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Anne L Coleman - One of the best experts on this subject based on the ideXlab platform.

  • association of open angle glaucoma with Perfusion Pressure status in the thessaloniki eye study
    American Journal of Ophthalmology, 2013
    Co-Authors: Fotis Topouzis, Alon Harris, Roy M Wilson, Panayiota Founti, Fei Yu, Eleftherios Anastasopoulos, Theofanis Pappas, Archimidis Koskosas, Angeliki Salonikiou, Anne L Coleman
    Abstract:

    Purpose To investigate the association of open-angle glaucoma (OAG), primary open-angle glaucoma (POAG), and pseudoexfoliative glaucoma (PEXG) with ocular Perfusion Pressure status (ocular Perfusion Pressure with or without antihypertensive treatment). Design Cross-sectional, population-based study. Methods A total of 2554 randomly selected, ≥ 60-year old subjects participated in the Thessaloniki Eye Study. Only clinic-visit participants (n = 2261), who had uniformly collected data, were included in the analyses. A logistic regression model was run for OAG in all clinic-visit participants; covariates included age, sex, diastolic ocular Perfusion Pressure, antihypertensive treatment, intraocular Pressure (IOP), IOP-lowering treatment, pseudoexfoliation, and vascular factors identified as risk factors for glaucoma in a previous analysis. Similar logistic regression models were run separately for POAG and PEXG. In addition, logistic regression models were run for OAG, POAG, and PEXG in subjects with and without antihypertensive treatment. Also, logistic regression models were run to assess the role of systolic ocular Perfusion Pressure in OAG, POAG, and PEXG. Results Among clinic-visits, 1212 subjects (53.7%) were using antihypertensive treatment. An association of borderline significance was found between low diastolic ocular Perfusion Pressure and POAG (OR = 0.84 per 10 mm Hg, 95% CI = 0.70-1.01, P  = .059). The effect of antihypertensive treatment on POAG was not statistically significant (OR = 1.20, 95% CI = 0.75-1.91, P  = .45). In subgroup analyses, diastolic ocular Perfusion Pressure was significantly associated with POAG in subjects using antihypertensive treatment (OR = 0.78 per 10 mm Hg, 95% CI = 0.62-0.97, P  = .028). No association was found between diastolic ocular Perfusion Pressure and PEXG, regardless of the use of antihypertensive treatment. No associations were found between systolic ocular Perfusion Pressure and OAG, POAG, or PEXG, regardless of the use of antihypertensive treatment. Conclusions Low diastolic ocular Perfusion Pressure may be associated with increased risk for POAG. This association was confirmed in subjects treated for systemic hypertension in subgroup analysis. This may support the hypothesis that the concept of ocular Perfusion Pressure status may be more relevant to glaucoma pathogenesis than ocular Perfusion Pressure alone.

  • blood Pressure Perfusion Pressure and glaucoma
    American Journal of Ophthalmology, 2010
    Co-Authors: Joseph Caprioli, Anne L Coleman
    Abstract:

    Purpose To provide a critical review of the relationships between blood Pressure, ocular blood flow, and glaucoma and the potential for glaucoma treatment through modulation of ocular Perfusion. Design Summaries of the pertinent literature and input from glaucoma researchers and specialists with relevant experience. Methods Review and interpretation of selected literature and the results of a 1-day group discussion involving glaucoma researchers and specialists with expertise in epidemiology, blood flow measurements, and cardiovascular physiology. Results Accurate, reproducible, and clinically relevant measurements of blood flow within the optic nerve head and associated capillary beds are not fully achievable with current methodology. Autoregulation of blood flow in the retina and optic nerve head occurs over a large range of intraocular Pressures and blood Pressures. Regulation of choroidal blood flow is provided by a mix of neurohumoral and local mechanisms. Vascular factors may be important in a subgroup of patients with primary open-angle glaucoma, and particularly in patients with normal-tension glaucoma and evidence of vasospasm. Low ocular Perfusion Pressure and low blood Pressure are associated with an increased risk of glaucoma in population-based studies. The physiologic nocturnal dip in blood Pressure is protective against systemic end-organ damage, but its effects on glaucoma are not well elaborated or understood. Large-scale longitudinal studies would be required to evaluate the risk of glaucomatous progression in non-dippers, dippers, and extreme nocturnal blood Pressure dippers. Conclusions Decreases in Perfusion Pressure and blood Pressure have been associated with glaucoma. However, there is no evidence to support the value of increasing a patient's blood Pressure as therapy for glaucoma. Such recommendations are not currently warranted, since we lack crucial information about the microvascular beds in which Perfusion is important in glaucoma, and the appropriate methods to evaluate their blood flow. There are also cardiovascular safety concerns associated with treatments designed to increase ocular Perfusion Pressure and blood flow by increasing blood Pressure, especially in elderly patients. For these reasons and with present evidence it is unlikely that safe and effective glaucoma treatments based on altering optic nerve Perfusion will soon be available.

  • Blood Pressure, Perfusion Pressure, and Glaucoma
    American Journal of Ophthalmology, 2010
    Co-Authors: Joseph Caprioli, Anne L Coleman
    Abstract:

    Purpose: To provide a critical review of the relationships between blood Pressure, ocular blood flow, and glaucoma and the potential for glaucoma treatment through modulation of ocular Perfusion. Design: Summaries of the pertinent literature and input from glaucoma researchers and specialists with relevant experience. Methods: Review and interpretation of selected literature and the results of a 1-day group discussion involving glaucoma researchers and specialists with expertise in epidemiology, blood flow measurements, and cardiovascular physiology. Results: Accurate, reproducible, and clinically relevant measurements of blood flow within the optic nerve head and associated capillary beds are not fully achievable with current methodology. Autoregulation of blood flow in the retina and optic nerve head occurs over a large range of intraocular Pressures and blood Pressures. Regulation of choroidal blood flow is provided by a mix of neurohumoral and local mechanisms. Vascular factors may be important in a subgroup of patients with primary open-angle glaucoma, and particularly in patients with normal-tension glaucoma and evidence of vasospasm. Low ocular Perfusion Pressure and low blood Pressure are associated with an increased risk of glaucoma in population-based studies. The physiologic nocturnal dip in blood Pressure is protective against systemic end-organ damage, but its effects on glaucoma are not well elaborated or understood. Large-scale longitudinal studies would be required to evaluate the risk of glaucomatous progression in non-dippers, dippers, and extreme nocturnal blood Pressure dippers. Conclusions: Decreases in Perfusion Pressure and blood Pressure have been associated with glaucoma. However, there is no evidence to support the value of increasing a patient's blood Pressure as therapy for glaucoma. Such recommendations are not currently warranted, since we lack crucial information about the microvascular beds in which Perfusion is important in glaucoma, and the appropriate methods to evaluate their blood flow. There are also cardiovascular safety concerns associated with treatments designed to increase ocular Perfusion Pressure and blood flow by increasing blood Pressure, especially in elderly patients. For these reasons and with present evidence it is unlikely that safe and effective glaucoma treatments based on altering optic nerve Perfusion will soon be available. © 2010 Elsevier Inc. All rights reserved.

Marek Czosnyka - One of the best experts on this subject based on the ideXlab platform.

  • Enhanced Visualization of Optimal Cerebral Perfusion Pressure Over Time to Support Clinical Decision Making.
    Critical care medicine, 2020
    Co-Authors: Marcel J H Aries, Joseph Donnelly, Marek Czosnyka, Robin Wesselink, Jan Willem J Elting, Ari Ercole, Natasha M Maurits, Peter Smielewski
    Abstract:

    Cerebrovascular reactivity can provide a continuously updated individualized target for management of cerebral Perfusion Pressure, termed optimal cerebral Perfusion Pressure. The objective of this project was to find a way of improving the optimal cerebral Perfusion Pressure methodology by introducing a new visualization method. Four severe traumatic brain injury patients with intracranial Pressure monitoring. Data were collected and pre-processed using ICM+ software. Sequential optimal cerebral Perfusion Pressure curves were used to create a color-coded maps of autoregulation - cerebral Perfusion Pressure relationship evolution over time. The visualization method addresses some of the main drawbacks of the original methodology and might bring the potential for its clinical application closer.

  • optimal cerebral Perfusion Pressure in centers with different treatment protocols
    Critical Care Medicine, 2018
    Co-Authors: Tim Howells, Peter Smielewski, Joseph Donnelly, Marek Czosnyka, Peter J Hutchinson, David K Menon, Per Enblad, Marcel J H Aries
    Abstract:

    The three centers in this study have different policies regarding cerebral Perfusion Pressure targets and use of vasopressors in traumatic brain injury patients. The aim was to determine if the different policies affected the estimation of cerebral Perfusion Pressure which optimizes the strength of cerebral autoregulation, termed "optimal cerebral Perfusion Pressure."Retrospective analysis of prospectively collected data.Three neurocritical care units at university hospitals in Cambridge, United Kingdom, Groningen, the Netherlands, and Uppsala, Sweden.A total of 104 traumatic brain injury patients were included: 35 each from Cambridge and Groningen, and 34 from Uppsala.None.In Groningen, the cerebral Perfusion Pressure target was greater than or equal to 50 and less than 70 mm Hg, in Uppsala greater than or equal to 60, and in Cambridge greater than or equal to 60 or preferably greater than or equal to 70. Despite protocol differences, median cerebral Perfusion Pressure for each center was above 70 mm Hg. Optimal cerebral Perfusion Pressure was calculated as previously published and implemented in the Intensive Care Monitoring+ software by the Cambridge group, now replicated in the Odin software in Uppsala. Periods with cerebral Perfusion Pressure above and below optimal cerebral Perfusion Pressure were analyzed, as were absolute difference between cerebral Perfusion Pressure and optimal cerebral Perfusion Pressure and percentage of monitoring time with a valid optimal cerebral Perfusion Pressure. Uppsala had the highest cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Uppsala patients were older than the other centers, and age is positively correlated with cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Optimal cerebral Perfusion Pressure was significantly lower in Groningen than in Cambridge. There were no significant differences in percentage of monitoring time with valid optimal cerebral Perfusion Pressure. Summary optimal cerebral Perfusion Pressure curves were generated for the combined patient data for each center. These summary curves could be generated for Groningen and Cambridge, but not Uppsala. The older age of the Uppsala patient cohort may explain the absence of a summary curve.Differences in optimal cerebral Perfusion Pressure calculation were found between centers due to demographics (age) and treatment (cerebral Perfusion Pressure targets). These factors should be considered in the design of trials to determine the efficacy of autoregulation-guided treatment.

  • individualizing thresholds of cerebral Perfusion Pressure using estimated limits of autoregulation
    Critical Care Medicine, 2017
    Co-Authors: Joseph Donnelly, Marek Czosnyka, Peter J Hutchinson, Ari Ercole, Hadie Adams, Chiara Robba, Luzius A Steiner, Danilo Cardim, Brenno Caetano Troca Cabella, David K Menon
    Abstract:

    Objectives:In severe traumatic brain injury, cerebral Perfusion Pressure management based on cerebrovascular Pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying “one” autoregulation-guided

  • optimal cerebral Perfusion Pressure in poor grade patients after subarachnoid hemorrhage
    Neurocritical Care, 2010
    Co-Authors: Philippe Bijlenga, Marek Czosnyka, John D Pickard, Karol P Budohoski, Martin Soehle, Peter J Kirkpatrick, Peter Smielewski
    Abstract:

    Background Cerebrovascular Pressure reactivity depends on cerebral Perfusion Pressure (CPP), with the optimal CPP (CPPopt) defined as Pressure at which cerebrovascular reactivity is functioning optimally, reaching minimal value of Pressure reactivity index (PRx). The study investigates the association between vasospasm, PRx, and CPPopt in poor grade patients (WFNS 4&5) after subarachnoid hemorrhage (SAH).

  • continuous monitoring of cerebrovascular Pressure reactivity allows determination of optimal cerebral Perfusion Pressure in patients with traumatic brain injury
    Critical Care Medicine, 2002
    Co-Authors: Luzius A Steiner, Marek Czosnyka, David K Menon, Stefan K Piechnik, Piotr Smielewski, Doris A Chatfield, John D Pickard
    Abstract:

    Objectives To define optimal cerebral Perfusion Pressure (CPPOPT) in individual head-injured patients using continuous monitoring of cerebrovascular Pressure reactivity. To test the hypothesis that patients with poor outcome were managed at a cerebral Perfusion Pressure (CPP) differing more from the

David K Menon - One of the best experts on this subject based on the ideXlab platform.

  • optimal cerebral Perfusion Pressure in centers with different treatment protocols
    Critical Care Medicine, 2018
    Co-Authors: Tim Howells, Peter Smielewski, Joseph Donnelly, Marek Czosnyka, Peter J Hutchinson, David K Menon, Per Enblad, Marcel J H Aries
    Abstract:

    The three centers in this study have different policies regarding cerebral Perfusion Pressure targets and use of vasopressors in traumatic brain injury patients. The aim was to determine if the different policies affected the estimation of cerebral Perfusion Pressure which optimizes the strength of cerebral autoregulation, termed "optimal cerebral Perfusion Pressure."Retrospective analysis of prospectively collected data.Three neurocritical care units at university hospitals in Cambridge, United Kingdom, Groningen, the Netherlands, and Uppsala, Sweden.A total of 104 traumatic brain injury patients were included: 35 each from Cambridge and Groningen, and 34 from Uppsala.None.In Groningen, the cerebral Perfusion Pressure target was greater than or equal to 50 and less than 70 mm Hg, in Uppsala greater than or equal to 60, and in Cambridge greater than or equal to 60 or preferably greater than or equal to 70. Despite protocol differences, median cerebral Perfusion Pressure for each center was above 70 mm Hg. Optimal cerebral Perfusion Pressure was calculated as previously published and implemented in the Intensive Care Monitoring+ software by the Cambridge group, now replicated in the Odin software in Uppsala. Periods with cerebral Perfusion Pressure above and below optimal cerebral Perfusion Pressure were analyzed, as were absolute difference between cerebral Perfusion Pressure and optimal cerebral Perfusion Pressure and percentage of monitoring time with a valid optimal cerebral Perfusion Pressure. Uppsala had the highest cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Uppsala patients were older than the other centers, and age is positively correlated with cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Optimal cerebral Perfusion Pressure was significantly lower in Groningen than in Cambridge. There were no significant differences in percentage of monitoring time with valid optimal cerebral Perfusion Pressure. Summary optimal cerebral Perfusion Pressure curves were generated for the combined patient data for each center. These summary curves could be generated for Groningen and Cambridge, but not Uppsala. The older age of the Uppsala patient cohort may explain the absence of a summary curve.Differences in optimal cerebral Perfusion Pressure calculation were found between centers due to demographics (age) and treatment (cerebral Perfusion Pressure targets). These factors should be considered in the design of trials to determine the efficacy of autoregulation-guided treatment.

  • individualizing thresholds of cerebral Perfusion Pressure using estimated limits of autoregulation
    Critical Care Medicine, 2017
    Co-Authors: Joseph Donnelly, Marek Czosnyka, Peter J Hutchinson, Ari Ercole, Hadie Adams, Chiara Robba, Luzius A Steiner, Danilo Cardim, Brenno Caetano Troca Cabella, David K Menon
    Abstract:

    Objectives:In severe traumatic brain injury, cerebral Perfusion Pressure management based on cerebrovascular Pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying “one” autoregulation-guided

  • continuous monitoring of cerebrovascular Pressure reactivity allows determination of optimal cerebral Perfusion Pressure in patients with traumatic brain injury
    Critical Care Medicine, 2002
    Co-Authors: Luzius A Steiner, Marek Czosnyka, David K Menon, Stefan K Piechnik, Piotr Smielewski, Doris A Chatfield, John D Pickard
    Abstract:

    Objectives To define optimal cerebral Perfusion Pressure (CPPOPT) in individual head-injured patients using continuous monitoring of cerebrovascular Pressure reactivity. To test the hypothesis that patients with poor outcome were managed at a cerebral Perfusion Pressure (CPP) differing more from the

John D Pickard - One of the best experts on this subject based on the ideXlab platform.

Peter Smielewski - One of the best experts on this subject based on the ideXlab platform.

  • Enhanced Visualization of Optimal Cerebral Perfusion Pressure Over Time to Support Clinical Decision Making.
    Critical care medicine, 2020
    Co-Authors: Marcel J H Aries, Joseph Donnelly, Marek Czosnyka, Robin Wesselink, Jan Willem J Elting, Ari Ercole, Natasha M Maurits, Peter Smielewski
    Abstract:

    Cerebrovascular reactivity can provide a continuously updated individualized target for management of cerebral Perfusion Pressure, termed optimal cerebral Perfusion Pressure. The objective of this project was to find a way of improving the optimal cerebral Perfusion Pressure methodology by introducing a new visualization method. Four severe traumatic brain injury patients with intracranial Pressure monitoring. Data were collected and pre-processed using ICM+ software. Sequential optimal cerebral Perfusion Pressure curves were used to create a color-coded maps of autoregulation - cerebral Perfusion Pressure relationship evolution over time. The visualization method addresses some of the main drawbacks of the original methodology and might bring the potential for its clinical application closer.

  • optimal cerebral Perfusion Pressure in centers with different treatment protocols
    Critical Care Medicine, 2018
    Co-Authors: Tim Howells, Peter Smielewski, Joseph Donnelly, Marek Czosnyka, Peter J Hutchinson, David K Menon, Per Enblad, Marcel J H Aries
    Abstract:

    The three centers in this study have different policies regarding cerebral Perfusion Pressure targets and use of vasopressors in traumatic brain injury patients. The aim was to determine if the different policies affected the estimation of cerebral Perfusion Pressure which optimizes the strength of cerebral autoregulation, termed "optimal cerebral Perfusion Pressure."Retrospective analysis of prospectively collected data.Three neurocritical care units at university hospitals in Cambridge, United Kingdom, Groningen, the Netherlands, and Uppsala, Sweden.A total of 104 traumatic brain injury patients were included: 35 each from Cambridge and Groningen, and 34 from Uppsala.None.In Groningen, the cerebral Perfusion Pressure target was greater than or equal to 50 and less than 70 mm Hg, in Uppsala greater than or equal to 60, and in Cambridge greater than or equal to 60 or preferably greater than or equal to 70. Despite protocol differences, median cerebral Perfusion Pressure for each center was above 70 mm Hg. Optimal cerebral Perfusion Pressure was calculated as previously published and implemented in the Intensive Care Monitoring+ software by the Cambridge group, now replicated in the Odin software in Uppsala. Periods with cerebral Perfusion Pressure above and below optimal cerebral Perfusion Pressure were analyzed, as were absolute difference between cerebral Perfusion Pressure and optimal cerebral Perfusion Pressure and percentage of monitoring time with a valid optimal cerebral Perfusion Pressure. Uppsala had the highest cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Uppsala patients were older than the other centers, and age is positively correlated with cerebral Perfusion Pressure/optimal cerebral Perfusion Pressure difference. Optimal cerebral Perfusion Pressure was significantly lower in Groningen than in Cambridge. There were no significant differences in percentage of monitoring time with valid optimal cerebral Perfusion Pressure. Summary optimal cerebral Perfusion Pressure curves were generated for the combined patient data for each center. These summary curves could be generated for Groningen and Cambridge, but not Uppsala. The older age of the Uppsala patient cohort may explain the absence of a summary curve.Differences in optimal cerebral Perfusion Pressure calculation were found between centers due to demographics (age) and treatment (cerebral Perfusion Pressure targets). These factors should be considered in the design of trials to determine the efficacy of autoregulation-guided treatment.

  • optimal cerebral Perfusion Pressure in poor grade patients after subarachnoid hemorrhage
    Neurocritical Care, 2010
    Co-Authors: Philippe Bijlenga, Marek Czosnyka, John D Pickard, Karol P Budohoski, Martin Soehle, Peter J Kirkpatrick, Peter Smielewski
    Abstract:

    Background Cerebrovascular Pressure reactivity depends on cerebral Perfusion Pressure (CPP), with the optimal CPP (CPPopt) defined as Pressure at which cerebrovascular reactivity is functioning optimally, reaching minimal value of Pressure reactivity index (PRx). The study investigates the association between vasospasm, PRx, and CPPopt in poor grade patients (WFNS 4&5) after subarachnoid hemorrhage (SAH).