The Experts below are selected from a list of 150 Experts worldwide ranked by ideXlab platform
Ulf De Faire - One of the best experts on this subject based on the ideXlab platform.
-
Antibodies to Endothelial Cells in Borderline Hypertension
Circulation, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De FaireAbstract: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, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De FaireAbstract: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, 1997Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De FaireAbstract: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
-
association of serum antibodies to heat shock protein 65 with Borderline Hypertension
Hypertension, 1997Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De FaireAbstract: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 <80 mm Hg, respectively) were recruited from a population screening program. Titers of antibodies to HSP65 were determined by enzyme-linked immunosorbent assay. The presence of carotid atherosclerosis was determined by B-mode ultrasonography. Twenty-seven individuals had atherosclerotic plaques; 48 were smokers (more than one to two cigarettes per day). Borderline hypertensive men had higher anti-HSP65 reactivity than normotensive control subjects ( P =.034). Smokers with atherosclerosis had low levels of antibodies to HSP65 compared with nonsmokers with atherosclerosis ( P =.002). Furthermore, when high-risk individuals (Borderline Hypertension plus plaque, n=15) were compared with matched low-risk individuals (normotensive with no plaque, n=15), the high-risk men had significantly enhanced antibody titers to HSP65 ( P =.041). In conclusion, we demonstrate that serum antibody titers to HSP65 are enhanced in individuals with Borderline Hypertension, which may indicate an ongoing immune reaction in the artery wall.
-
Carotid Intima-Media Thickness and Plaque in Borderline Hypertension
Stroke, 1995Co-Authors: Carola Lemne, Tomas Jogestrand, Ulf De FaireAbstract:Background and Purpose In this study, we investigated intima-media thickness and plaque occurrence in the carotid arteries of men with Borderline Hypertension compared with that in normotensive control subjects and investigated the relations of these variables to atherosclerotic risk factors. Methods Using B-mode ultrasonography, we compared carotid artery intima-media thickness and plaque occurrence in men with Borderline Hypertension (diastolic blood pressure of 85 to 94 mm Hg, n=73) with that in age-matched normotensive control subjects (diastolic blood pressure of 80 mm Hg, n=72). We evaluated the relationships of intima-media thickness and plaque occurrence to atherosclerotic risk factors such as age, smoking, lipoprotein levels, and fasting insulin levels. Results The Borderline hypertensive group exhibited a slight increase in overall intima-media thickness (0.73 versus 0.69 mm, P=.07), which was most evident in the right carotid artery (0.72 versus 0.67 mm, P
Carola Lemne - One of the best experts 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, 1999Co-Authors: Ruihua Wu, Carola Lemne, U De Faire, Johan FrostegårdAbstract: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, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De FaireAbstract: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, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De FaireAbstract: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.
-
insulin like growth factor binding protein 1 as a marker of the metabolic syndrome a study in Borderline Hypertension
Blood Pressure, 1998Co-Authors: Carola Lemne, Kerstin BrismarAbstract:Aim: To evaluate insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein-1 (IGFBP-1) in Borderline Hypertension (BHT) in relation to plasma lipoprotein and insulin levels, anthropometric variables and 24-h ambulatory blood pressure (BP). Seventy-five BHT men diastolic BP (DBP) 85-94 mmHg) and 75 age-matched normotensive controls (NT, DBP < 80 mmHg) were recruited from a population-based screening program. Results
-
Association of Serum Antibodies to Heat-Shock Protein 65 With Borderline Hypertension
Hypertension, 1997Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De FaireAbstract: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
Johan Frostegård - One of the best experts 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, 1999Co-Authors: Ruihua Wu, Carola Lemne, U De Faire, Johan FrostegårdAbstract: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, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Caroline Gillis-haegerstrand, Carola Lemne, Ulf De FaireAbstract: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, 1998Co-Authors: Johan Frostegård, Ruihua Wu, Carola Lemne, Caroline Gillishaegerstrand, Ulf De FaireAbstract: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, 1997Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De FaireAbstract: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
-
association of serum antibodies to heat shock protein 65 with Borderline Hypertension
Hypertension, 1997Co-Authors: Johan Frostegård, Carola Lemne, Birger Andersson, Rolf Kiessling, Ulf De FaireAbstract: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 <80 mm Hg, respectively) were recruited from a population screening program. Titers of antibodies to HSP65 were determined by enzyme-linked immunosorbent assay. The presence of carotid atherosclerosis was determined by B-mode ultrasonography. Twenty-seven individuals had atherosclerotic plaques; 48 were smokers (more than one to two cigarettes per day). Borderline hypertensive men had higher anti-HSP65 reactivity than normotensive control subjects ( P =.034). Smokers with atherosclerosis had low levels of antibodies to HSP65 compared with nonsmokers with atherosclerosis ( P =.002). Furthermore, when high-risk individuals (Borderline Hypertension plus plaque, n=15) were compared with matched low-risk individuals (normotensive with no plaque, n=15), the high-risk men had significantly enhanced antibody titers to HSP65 ( P =.041). In conclusion, we demonstrate that serum antibody titers to HSP65 are enhanced in individuals with Borderline Hypertension, which may indicate an ongoing immune reaction in the artery wall.
Olli T Raitakari - One of the best experts on this subject based on the ideXlab platform.
-
increased arterial intima media thickness and in vivo ldl oxidation in young men with Borderline Hypertension
Hypertension, 2000Co-Authors: Jyri O Toikka, Hanna Laine, Markku Ahotupa, Arto Haapanen, Jorma Viikari, Jaakko Hartiala, Olli T RaitakariAbstract:Abstract —We used Borderline Hypertension as a model for preHypertension to examine the early influences of elevated blood pressure on subclinical atherosclerosis, lipoprotein oxidation, and cardiac adaptation. Healthy men (age 37±4 years) were classified prospectively into 2 groups on the basis of having either Borderline Hypertension (systolic 130 to 140 mm Hg or diastolic 85 to 89 mm Hg, n=16) or normal ( P P P P P =0.10). The current study demonstrates evidence of increased subclinical atherosclerosis and ox-LDL in Borderline Hypertension. These results are consistent with the idea that enhanced ox-LDL may be one of the pathophysiological events related to development of atherosclerosis in men with Borderline elevated blood pressure.
-
early impairment of coronary flow reserve in young men with Borderline Hypertension
Journal of the American College of Cardiology, 1998Co-Authors: Hanna Laine, Jorma Viikari, Olli T Raitakari, Harri Niinikoski, Ollipekka Pitkanen, Hidehiro Iida, Pirjo Nuutila, Juhani KnuutiAbstract:Abstract Objectives. The purpose of this study was to investigate whether functional abnormalities in coronary vasomotion are present in young healthy asymptomatic men fulfilling the World Health Organization (WHO) criteria for Borderline Hypertension. Background. Previous studies have reported reduced coronary flow reserve in middle-aged subjects with sustained Hypertension and Hypertension-induced microvascular heart disease or left ventricular hypertrophy. Methods. Myocardial blood flow was measured at baseline and during dipyridamole-induced hyperemia by means of positron emission tomography and oxygen-15–labeled water in asymptomatic young men with Borderline Hypertension (group 1: n = 16, mean ± SD age 37 ± 4 years, 24-h ambulatory blood pressure 135 ± 10/81 ± 9 mm Hg) and matched healthy control subjects (group 2: n = 19, age 35 ± 3 years, 24-h ambulatory blood pressure 119 ± 8/69 ± 8 mm Hg, p Results. LV mass, dimensions and diastolic function were similar in the study groups. Baseline myocardial blood flow was similar (0.83 ± 0.21 vs. 0.80 ± 0.22 ml/g per min, group 1 vs. group 2, respectively, p = NS), and a significant increase in flow was detected after dipyridamole infusion (0.56 mg/kg body weight in 4 min intravenously) in both groups. However, the flow response to dipyridamole was significantly lower in group 1, leading to lower hyperemic flow in group 1 than in group 2 (2.85 ± 1.20 vs. 3.80 ± 1.44 ml/g per min, respectively). Consequently, the coronary flow response was lower in hypertensive than in normotensive men (3.46 ± 1.23 vs. 4.99 ± 2.5 ml/g per min, group 1 vs. group 2, respectively, p Conclusions. These results demonstrate reduced coronary reactivity present in young asymptomatic men with Borderline Hypertension and no signs of Hypertension-induced angina or left ventricular hypertrophy. Because baseline basal myocardial blood flow was unchanged, the reduction in coronary flow reserve depends on an impaired maximal vasodilator capacity.
Hanna Laine - One of the best experts on this subject based on the ideXlab platform.
-
increased arterial intima media thickness and in vivo ldl oxidation in young men with Borderline Hypertension
Hypertension, 2000Co-Authors: Jyri O Toikka, Hanna Laine, Markku Ahotupa, Arto Haapanen, Jorma Viikari, Jaakko Hartiala, Olli T RaitakariAbstract:Abstract —We used Borderline Hypertension as a model for preHypertension to examine the early influences of elevated blood pressure on subclinical atherosclerosis, lipoprotein oxidation, and cardiac adaptation. Healthy men (age 37±4 years) were classified prospectively into 2 groups on the basis of having either Borderline Hypertension (systolic 130 to 140 mm Hg or diastolic 85 to 89 mm Hg, n=16) or normal ( P P P P P =0.10). The current study demonstrates evidence of increased subclinical atherosclerosis and ox-LDL in Borderline Hypertension. These results are consistent with the idea that enhanced ox-LDL may be one of the pathophysiological events related to development of atherosclerosis in men with Borderline elevated blood pressure.
-
early impairment of coronary flow reserve in young men with Borderline Hypertension
Journal of the American College of Cardiology, 1998Co-Authors: Hanna Laine, Jorma Viikari, Olli T Raitakari, Harri Niinikoski, Ollipekka Pitkanen, Hidehiro Iida, Pirjo Nuutila, Juhani KnuutiAbstract:Abstract Objectives. The purpose of this study was to investigate whether functional abnormalities in coronary vasomotion are present in young healthy asymptomatic men fulfilling the World Health Organization (WHO) criteria for Borderline Hypertension. Background. Previous studies have reported reduced coronary flow reserve in middle-aged subjects with sustained Hypertension and Hypertension-induced microvascular heart disease or left ventricular hypertrophy. Methods. Myocardial blood flow was measured at baseline and during dipyridamole-induced hyperemia by means of positron emission tomography and oxygen-15–labeled water in asymptomatic young men with Borderline Hypertension (group 1: n = 16, mean ± SD age 37 ± 4 years, 24-h ambulatory blood pressure 135 ± 10/81 ± 9 mm Hg) and matched healthy control subjects (group 2: n = 19, age 35 ± 3 years, 24-h ambulatory blood pressure 119 ± 8/69 ± 8 mm Hg, p Results. LV mass, dimensions and diastolic function were similar in the study groups. Baseline myocardial blood flow was similar (0.83 ± 0.21 vs. 0.80 ± 0.22 ml/g per min, group 1 vs. group 2, respectively, p = NS), and a significant increase in flow was detected after dipyridamole infusion (0.56 mg/kg body weight in 4 min intravenously) in both groups. However, the flow response to dipyridamole was significantly lower in group 1, leading to lower hyperemic flow in group 1 than in group 2 (2.85 ± 1.20 vs. 3.80 ± 1.44 ml/g per min, respectively). Consequently, the coronary flow response was lower in hypertensive than in normotensive men (3.46 ± 1.23 vs. 4.99 ± 2.5 ml/g per min, group 1 vs. group 2, respectively, p Conclusions. These results demonstrate reduced coronary reactivity present in young asymptomatic men with Borderline Hypertension and no signs of Hypertension-induced angina or left ventricular hypertrophy. Because baseline basal myocardial blood flow was unchanged, the reduction in coronary flow reserve depends on an impaired maximal vasodilator capacity.
