The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform
Samuel J. Mann - One of the best experts on this subject based on the ideXlab platform.
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Abstract P108: The Cause and Treatment of Paroxysmal Hypertension
Hypertension, 2020Co-Authors: Samuel J. Mann, Kaushal SolankiAbstract:Introduction: The cause and treatment of Paroxysmal Hypertension (PH) (“pseudopheochromocytoma”) in the 98-99% of patients who do not have a pheochromocytoma has long been a mystery. It has been li...
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Labile and Paroxysmal Hypertension: Common Clinical Dilemmas in Need of Treatment Studies
Current Cardiology Reports, 2015Co-Authors: Samuel J. MannAbstract:Although “labile Hypertension” is regularly encountered by clinicians, there is a paucity of information available to guide therapeutic decisions. This review discusses its clinical relevance, the limitations of current knowledge, and possible directions for future research and clinical management. Results of studies that assessed measures of blood pressure variability or reactivity are reviewed. The limited information about effects of antihypertensive drugs on blood pressure variability is discussed. Two different clinical presentations are differentiated: labile Hypertension and Paroxysmal Hypertension . Labile Hypertension remains a clinical impression without defined criteria or treatment guidance. Paroxysmal Hypertension, also called pseudopheochromocytoma, presents as dramatic episodes of abrupt and severe blood pressure elevation. The disorder can be disabling. Although it regularly raises suspicion of a pheochromocytoma, such a tumor is found in
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labile and Paroxysmal Hypertension common clinical dilemmas in need of treatment studies
Current Cardiology Reports, 2015Co-Authors: Samuel J. MannAbstract:Although “labile Hypertension” is regularly encountered by clinicians, there is a paucity of information available to guide therapeutic decisions. This review discusses its clinical relevance, the limitations of current knowledge, and possible directions for future research and clinical management. Results of studies that assessed measures of blood pressure variability or reactivity are reviewed. The limited information about effects of antihypertensive drugs on blood pressure variability is discussed. Two different clinical presentations are differentiated: labile Hypertension and Paroxysmal Hypertension. Labile Hypertension remains a clinical impression without defined criteria or treatment guidance. Paroxysmal Hypertension, also called pseudopheochromocytoma, presents as dramatic episodes of abrupt and severe blood pressure elevation. The disorder can be disabling. Although it regularly raises suspicion of a pheochromocytoma, such a tumor is found in <2 % of patients. The cause, which involves both emotional factors and the sympathetic nervous system, and treatment approaches, are presented.
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Severe Paroxysmal Hypertension (pseudopheochromocytoma).
Current hypertension reports, 2008Co-Authors: Samuel J. MannAbstract:Paroxysmal Hypertension always engenders a search for a catecholamine-secreting pheochromocytoma, Yet
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severe Paroxysmal Hypertension pseudopheochromocytoma
Current Hypertension Reports, 2008Co-Authors: Samuel J. MannAbstract:Paroxysmal Hypertension always engenders a search for a catecholamine-secreting pheochromocytoma, Yet <2% turn out to have this tumor, and its cause and management have remained a mystery, and the subject of remarkably few papers. This review presents an approach to understanding and treating this disorder, which is increasingly known as “pseudopheochromocytoma.” Patients experience symptomatic blood pressure surges likely linked to stimulation of the sympathetic nervous system. Psychological characteristics of patients with this disorder suggest a psychological basis, attributable to repressed emotion related either to prior emotional trauma or to a repressive (non-emotional) coping style. Interventions based on this understanding appear helpful in most cases. Paroxysms can be treated with an anxiolytic (e.g. alprazolam) and/or oral clonidine; an anxiolytic plus intravenous labetalol are usually effective in severe paroxysms. For preventive therapy, antidepressant agents appear effective in most patients. Although the role of psychotherapy is unclear, reassurance that an acute cardiovascular event is unlikely to occur during a paroxysm can be helpful. Fortunately, with appropriately selected intervention, attacks can be reduced or eliminated in most patients.
Karel Pacak - One of the best experts on this subject based on the ideXlab platform.
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Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma
Annals of the New York Academy of Sciences, 2008Co-Authors: Graeme Eisenhofer, Yehonatan Sharabi, Karel PacakAbstract:Among overall numbers of patients tested for pheochromocytoma, less than 2% harbor the tumor. Among the rest, there is often no satisfactory explanation for the signs and symptoms leading to suspicion of pheochromocytoma. This group includes patients with severe symptomatic Paroxysmal Hypertension, often referred to as pseudopheochromocytoma, a condition that can be debilitating for patients and perplexing for clinicians. Similar to patients with the real tumor, patients with pseudopheochromocytoma can be misdiagnosed with panic disorder. However, pseudopheochromocytoma is characterized by an absence of panic or emotional distress preceding the onset of Hypertension and symptoms of catecholamine excess. Because the clinical manifestations of pseudopheochromocytoma are similar, if not identical, to those due to excess circulating catecholamines in patients with the tumor, the most attractive explanation for the disorder is that it involves altered function of the autonomic nervous system. In line with this hypothesis, recent findings suggest that enhanced adrenal release of epinephrine and exaggerated cardiovascular responsiveness to catecholamines both contribute to the Paroxysmal Hypertension and symptoms of catecholamine excess in pseudopheochromocytoma. From this pattern, one would predict that therapeutic interventions that inhibit adrenal secretion of epinephrine or block adrenoceptor-mediated responses to catecholamines might provide a logical approach to therapy.
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Sympathoadrenal function in patients with Paroxysmal Hypertension: pseudopheochromocytoma.
Journal of hypertension, 2007Co-Authors: Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Karel Pacak, Graeme EisenhoferAbstract:ObjectivesThe causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded (‘pseudopheochromocytoma’) usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal m
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Sympathoadrenal function in patients with Paroxysmal Hypertension : pseudopheochromocytoma. Commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P
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sympathoadrenal function in patients with Paroxysmal Hypertension pseudopheochromocytoma commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P<0.05) baseline plasma concentrations of epinephrine, 80% higher (P<0.01) baseline plasma concentrations of metanephrine, and sixfold larger (P<0.05) increases in plasma epinephrine after glucagon. Adrenal 18 F-fluorodopamine-derived radioactivity did not differ between groups. Compared with changes in plasma norepinephrine, falls in blood pressure after trimethaphan were 13-fold larger (P<0.005) and increases in blood pressure after yohimbine were threefold larger (P<0.01) in pseudopheochromocytoma patients than in controls. Conclusion Patients with pseudopheochromocytoma exhibit a pattern of normal sympathetic noradrenergic outflow, adrenomedullary activation, and augmented blood pressure responses to changes in the sympathoneural release of norepinephrine.
Yehonatan Sharabi - One of the best experts on this subject based on the ideXlab platform.
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Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma
Annals of the New York Academy of Sciences, 2008Co-Authors: Graeme Eisenhofer, Yehonatan Sharabi, Karel PacakAbstract:Among overall numbers of patients tested for pheochromocytoma, less than 2% harbor the tumor. Among the rest, there is often no satisfactory explanation for the signs and symptoms leading to suspicion of pheochromocytoma. This group includes patients with severe symptomatic Paroxysmal Hypertension, often referred to as pseudopheochromocytoma, a condition that can be debilitating for patients and perplexing for clinicians. Similar to patients with the real tumor, patients with pseudopheochromocytoma can be misdiagnosed with panic disorder. However, pseudopheochromocytoma is characterized by an absence of panic or emotional distress preceding the onset of Hypertension and symptoms of catecholamine excess. Because the clinical manifestations of pseudopheochromocytoma are similar, if not identical, to those due to excess circulating catecholamines in patients with the tumor, the most attractive explanation for the disorder is that it involves altered function of the autonomic nervous system. In line with this hypothesis, recent findings suggest that enhanced adrenal release of epinephrine and exaggerated cardiovascular responsiveness to catecholamines both contribute to the Paroxysmal Hypertension and symptoms of catecholamine excess in pseudopheochromocytoma. From this pattern, one would predict that therapeutic interventions that inhibit adrenal secretion of epinephrine or block adrenoceptor-mediated responses to catecholamines might provide a logical approach to therapy.
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Sympathoadrenal function in patients with Paroxysmal Hypertension: pseudopheochromocytoma.
Journal of hypertension, 2007Co-Authors: Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Karel Pacak, Graeme EisenhoferAbstract:ObjectivesThe causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded (‘pseudopheochromocytoma’) usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal m
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Sympathoadrenal function in patients with Paroxysmal Hypertension : pseudopheochromocytoma. Commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P
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sympathoadrenal function in patients with Paroxysmal Hypertension pseudopheochromocytoma commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P<0.05) baseline plasma concentrations of epinephrine, 80% higher (P<0.01) baseline plasma concentrations of metanephrine, and sixfold larger (P<0.05) increases in plasma epinephrine after glucagon. Adrenal 18 F-fluorodopamine-derived radioactivity did not differ between groups. Compared with changes in plasma norepinephrine, falls in blood pressure after trimethaphan were 13-fold larger (P<0.005) and increases in blood pressure after yohimbine were threefold larger (P<0.01) in pseudopheochromocytoma patients than in controls. Conclusion Patients with pseudopheochromocytoma exhibit a pattern of normal sympathetic noradrenergic outflow, adrenomedullary activation, and augmented blood pressure responses to changes in the sympathoneural release of norepinephrine.
Christopher J. Mathias - One of the best experts on this subject based on the ideXlab platform.
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Orthostatic hypotension and Paroxysmal Hypertension in humans with high spinal cord injury.
Progress in brain research, 2006Co-Authors: Christopher J. MathiasAbstract:The spinal cord is essential for normal autonomic nervous system regulation of the cardiovascular system as the preganglionic neurons controlling the heart and blood vessels originate in the thoracolumbar spinal segments. The site and extent of a spinal cord injury determine the degree of autonomic involvement in cardiovascular dysfunction after the injury. After complete cervical cord lesions the entire sympathetic outflow is separated from cerebral control; this may cause orthostatic hypotension. Commonly after traumatic injuries to the spinal cord, one or more segments are totally destroyed. However, the distal portion of the spinal cord often retains function and activation of spinal cord reflexes working independently of the brain can result in Paroxysmal Hypertension. This chapter will focus on orthostatic hypotension and Paroxysmal Hypertension in cord-injured people with lesions affecting the cervical and upper thoracic spinal cord. Conditions promoting these abnormalities in blood pressure will be elaborated. Possible mechanisms for the hypo- and Hypertension will be discussed, as will strategies for managing these problems.
Marilla Geraci - One of the best experts on this subject based on the ideXlab platform.
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Sympathoadrenal function in patients with Paroxysmal Hypertension: pseudopheochromocytoma.
Journal of hypertension, 2007Co-Authors: Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Karel Pacak, Graeme EisenhoferAbstract:ObjectivesThe causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded (‘pseudopheochromocytoma’) usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal m
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Sympathoadrenal function in patients with Paroxysmal Hypertension : pseudopheochromocytoma. Commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P
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sympathoadrenal function in patients with Paroxysmal Hypertension pseudopheochromocytoma commentary
Journal of Hypertension, 2007Co-Authors: Isla S. Mackenzie, Yehonatan Sharabi, David S. Goldstein, Oladi Bentho, Ahmed Saleem, Sandra Pechnik, Marilla Geraci, Courtney Holmes, Morris J. Brown, Karel PacakAbstract:Objectives The causes of Paroxysmal Hypertension in patients in whom pheochromocytoma has been excluded ('pseudopheochromocytoma') usually remain unclear. Blood pressure disturbances and symptoms of catecholamine excess in these patients may reflect activation of the sympathetic nervous and adrenal medullary systems. We therefore examined sympathoadrenal function in patients with pseudopheochromocytoma compared with age-matched control subjects in whom there was no suspicion of pheochromocytoma. Methods Plasma catecholamines and hemodynamics were examined in response to intravenous glucagon, yohimbine, and trimethaphan in 11 patients with pseudopheochromocytoma and a comparison group of nine normotensive and five hypertensive volunteers. Adrenomedullary function was also assessed by abdominal 18 F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, the O-methylated metabolite of epinephrine. Results Compared with controls, patients with pseudopheochromocytoma had normal plasma concentrations of norepinephrine, but 120% higher (P<0.05) baseline plasma concentrations of epinephrine, 80% higher (P<0.01) baseline plasma concentrations of metanephrine, and sixfold larger (P<0.05) increases in plasma epinephrine after glucagon. Adrenal 18 F-fluorodopamine-derived radioactivity did not differ between groups. Compared with changes in plasma norepinephrine, falls in blood pressure after trimethaphan were 13-fold larger (P<0.005) and increases in blood pressure after yohimbine were threefold larger (P<0.01) in pseudopheochromocytoma patients than in controls. Conclusion Patients with pseudopheochromocytoma exhibit a pattern of normal sympathetic noradrenergic outflow, adrenomedullary activation, and augmented blood pressure responses to changes in the sympathoneural release of norepinephrine.