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Borderline Hypertension

The Experts below are selected from a list of 150 Experts worldwide ranked by ideXlab platform

Ulf De Faire – 1st expert on this subject based on the ideXlab platform

  • Antibodies to Endothelial Cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and

  • antibodies to endothelial cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and <80 mm Hg, respectively) were recruited from a population screening program. Antibody levels were determined by ELISA. Presence of carotid atherosclerosis was determined by B-mode ultrasonography, and 29 individuals had atherosclerotic plaques. BHT men had significantly higher aEC and abeta2GP1 levels of IgG class than NT control subjects (P=0.029 and P=0.0001, respectively). aEC levels of IgM class were higher in BHT (P=0.012), but not abeta2GP1 levels. There was no correlation between aCL levels and BHT. Individuals with atherosclerotic plaques had significantly higher aEC levels of both IgG (P=0.042) and IgM subclasses (P=0.018) than those without plaques, but no difference was found in aCL and abeta2GP1 levels. Endothelin and aECs of IgM class were significantly associated. CONCLUSIONS: We demonstrate the first evidence of a significant elevation of aEC and abeta2GP1 levels in Borderline Hypertension. These findings provide a new link between Hypertension and atherosclerosis and indicate that humoral immune reactions to the endothelium may play an important role in both conditions.

  • Association of Serum Antibodies to Heat-Shock Protein 65 With Borderline Hypertension
    Hypertension, 1997
    Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De Faire

    Abstract:

    Heat-shock proteins protect cells from damage but are also often the target of immune responses in inflammation and may therefore both induce and perpetuate the chronic inflammation characterizing atherosclerosis. Hypertension is a well-established risk factor for atherosclerosis, and recently, Borderline Hypertension also has been related to atherosclerosis. The present study investigated the possible role of heat-shock proteins in Borderline Hypertension and their relation to atherosclerosis by investigating antibody titers against the 65-kD heat-shock protein (HSP65). Sixty-six men with Borderline Hypertension and 67 age-matched normotensive men (diastolic pressure, 85 to 94 and

Carola Lemne – 2nd expert on this subject based on the ideXlab platform

  • antibodies to platelet activating factor are associated with Borderline Hypertension early atherosclerosis and the metabolic syndrome
    Journal of Internal Medicine, 1999
    Co-Authors: Ruihua Wu, Carola Lemne, U De Faire, Johan Frostegård

    Abstract:

    Abstract. Wu R, Lemne C, de Faire U, Frostegard J (Karolinska Hospital and Karolinska Institute, Stockholm, Sweden). Antibodies to platelet-activating factor (PAF) are associated with Borderline Hypertension, early atherosclerosis and the metabolic syndrome. J Intern Med 1999; 246: 389–397.

    Objective. Platelet-activating factor (PAF) is a phospholipid inflammatory mediator which is synthesized by a variety of cells, including monocytes and endothelial cells, and PAF can be retained in activated endothelial cell membranes. Furthermore, PAF-like lipids are produced in other phospholipid membranes as in oxidized LDL. Atherosclerosis is a chronic inflammation in the artery wall, but little is known about the role of immune reactions in the early stages of development of cardiovascular disease. In the present study we investigated if there are antibodies to PAF (aPAF) that may play a role in Borderline Hypertension and early atherosclerosis.

    Design. Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure 85–94 and <80 mmHg, respectively) were recruited from a population screening programme. Antibody levels were determined by use of ELISA. Carotid intima-media (IM)-thickness and atherosclerosis was determined by B-mode ultrasonography. Results. BHT men had 49.3% higher aPAF levels of IgG class than NT controls (P = 0.0007). Antibodies to the biologically inactive lysoPAF did not differ between BHT and NT group. aPAF levels were associated with IM-thickness in the left (P = 0.02) and right (P = 0.009) carotid artery. Furthermore, aPAF levels were enhanced in individuals with the metabolic syndrome (n = 44) as compared to those without (n = 102; P = 0.009), and also significantly associated with insulin levels (P = 0.02) and insulin resistance (P = 0.02). Conclusions. aPAF antibodies may reflect early vascular changes and thus serve as novel markers for disease, and they may also be pathogenic, by eliciting an inflammatory reaction in the vascular wall.

  • Antibodies to Endothelial Cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and

  • antibodies to endothelial cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and <80 mm Hg, respectively) were recruited from a population screening program. Antibody levels were determined by ELISA. Presence of carotid atherosclerosis was determined by B-mode ultrasonography, and 29 individuals had atherosclerotic plaques. BHT men had significantly higher aEC and abeta2GP1 levels of IgG class than NT control subjects (P=0.029 and P=0.0001, respectively). aEC levels of IgM class were higher in BHT (P=0.012), but not abeta2GP1 levels. There was no correlation between aCL levels and BHT. Individuals with atherosclerotic plaques had significantly higher aEC levels of both IgG (P=0.042) and IgM subclasses (P=0.018) than those without plaques, but no difference was found in aCL and abeta2GP1 levels. Endothelin and aECs of IgM class were significantly associated. CONCLUSIONS: We demonstrate the first evidence of a significant elevation of aEC and abeta2GP1 levels in Borderline Hypertension. These findings provide a new link between Hypertension and atherosclerosis and indicate that humoral immune reactions to the endothelium may play an important role in both conditions.

Johan Frostegård – 3rd expert on this subject based on the ideXlab platform

  • antibodies to platelet activating factor are associated with Borderline Hypertension early atherosclerosis and the metabolic syndrome
    Journal of Internal Medicine, 1999
    Co-Authors: Ruihua Wu, Carola Lemne, U De Faire, Johan Frostegård

    Abstract:

    Abstract. Wu R, Lemne C, de Faire U, Frostegard J (Karolinska Hospital and Karolinska Institute, Stockholm, Sweden). Antibodies to platelet-activating factor (PAF) are associated with Borderline Hypertension, early atherosclerosis and the metabolic syndrome. J Intern Med 1999; 246: 389–397.

    Objective. Platelet-activating factor (PAF) is a phospholipid inflammatory mediator which is synthesized by a variety of cells, including monocytes and endothelial cells, and PAF can be retained in activated endothelial cell membranes. Furthermore, PAF-like lipids are produced in other phospholipid membranes as in oxidized LDL. Atherosclerosis is a chronic inflammation in the artery wall, but little is known about the role of immune reactions in the early stages of development of cardiovascular disease. In the present study we investigated if there are antibodies to PAF (aPAF) that may play a role in Borderline Hypertension and early atherosclerosis.

    Design. Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure 85–94 and <80 mmHg, respectively) were recruited from a population screening programme. Antibody levels were determined by use of ELISA. Carotid intima-media (IM)-thickness and atherosclerosis was determined by B-mode ultrasonography. Results. BHT men had 49.3% higher aPAF levels of IgG class than NT controls (P = 0.0007). Antibodies to the biologically inactive lysoPAF did not differ between BHT and NT group. aPAF levels were associated with IM-thickness in the left (P = 0.02) and right (P = 0.009) carotid artery. Furthermore, aPAF levels were enhanced in individuals with the metabolic syndrome (n = 44) as compared to those without (n = 102; P = 0.009), and also significantly associated with insulin levels (P = 0.02) and insulin resistance (P = 0.02). Conclusions. aPAF antibodies may reflect early vascular changes and thus serve as novel markers for disease, and they may also be pathogenic, by eliciting an inflammatory reaction in the vascular wall.

  • Antibodies to Endothelial Cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and

  • antibodies to endothelial cells in Borderline Hypertension
    Circulation, 1998
    Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De Faire

    Abstract:

    BACKGROUND: Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in Borderline Hypertension. METHODS AND RESULTS: Seventy-three men with Borderline Hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and <80 mm Hg, respectively) were recruited from a population screening program. Antibody levels were determined by ELISA. Presence of carotid atherosclerosis was determined by B-mode ultrasonography, and 29 individuals had atherosclerotic plaques. BHT men had significantly higher aEC and abeta2GP1 levels of IgG class than NT control subjects (P=0.029 and P=0.0001, respectively). aEC levels of IgM class were higher in BHT (P=0.012), but not abeta2GP1 levels. There was no correlation between aCL levels and BHT. Individuals with atherosclerotic plaques had significantly higher aEC levels of both IgG (P=0.042) and IgM subclasses (P=0.018) than those without plaques, but no difference was found in aCL and abeta2GP1 levels. Endothelin and aECs of IgM class were significantly associated. CONCLUSIONS: We demonstrate the first evidence of a significant elevation of aEC and abeta2GP1 levels in Borderline Hypertension. These findings provide a new link between Hypertension and atherosclerosis and indicate that humoral immune reactions to the endothelium may play an important role in both conditions.