Neurovascular compression of the medulla: can it cause neurogenic hypertension?
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Biomedical subjects
Publications and source records attributed to Thomas G Pickering.
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Blood pressure strongly predicts microalbuminuria and later progression to renal failure in people with diabetes. Ambulatory blood pressure monitoring seems to be superior to office blood pressure in predicting progression to microalbuminuria in type 1 diabetes. The associations of ambulatory blood pressure with office blood pressure and microalbuminuria in type 2 diabetes remain unclear. We studied the association of office blood pressure taken with an automated device and ambulatory blood pressure with spot urine albumin:creatinine ratio in 1180 older people with type 2 diabetes participating in the Informatics for Diabetes Education and Telemedicine Study. Office and awake systolic blood pressure were independently associated with albuminuria (P<0.001 for both) in a multivariate linear regression analysis that adjusted for age, gender, duration of diabetes, hemoglobin A1c, number of antihypertensive medications, and use of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Twelve percent of participants had well-controlled office blood pressure but not ambulatory blood pressure, whereas 14% had well-controlled ambulatory but not office blood pressure. The prevalence of microalbuminuria and macroalbuminuria in these subgroups was intermediate between those with well-controlled or uncontrolled blood pressure by both methods. We found, in a multiethnic group of older subjects with type 2 diabetes, that office systolic blood pressure and awake systolic ambulatory blood pressure exhibited independent associations with degree of albuminuria.
Depriving healthy subjects of sleep has been shown to acutely increase blood pressure and sympathetic nervous system activity. Prolonged short sleep durations could lead to hypertension through extended exposure to raised 24-hour blood pressure and heart rate, elevated sympathetic nervous system activity, and increased salt retention. Such forces could lead to structural adaptations and the entrainment of the cardiovascular system to operate at an elevated pressure equilibrium. Sleep disorders are associated with cardiovascular disease, but we are not aware of any published prospective population studies that have shown a link between short sleep duration and the incidence of hypertension in subjects without apparent sleep disorders. We assessed whether short sleep duration would increase the risk for hypertension incidence by conducting longitudinal analyses of the first National Health and Nutrition Examination Survey (n=4810) using Cox proportional hazards models and controlling for covariates. Hypertension incidence (n=647) was determined by physician diagnosis, hospital record, or cause of death over the 8- to 10-year follow-up period between 1982 and 1992. Sleep durations of < or =5 hours per night were associated with a significantly increased risk of hypertension (hazard ratio, 2.10; 95% CI, 1.58 to 2.79) in subjects between the ages of 32 and 59 years, and controlling for the potential confounding variables only partially attenuated this relationship. The increased risk continued to be significant after controlling for obesity and diabetes, which was consistent with the hypothesis that these variables would act as partial mediators. Short sleep duration could, therefore, be a significant risk factor for hypertension.
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BACKGROUND: The relationship between urinary albumin excretion and blood pressure (BP) has been found to be positive in hypertensive and normotensive subjects. It is not known, in a normotensive and nondiabetic sample, whether elevated urinary albumin levels predict future increases in BP. METHODS: In this prospective study, we followed a cohort of 108 individuals who were initially free of hypertension and diabetes for an average of 7.7 years. Urinary albumin excretion was determined at baseline by radioimmunoassay in a 24-h collection. Ambulatory BP monitoring was used to assess BP at baseline and at 7.5-year follow-up. Regression models were used to evaluate the relationship of baseline urinary albumin-to-creatinine ratio to baseline BP and average rate of change in BP before and after controlling for several potential confounding variables. RESULTS: Baseline albumin-to-creatinine ratio was not associated with baseline ambulatory BP, but was positively associated with change in ambulatory BP. Before and after controlling for sex, race/ethnicity, age, body mass index at baseline, and change in body mass index, urinary albumin-to-creatinine ratio was found to be a significant independent predictor of change in awake and sleep systolic and diastolic BPs (all P < .05). It also independently predicted hypertension status at follow-up. CONCLUSIONS: In healthy normotensive individuals, the urinary albumin-to-creatinine ratio predicts change in ambulatory BPs 7.5 years later. This finding suggests that urinary albumin excretion may be an important marker for processes that increase BP over time.
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BACKGROUND: A limitation of blood pressure measurements made in the physician's office is the transient elevation in pressure seen in many patients that does not appear to be linked to target organ damage or prognosis. This has been labeled the 'white-coat effect' (WCE), computed as the difference between blood pressure measurements taken by the physician and the ambulatory level or resting measures. It is unclear, however, which resting measure is most appropriate. The awake ambulatory blood pressure is the most widely used. However, while arguably the most useful measure for prediction of clinical outcomes, it is less appropriate for use as a resting measure, because it is influenced by many factors, including posture and physical activity level. Resting levels taken in the clinic may also be elevated, and will therefore underestimate the WCE. METHODS: We addressed this question by taking resting measures in a non-medical setting on the day before patients were seen at a Hypertension Clinic (day 1), and comparing these with resting measures taken on the following day, in the clinic before the patient saw the physician. RESULTS: As predicted, the day 1 resting levels were lower than those taken in the clinic prior to seeing the physician (P < 0.05 and P < 0.001 for systolic and diastolic pressures, respectively) in both normotensive and hypertensive patients. Using the day 1 resting levels, the estimated WCE for hypertensive patients was 5.3/6.9 mmHg (systolic/diastolic blood pressures), compared with estimates, using the clinic resting levels, of 0.3/0.5 mmHg. The pattern of changes was different in normotensive patients and hypertensive patients, with the physician pressures being slightly lower than day 1 pressures in the former, and substantially higher in the latter. Heart rate changes were similar and modest in both groups. CONCLUSION: The WCE may not just be limited to that narrow interval in which the patient actually sees the physician, but may generalize to the clinic setting, rendering a clinic 'resting' level invalid. While it is strongly positive in most hypertensive patients, it is frequently negative in normotensive patients. Our results suggest that improved methods of measuring blood pressure in the clinic setting are unlikely to resolve the confounding influence of the WCE, and that greater reliance will need to be placed on out-of-office monitoring.
BACKGROUND: Ambulatory blood pressure is a better predictor of target organ damage and the risk of adverse cardiovascular events than office measurements. Whether this is due to the greater reliability owing to the larger number of measurements that are usually taken using ambulatory monitoring, or the greater validity of these measurements independent of the number, remains controversial. METHODS: We addressed this issue by comparing physician readings and ambulatory measurements as predictors of left ventricular mass index. The number of readings was controlled by using the average of three physician readings and randomly selecting three awake readings from a 24-h ambulatory recording. RESULTS: In a multiple regression analysis that included both the ambulatory and physician blood pressure measurements, only the ambulatory systolic measurements significantly predicted left ventricular mass index (B=0.37, t=3.11, P=0.002); the coefficient for physician's systolic measurements was essentially zero (B=-0.01, t=-0.26, NS). CONCLUSIONS: These findings suggest that the superiority of ambulatory blood pressure as a predictor of target organ damage, compared with physician measurements, cannot be adequately/fully explained by the impact of the larger number of measurements obtained with ambulatory monitoring.
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Whether systolic blood pressure (SBP) or pulse pressure (PP) is more predictive of coronary heart disease remains controversial. The authors analyzed 6032 participants in the first National Health and Nutritional Examination Survey (NHANES I) followed up for an average of 16 years. Blood pressure was measured at baseline and coronary heart disease outcomes were determined from hospital or mortality records. Cox proportional hazard analyses were used to estimate the multivariate-adjusted relative risk (RR) for increases of 10 mm Hg or 1 SD in SBP and PP, and the RR associated with PP was greater than the RR associated with SBP when using an increase of 10 mm Hg. However, when using an increase of 1 SD, the RR associated with SBP was larger than for PP. Although both are predictors, the authors conclude that SBP has a larger RR than PP for coronary heart disease events.