Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated pl...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kim, Dan A. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014transfer abstract |
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| Umfang: |
6 |
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| Übergeordnetes Werk: |
Enthalten in: PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems - Zhang, Meng ELSEVIER, 2017, official journal of the American College of Cardiology, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:114 ; year:2014 ; number:2 ; day:15 ; month:07 ; pages:181-186 ; extent:6 |
| Links: |
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| DOI / URN: |
10.1016/j.amjcard.2014.04.023 |
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| 520 | |a Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. | ||
| 520 | |a Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. | ||
| 700 | 1 | |a McClure, Willie G. |4 oth | |
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| 700 | 1 | |a Vaidya, Dhananjay |4 oth | |
| 700 | 1 | |a Williams, Marlene S. |4 oth | |
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10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
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10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
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10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
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10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
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10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
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Enthalten in PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems Amsterdam [u.a.] volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 |
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In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. 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platelet response to serotonin in patients with stable coronary heart disease |
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Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
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Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
| abstractGer |
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
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Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
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