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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

Interconnection of relative risk effects of selective serotonin reuptake inhibitor use and serological biomarkers for CHD. ACR denotes, albumin-to-creatinine ratio; Adipon, adiponectin; ApoB, Apolipoprotein-B; BDNF, brain-derived neurotrophic factor; BNP, B-type natriuretic peptide; Cort, cortisol; CRP, C-reactive protein; Cysteine, Homocysteine; Fibrin, fibrinogen; GDF-15, growth-differentiation factor-15; HbA1c, glycated hemoglobin A1c; HDL, high-density lipoprotein; IGF-1, insulin-like growth factor-1; IL-6, interleukin-6; LDL, low-density lipoprotein; MPO, myeloperoxidase; RANKL or OPG, osteoprotegerin; TNF-α, tumor necrosis factor-α; Trigl, triglycerides; Trop, troponins
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Fig4: Interconnection of relative risk effects of selective serotonin reuptake inhibitor use and serological biomarkers for CHD. ACR denotes, albumin-to-creatinine ratio; Adipon, adiponectin; ApoB, Apolipoprotein-B; BDNF, brain-derived neurotrophic factor; BNP, B-type natriuretic peptide; Cort, cortisol; CRP, C-reactive protein; Cysteine, Homocysteine; Fibrin, fibrinogen; GDF-15, growth-differentiation factor-15; HbA1c, glycated hemoglobin A1c; HDL, high-density lipoprotein; IGF-1, insulin-like growth factor-1; IL-6, interleukin-6; LDL, low-density lipoprotein; MPO, myeloperoxidase; RANKL or OPG, osteoprotegerin; TNF-α, tumor necrosis factor-α; Trigl, triglycerides; Trop, troponins

Mentions: The serological biomarkers which are modified by use of SSRI’s are presented in Fig. 4. Figure 4 is a ‘connection graph’ presented in the same manner as was Fig. 3. The ‘connection graph’ for SSRI antidepressants elucidates known changes in serological biomarkers. The paths upon which SSRI’s may act to influence these biomarkers are indicated on the connection lines.Fig. 4


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

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

Interconnection of relative risk effects of selective serotonin reuptake inhibitor use and serological biomarkers for CHD. ACR denotes, albumin-to-creatinine ratio; Adipon, adiponectin; ApoB, Apolipoprotein-B; BDNF, brain-derived neurotrophic factor; BNP, B-type natriuretic peptide; Cort, cortisol; CRP, C-reactive protein; Cysteine, Homocysteine; Fibrin, fibrinogen; GDF-15, growth-differentiation factor-15; HbA1c, glycated hemoglobin A1c; HDL, high-density lipoprotein; IGF-1, insulin-like growth factor-1; IL-6, interleukin-6; LDL, low-density lipoprotein; MPO, myeloperoxidase; RANKL or OPG, osteoprotegerin; TNF-α, tumor necrosis factor-α; Trigl, triglycerides; Trop, troponins
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig4: Interconnection of relative risk effects of selective serotonin reuptake inhibitor use and serological biomarkers for CHD. ACR denotes, albumin-to-creatinine ratio; Adipon, adiponectin; ApoB, Apolipoprotein-B; BDNF, brain-derived neurotrophic factor; BNP, B-type natriuretic peptide; Cort, cortisol; CRP, C-reactive protein; Cysteine, Homocysteine; Fibrin, fibrinogen; GDF-15, growth-differentiation factor-15; HbA1c, glycated hemoglobin A1c; HDL, high-density lipoprotein; IGF-1, insulin-like growth factor-1; IL-6, interleukin-6; LDL, low-density lipoprotein; MPO, myeloperoxidase; RANKL or OPG, osteoprotegerin; TNF-α, tumor necrosis factor-α; Trigl, triglycerides; Trop, troponins
Mentions: The serological biomarkers which are modified by use of SSRI’s are presented in Fig. 4. Figure 4 is a ‘connection graph’ presented in the same manner as was Fig. 3. The ‘connection graph’ for SSRI antidepressants elucidates known changes in serological biomarkers. The paths upon which SSRI’s may act to influence these biomarkers are indicated on the connection lines.Fig. 4

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