conceptual model of general health factors, salient CHD pathogenetic pathways and CHD hallmarks. Note. From “How do high glycemic load diets influence coronary heart disease?” by Mathews M, Liebenberg L, Mathews EH Nutr Metab 2015;12:6 [9]. The affective pathway of pharmacotherapeutics, boxes, is shown in Fig. 1, and salient serological biomarkers are indicated by tags (). The blunted arrows denote antagonize or inhibit and pointed arrows denote up-regulate or facilitate. ACE denotes angiotensin-converting-enzyme; BDNF, brain-derived neurotrophic factor; β-blocker, beta-adrenergic antagonists; BNP, B-type natriuretic peptide; COX, cyclooxygenase; CRP, C-reactive protein; D-dimer, fibrin degradation product D; FFA, free fatty acids; GCF, gingival crevicular fluid; HDL, high-density lipoprotein; HbA1c, glycated hemoglobin A1c; Hs, homocysteine; ICAM, intracellular adhesion molecule; IGF-1, insulin-like growth factor-1; IL, interleukin; LDL, low-density lipoprotein; MAPK, mitogen-activated protein (MAP) kinase; MCP, monocyte chemoattractant protein; MIF, macrophage migration inhibitory factor; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NFκβ, nuclear factor-κβ; NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; OPG, osteoprotegerin; oxLDL, oxidized LDL; P. gingivalis, Porphyromonas gingivalis; PAI, plasminogen activator inhibitor; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; ROS, reactive oxygen species; SCD-40, recombinant human sCD40 ligand; SMC, smooth muscle cell; SSRI, serotonin reuptake inhibitors; TF, tissue factor; TMAO, an oxidation product of trimethylamine (TMA); TNF-α , tumor necrosis factor-α; vWF, von Willebrand factor; VCAM, vascular cell adhesion molecule

Mentions: The integrated model in Fig. 1 schematically illustrates the complexity of CHD and shows all theoretical pathogenetic pathways between the health factors and CHD. The health factors that are described by the integrated model include both modifiable lifestyle effects and underlying comorbid disorders such as depression. A more detailed discussion of Fig. 1, relevant to depression, is given in next section.Fig. 1


The mechanisms by which antidepressants may reduce coronary heart disease risk.

Mathews MJ, Mathews EH, Liebenberg L - BMC Cardiovasc Disord (2015)

Conceptual model of general health factors, salient CHD pathogenetic pathways and CHD hallmarks. Note. From “How do high glycemic load diets influence coronary heart disease?” by Mathews M, Liebenberg L, Mathews EH Nutr Metab 2015;12:6 [9]. The affective pathway of pharmacotherapeutics, boxes, is shown in Fig. 1, and salient serological biomarkers are indicated by tags (). The blunted arrows denote antagonize or inhibit and pointed arrows denote up-regulate or facilitate. ACE denotes angiotensin-converting-enzyme; BDNF, brain-derived neurotrophic factor; β-blocker, beta-adrenergic antagonists; BNP, B-type natriuretic peptide; COX, cyclooxygenase; CRP, C-reactive protein; D-dimer, fibrin degradation product D; FFA, free fatty acids; GCF, gingival crevicular fluid; HDL, high-density lipoprotein; HbA1c, glycated hemoglobin A1c; Hs, homocysteine; ICAM, intracellular adhesion molecule; IGF-1, insulin-like growth factor-1; IL, interleukin; LDL, low-density lipoprotein; MAPK, mitogen-activated protein (MAP) kinase; MCP, monocyte chemoattractant protein; MIF, macrophage migration inhibitory factor; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NFκβ, nuclear factor-κβ; NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; OPG, osteoprotegerin; oxLDL, oxidized LDL; P. gingivalis, Porphyromonas gingivalis; PAI, plasminogen activator inhibitor; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; ROS, reactive oxygen species; SCD-40, recombinant human sCD40 ligand; SMC, smooth muscle cell; SSRI, serotonin reuptake inhibitors; TF, tissue factor; TMAO, an oxidation product of trimethylamine (TMA); TNF-α , tumor necrosis factor-α; vWF, von Willebrand factor; VCAM, vascular cell adhesion molecule
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4522054&req=5

Fig1: Conceptual model of general health factors, salient CHD pathogenetic pathways and CHD hallmarks. Note. From “How do high glycemic load diets influence coronary heart disease?” by Mathews M, Liebenberg L, Mathews EH Nutr Metab 2015;12:6 [9]. The affective pathway of pharmacotherapeutics, boxes, is shown in Fig. 1, and salient serological biomarkers are indicated by tags (). The blunted arrows denote antagonize or inhibit and pointed arrows denote up-regulate or facilitate. ACE denotes angiotensin-converting-enzyme; BDNF, brain-derived neurotrophic factor; β-blocker, beta-adrenergic antagonists; BNP, B-type natriuretic peptide; COX, cyclooxygenase; CRP, C-reactive protein; D-dimer, fibrin degradation product D; FFA, free fatty acids; GCF, gingival crevicular fluid; HDL, high-density lipoprotein; HbA1c, glycated hemoglobin A1c; Hs, homocysteine; ICAM, intracellular adhesion molecule; IGF-1, insulin-like growth factor-1; IL, interleukin; LDL, low-density lipoprotein; MAPK, mitogen-activated protein (MAP) kinase; MCP, monocyte chemoattractant protein; MIF, macrophage migration inhibitory factor; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NFκβ, nuclear factor-κβ; NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; OPG, osteoprotegerin; oxLDL, oxidized LDL; P. gingivalis, Porphyromonas gingivalis; PAI, plasminogen activator inhibitor; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; ROS, reactive oxygen species; SCD-40, recombinant human sCD40 ligand; SMC, smooth muscle cell; SSRI, serotonin reuptake inhibitors; TF, tissue factor; TMAO, an oxidation product of trimethylamine (TMA); TNF-α , tumor necrosis factor-α; vWF, von Willebrand factor; VCAM, vascular cell adhesion molecule
Mentions: The integrated model in Fig. 1 schematically illustrates the complexity of CHD and shows all theoretical pathogenetic pathways between the health factors and CHD. The health factors that are described by the integrated model include both modifiable lifestyle effects and underlying comorbid disorders such as depression. A more detailed discussion of Fig. 1, relevant to depression, is given in next section.Fig. 1

Bottom Line: Using biomarker relative risk data the pathogenetic effects are representable as measurable effects based on changes in biomarkers.The use of selective serotonin reuptake inhibitors (SSRIs) is postulated to have potential to decrease CHD risk.These effects might be mediated with the use of SSRI's.

View Article: PubMed Central - PubMed

Affiliation: CRCED Pretoria, North-West University, P.O. Box 11207, Silver Lakes, 0054, South Africa. mjmathews@rems2.com.

ABSTRACT

Background: Depression is known to increase the risk for coronary heart disease (CHD) likely through various pathogenetic actions. Understanding the links between depression and CHD and the effects of mediating these links may prove beneficial in CHD prevention.

Methods: An integrated model of CHD was used to elucidate pathogenetic pathways of importance between depression and CHD. Using biomarker relative risk data the pathogenetic effects are representable as measurable effects based on changes in biomarkers.

Results: A 'connection graph' presents interactions by illustrating the relationship between depression and the biomarkers of CHD. The use of selective serotonin reuptake inhibitors (SSRIs) is postulated to have potential to decrease CHD risk. Comparing the 'connection graph' of SSRI's to that of depression elucidates the possible actions through which risk reduction may occur.

Conclusions: The CHD effects of depression appear to be driven by increased inflammation and altered metabolism. These effects might be mediated with the use of SSRI's.

No MeSH data available.


Related in: MedlinePlus