Jesús D Melgarejo1, Joseph H Lee2, Michele Petitto3, Juan B Yépez3, Felipe A Murati3, Zhezhen Jin4, Carlos A Chávez1, Rosa V Pirela1, Gustavo E Calmón5, Winston Lee6, Matthew P Johnson7, Luis J Mena8, Lama A Al-Aswad9, Joseph D Terwilliger10, Rando Allikmets11, Gladys E Maestre12, C Gustavo De Moraes6. 1. Laboratory of Neurosciences, Faculty of Medicine at University of Zulia-Maracaibo, Zulia, Venezuela. 2. The Taub Institute for Research in Alzheimer's Disease and the Aging Brain and the G.H. Sergievsky Center at Columbia University, New York, New York; Department of Epidemiology, School of Public Health, Columbia University, New York, New York. 3. Glaucoma and Retina Units, Eye Clinic of Maracaibo, Maracaibo, Zulia, Venezuela. 4. Department of Biostatistics, Columbia University, New York, New York. 5. Laboratory of Ambulatory Recordings, Cardiovascular Institute (IECLUZ) at University of Zulia, Maracaibo, Zulia, Venezuela. 6. Department of Ophthalmology, Columbia University, New York, New York. 7. South Texas Diabetes and Obesity Institute, School of Medicine, University of Texas Rio Grande Valley, Brownsville, Texas. 8. Department of Informatics, Polytechnic University of Sinaloa, Mazatlán, México. 9. Department of Epidemiology, School of Public Health, Columbia University, New York, New York. 10. Department of Genetics and Development, Department of Psychiatry, and G.H. Sergievsky Center, Columbia University, New York, New York; Division of Medical Genetics, New York State Psychiatric Institute, New York, New York; Division of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland. 11. Department of Ophthalmology, Columbia University, New York, New York; Department of Pathology & Cell Biology, Columbia University, New York, New York. 12. Laboratory of Neurosciences, Faculty of Medicine at University of Zulia-Maracaibo, Zulia, Venezuela; Department of Biomedical Sciences, Division of Neurosciences, University of Texas Rio Grande Valley School of Medicine, Brownsville, Texas. Electronic address: gladys.maestre@utrgv.edu.
Abstract
PURPOSE: To determine which nocturnal blood pressure (BP) parameters (low levels or extreme dipper status) are associated with an increased risk of glaucomatous damage in Hispanics. DESIGN: Observational cross-sectional study. PARTICIPANTS: A subset (n = 93) of the participants from the Maracaibo Aging Study (MAS) who met the study eligibility criteria were included. These participants, who were at least 40 years of age, had measurements for optical tomography coherence, visual field (VF) tests, 24-hour BP, office BP, and intraocular pressure <22 mmHg. METHODS: Univariate and multivariate logistic regression analyses under the generalized estimating equations (GEE) framework were used to examine the relationships between glaucomatous damage and BP parameters, with particular attention to decreases in nocturnal BP. MAIN OUTCOME MEASURES: Glaucomatous optic neuropathy (GON) based on the presence of optic nerve damage and VF defects. RESULTS: The mean age was 61.9 years, and 87.1% were women. Of 185 eyes evaluated, 19 (26.5%) had signs of GON. Individuals with GON had significantly lower 24-hour and nighttime diastolic BP levels than those without. However, results of the multivariate GEE models indicated that the glaucomatous damage was not related to the average systolic or diastolic BP levels measured over 24 hours, daytime, or nighttime. In contrast, extreme decreases in nighttime systolic and diastolic BP (>20% compared with daytime BP) were significant risk factors for glaucomatous damage (odds ratio, 19.78 and 5.55, respectively). CONCLUSIONS: In this population, the link between nocturnal BP and GON is determined by extreme dipping effects rather than low nocturnal BP levels alone. Further studies considering extreme decreases in nocturnal BP in individuals at high risk of glaucoma are warranted.
PURPOSE: To determine which nocturnal blood pressure (BP) parameters (low levels or extreme dipper status) are associated with an increased risk of glaucomatous damage in Hispanics. DESIGN: Observational cross-sectional study. PARTICIPANTS: A subset (n = 93) of the participants from the Maracaibo Aging Study (MAS) who met the study eligibility criteria were included. These participants, who were at least 40 years of age, had measurements for optical tomography coherence, visual field (VF) tests, 24-hour BP, office BP, and intraocular pressure <22 mmHg. METHODS: Univariate and multivariate logistic regression analyses under the generalized estimating equations (GEE) framework were used to examine the relationships between glaucomatous damage and BP parameters, with particular attention to decreases in nocturnal BP. MAIN OUTCOME MEASURES: Glaucomatous optic neuropathy (GON) based on the presence of optic nerve damage and VF defects. RESULTS: The mean age was 61.9 years, and 87.1% were women. Of 185 eyes evaluated, 19 (26.5%) had signs of GON. Individuals with GON had significantly lower 24-hour and nighttime diastolic BP levels than those without. However, results of the multivariate GEE models indicated that the glaucomatous damage was not related to the average systolic or diastolic BP levels measured over 24 hours, daytime, or nighttime. In contrast, extreme decreases in nighttime systolic and diastolic BP (>20% compared with daytime BP) were significant risk factors for glaucomatous damage (odds ratio, 19.78 and 5.55, respectively). CONCLUSIONS: In this population, the link between nocturnal BP and GON is determined by extreme dipping effects rather than low nocturnal BP levels alone. Further studies considering extreme decreases in nocturnal BP in individuals at high risk of glaucoma are warranted.
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