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At least 379 records · Page 21Linked to original sources
PubMed2006

The effect of acute hypertension on left ventricular diastolic pressures in a canine model of left ventricular dysfunction with a preserved ejection fraction and elevated left ventricular filling pressures.

BACKGROUND: Decompensated heart failure with preserved left ventricular (LV) ejection fraction (EF) is often accompanied by hypertensive episodes. We hypothesized that acute increase in arterial pressure results in elevated early and late diastolic LV pressures as a result of further impaired LV relaxation. METHODS: To test this hypothesis, we used a chronic canine model of LV systolic dysfunction with preserved LV function (LVDPEF) (EF > 50%) and elevated LV end-diastolic pressure using coronary microsphere embolization. At baseline and with LVDPEF, each dog was paced 10 beats above their baseline heart rate and high-fidelity LV pressures, echocardiographic LV volumes, and transmitral Doppler were obtained before and after methoxamine pressure loading. RESULTS: With normal LV function, LV pressures at peak negative dP/dt (+18 mm Hg, P < .05) and at LV pressure minimum (+3.6 mm Hg, P < .01) increased. Both tau (P < .05) and LV end-diastolic pressure increased (5 +/- 3 vs 13 +/- 4 mm Hg, P < .01). EF was unchanged, although LV end-diastolic volume increased (P < .01). Pressure loading with LVDPEF resulted in a timing delay (P < .05) and a greater increase in LV pressures at peak negative dP/dt (+45 mm Hg) and LV minimal pressure (+7.5 mm Hg) as compared with normal LV function (P < .01). LV end-diastolic pressure increased (9 +/- 2-23 +/- 5 mm Hg, P < .001), diastolic filling period shortened (288 +/- 51-204 +/- 54 milliseconds, P < .01), and tau increased (P < .001). EF declined from 54 +/- 9% to 43 +/- 9% (P < .05) and LV size increased (P < .01). CONCLUSIONS: Pressure loading with normal LV function and with LVDPEF results in increased LV diastolic pressures, which are further exaggerated with LVDPEF as a result of prolonged relaxation and shortened diastolic filling.

Acute Disease↗
PubMed2006

Effect of peak pressure and pressure gradient on subsurface shear stresses in the neuropathic foot.

The pressure distribution on the plantar surface of the foot may provide insights into the stresses within the subsurface tissues of patients with diabetes mellitus and peripheral neuropathy (PN) who are at risk for skin breakdown. The purposes of this study were to (1) estimate the stress distribution in the subsurface soft tissue from a measured surface pressure distribution and determine any differences between values in the forefoot and rearfoot, and (2) determine the relationship between maximum shear stress (MSS) (magnitude and depth) and characteristics of the pressure distribution. The measured in-shoe pressure distributions during walking characterized by the peak plantar pressure and maximum pressure gradient on the plantar surface of the feet for 20 subjects with diabetes, PN and history of a mid foot or forefoot plantar ulcer were analyzed. The effects of peak pressure and maximum pressure gradient at the peak pressure location on the stress components in the subsurface soft tissue were studied using a potential function method to estimate the subsurface tissue stress. The calculated MSSs are larger in magnitude and located closer to the surface in the forefoot, where most skin breakdown occurs, compared to the rearfoot. In addition, the MSS (magnitude and depth) is highly correlated with the pressure gradient (r=-0.77 & 0.61) and the peak pressure (r=-0.61 & 0.91). The peak pressure and the maximum pressure gradient obtained from the surface pressure distribution appear to be important variables to identify where MSSs are located in the subsurface tissues on the plantar foot that may lead to skin break down.

Aged↗
PubMed2003

Blood pressure and pulse pressure development in a population sample of women with special reference to basal body mass and distribution of body fat and their changes during 24 years.

OBJECTIVE: To study blood pressure and pulse pressure longitudinally and their association with basal and change of body mass index (BMI) and waist to hip ratio (WHR). DESIGN: A prospective population study of 1462 women in Gothenburg, Sweden, aged 38-60 y at baseline, with a longitudinal follow-up of 24 y. OUTCOME MEASURES: Incidence of hypertension, systolic and diastolic blood pressure, and pulse pressure at baseline and after 12 and 24 y of follow-up. RESULTS: Systolic and diastolic blood pressure as well as pulse pressure increased with age and turned down again at high age. BMI and WHR at baseline were each independently associated with baseline systolic and diastolic blood pressure, but only BMI with pulse pressure. However, baseline BMI and WHR were not associated with change of systolic, diastolic or pulse pressure during 12 or 24 y of follow-up. Increase in BMI during the follow-up period was associated with increase in systolic and diastolic blood pressure but not with increase in pulse pressure. There were no such associations with WHR changes which, were either unrelated or in one analysis inversely related with blood pressure changes. When considering incidence of hypertension during the first 12 y of follow-up, BMI and change in BMI were significant predictors, independent of WHR. CONCLUSION: Age, BMI and increments in BMI seem to be strong predictors for hypertension and increased systolic and diastolic blood pressure in women. In contrast, WHR plays a lesser and uncertain role in the development of hypertension in middle-aged women. Changes in BMI seem not to be accompanied by changes in pulse pressure during a long time follow-up.

Adipose Tissue↗
PubMed2001

Renal pelvic pressure responds with augmented increases to increments in intraabdominal pressure.

BACKGROUND/PURPOSE: Flow of a fluid through a collapsible tube is under the influence of various factors including the external compressing pressure. Because the intraabdominal pressure may compress the ureter, an experimental study has been planned to determine and compare the normal intraabdominal and renal pelvic pressures and the alterations in renal pelvic pressure in response to the increments in intraabdominal pressure in the rabbits. METHODS: Eight adult rabbits were used for the experiment. Under general anesthesia, an urethral catheter, a nasogastric tube, and an intraperitoneal catheter were placed to measure intravesical (IVP), intragastric (IGP), and intraabdominal pressures (IAP), respectively. Intracranial pressure monitorization catheter was placed into the renal pelvis to monitor intrapelvic pressure (IPP). Basal pressure measurements have been recorded. The pressures have been recorded in every 5 minutes, and IAP has been increased gradually about 3 to 4 cm of water pressure in every step for 30-minute periods. RESULTS: Increases in the intrapelvic pressure values have been significantly higher than the increases in the IAP (P < .001). A significant correlation has been found between IPP and IAP (P = .000, r = 0.866). By using linear regression analysis the relationship has been found to be IPP = 7.303 + 1.985 (IAP). Intragastric pressure values have been higher compared with IAP values (P < .001), whereas intravesical pressures have not differed from IAP (P > .05). CONCLUSIONS: Elevations in IAP results in augmented increases in the IPP. Poiseuille and Laplace Laws suggest this augmented increase to resemble proximal ureteric obstruction. Increases in IAP may simulate proximal ureteric obstruction and may take part in the pathogenesis of hydronephrosis. J Pediatr Surg 36:901-904.

Animals↗
PubMed2000

Selectivity of oxymetazoline for urethral pressure vs blood pressure in the anaesthetized female rabbit.

OBJECTIVE: The aim of this study was to test alpha-adrenergic reference agonists for tissue selectivity in the urethra and to pharmacologically characterize the functional alpha-adrenoceptor type of the female rabbit urethra in vivo. MATERIAL AND METHODS: The effect of alpha-adrenergic agonists and antagonists on the urethral pressure was compared with that on blood pressure and heart rate measured simultaneously in the anaesthetized female rabbit. RESULTS: Oxymetazoline, NS-49, phenylephrine and phenylpropanolamine enhanced the urethral pressure in a dose-dependent manner. Phenylephrine and phenylpropanolamine also enhanced the blood pressure with significantly lower ED50 (dose that gives half of the maximal enhancing effect) values than for the urethral pressure. This was in contrast to oxymetazoline and NS-49. The ED50 values for oxymetazoline on urethral pressure, and systolic and diastolic blood pressure were 0.00067, 0.0030 and 0.0020 mg/kg, respectively. The ED50 values for NS-49 on urethral pressure, and systolic and diastolic blood pressure were 0.019, 0.21 and 0.18 mg/kg, respectively. Clonidine and UK 14,304 had no effect on urethral or blood pressure. The oxymetazoline-evoked increase in urethral pressure was inhibited by WB-4101 with an ID50 (dose that gives half of the inhibitory effect) significantly lower than that for rauwolscine. CONCLUSIONS: The results suggest that in the female rabbit in vivo activation of alpha1-adrenoceptors increased the urethral pressure. Phenylephrine and phenylpropanolamine, in contrast to oxymetazoline and NS-49, selectively enhanced blood pressure as compared with urethral pressure. Provided that the present results also have validity in humans, it would seem possible to develop urethra-selective drugs for treatment of stress incontinence with few or no cardiovascular side-effects.

Adrenergic alpha-Agonists↗
PubMed1981

Behavioral treatment of high blood pressure. I. Analyses of intra- and interdaily variations of blood pressure during a one-month, baseline period.

A group of 125 patients was enrolled in a study designed to evaluate the effectiveness of two behavioral treatments of high blood pressure, "relaxation' and systolic blood pressure "biofeedback." All patients monitored their pressures three times daily and also had their pressures recorded by a health professional weekly for a one-month, baseline period. This article reports only the results form the baseline period. The main findings are: 1) extensive self-monitoring of blood pressure is feasible and practical; 2) systolic pressure rises throughout the day, but is highest in the afternoon; 3) diastolic pressure falls form morning to evening, but is highest in the afternoon; 4) intradaily range of systolic but not diastolic blood pressure is higher among women than among men; 5) both systolic and diastolic pressures fall throughout the first 3 weeks; 6) standard deviations and ranges of self-determined blood pressures are highly intercorrelated; however, changes in professionally measured blood pressures are poorly correlated with these indices of blood pressure lability; 7) systolic pressure levels, rates of decline throughout the baseline period and lability indices are correlated with age, but comparable measures of diastolic blood pressure are not correlated with age.

Adult↗
PubMed2001

Assessment of outcomes other than systolic and diastolic blood pressure: pulse pressure, arterial stiffness and heart rate.

In recent years, studies have shown that parameters derived from the arterial pressure wave other than systolic and diastolic blood pressure provide important information on cardiovascular status. Among these parameters, pulse pressure, arterial stiffness and heart rate have emerged as independent markers of cardiovascular risk in different populations. Although a number of studies have used casual measurements of these parameters in a clinic setting, others have focused on their assessment under ambulatory conditions. The pulse pressure represents the amplitude of the pressure wave signal (systolic minus diastolic blood pressure), higher pulse pressure values having been reported in patients possessing cardiovascular risk factors. Close associations between a high pulse pressure and several surrogate end-points have been described. Furthermore, epidemiological studies have shown that a high pulse pressure is an independent predictor of hard end-points in several populations. Arterial stiffness represents one of the major haemodynamic factors determining pulse pressure. Pulse wave velocity, measured from the initial upstroke of the pressure wave, constitutes an established index of arterial stiffness. Studies have reported stiffer arteries in patients with cardiovascular pathology even at an early stage of disease. Close correlations between arterial stiffness and several surrogate markers have been reported, and arterial stiffness and its changes have recently been shown to be an independent predictor of hard end-points in patients with a high cardiovascular risk. Methods to evaluate arterial stiffness under ambulatory conditions are emerging. Heart rate represents the frequency of the cyclical strain of the arterial wall, clinical studies having shown that ambulatory heart rate is correlated to several surrogate markers. A few epidemiological studies have analysed the value of ambulatory heart rate as an independent predictor of hard end-points, but their positive findings need to be confirmed. The analysis of the pressure wave thus allows the determination of several haemodynamic indices other than systolic and diastolic blood pressure. Pulse pressure, arterial stiffness and heart rate constitute other outcomes that may be useful as additional factors in risk assessment for future therapeutic decision-making.

Arteries↗
PubMed2001

Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man.

Peripheral pulse pressure provides a surrogate measure of arterial stiffness. Analysis of the central pressure waveform allows assessment of central pulse pressure and arterial stiffness. The aim of the present study was to assess the effect of vasoconstrictor drugs on pulse pressure amplification and arterial stiffness in vivo. Eight healthy male subjects (mean age 30 years) received an infusion of angiotensin II (1, 3, 6 and 10 ng kg(-1) min(-1)), noradrenaline (10, 30, 60 and 100 ng kg(-1) min(-1)) and matching placebo, in random order, on separate occasions. Peripheral blood pressure and cardiac index were recorded non-invasively. Pulse wave analysis was used to determine augmentation index (AIx), which provides a measure of systemic arterial stiffness, aortic stiffness and central arterial pressure. Infusion of both active drugs resulted in a significant increase in peripheral mean arterial pressure (PMAP), peripheral vascular resistance, AIx, aortic stiffness and central pulse pressure, but only angiotensin II reduced cardiac index. Peripheral pulse pressure was unaffected by infusion of angiotensin II but increased with noradrenaline, which also produced a greater reduction in pulse pressure amplification than angiotensin II. However, the linear relationship of PMAP with both AIx and aortic stiffness did not differ significantly between drugs. These results demonstrate that intravenous infusion of angiotensin II and noradrenaline increase aortic and systemic arterial stiffness. Despite a similar effect on both parameters, for a given change in PMAP, the two drugs had divergent effects on peripheral pulse pressure and pulse pressure amplification. These data reveal that assessment of peripheral pulse pressure does not always reliably predict changes in central pulse pressure or arterial stiffness.

Adult↗
PubMed1998

Contribution of parental blood pressures to association between low birth weight and adult high blood pressure: cross sectional study.

OBJECTIVE: To examine the possibility that low birth weight is a feature of the inherited predisposition to high blood pressure. DESIGN: Cross sectional study. SETTING: Primary care medical centre in Edinburgh. SUBJECTS: One offspring of 452 families (231 men and 221 women aged 16-26 years) in whom blood pressure, weight, and height were measured in 1986 and whose parents had blood pressure measured in 1979. Birth weights were obtained from case records (270 offspring) or by questionnaires sent to the mothers (182 offspring). MAIN OUTCOME MEASURES: Birth weight and adult systolic blood pressure in offspring in relation to parental blood pressure. RESULTS: If parental blood pressures were not considered, a 1 kg decrease in birth weight was associated with a 2.24 mm Hg increase in systolic blood pressure of offspring (P = 0.06) after correction for current weight and sex. However, parental blood pressures correlated positively with blood pressure of offspring, and higher maternal blood pressure was associated with lower birth weight (-3.03 g/mm Hg, P < 0.01). After correction for parental blood pressures, a 1 kg decrease in birth weight was associated with only a 1.71 mm Hg increase in the systolic blood pressure of the offspring (P = 0.15). CONCLUSIONS: Low birth weight is a feature of the inherited predisposition to hypertension, perhaps because it is associated with higher maternal blood pressure during pregnancy. Parental blood pressure may be an important confounding factor in the relation between low birth weight and subsequent hypertension.

Adolescent↗
PubMed1992

Effect of reduced expiratory pressure on pharyngeal size during nasal positive airway pressure in patients with sleep apnoea: evaluation by continuous computed tomography.

BACKGROUND: This study aimed to determine whether reducing the expiratory pressure during nasal positive airway pressure for reasons of comfort causes a substantial decrease in the upper airway calibre. METHODS: Eight patients with obstructive sleep apnoea were studied. Continuous computed tomography (each run lasting 12 seconds) was used to measure minimum and maximum pharyngeal cross sectional areas at the velopharynx and the hypopharynx. Pharyngeal areas were measured while patients were awake and breathing without assistance, during the application of 12 cm H2O continuous positive airway pressure, and during bi-level positive airway pressure with an inspiratory pressure of 12 cm H2O and an expiratory pressure of 6 cm H2O. RESULTS: Nasal continuous positive airway pressure significantly increased the mean minimum and maximum upper airway areas at both the velopharynx and the hypopharynx compared with normal unassisted breathing. Bi-level positive airway pressure did not show a statistically significant increase in the minimum upper airway area at either level compared with normal unassisted breathing. The minimum areas of the velopharynx and hypopharynx were smaller with bi-level than continuous positive airways pressure in six of eight and eight of eight patients respectively but these were still greater than during unassisted breathing in seven of eight and six of eight patients respectively. CONCLUSIONS: Continuous positive airway pressure at 12 cm H2O is more effective in splinting the pharynx open than bi-level positive airway pressure with an inspiratory positive airway pressure of 12 cm H2O and an expiratory pressure of 6 cm H2O in patients with obstructive sleep apnoea during wakefulness, suggesting an important role for expiratory positive airway pressure. The clinical importance of this finding needs to be evaluated during sleep.

Humans↗
PubMed1986

Microvascular pressure in venules of skeletal muscle during arterial pressure reduction.

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40-185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.

Animals↗
PubMed1985

Effects of pleural pressure and abdominal pressure on diaphragmatic blood flow.

The aim of this experiment was to determine if blood flow to the diaphragm is affected by generating the transdiaphragmatic pressure mainly with positive abdominal pressure or mainly with negative pleural pressure, during both sustained and intermittent diaphragmatic contractions. Diaphragmatic blood flow was measured in anesthetized mongrel dogs by the radionuclide-labeled microsphere method. Sustained and intermittent tetanic diaphragmatic contractions were produced with 1) free abdomen and closed chest (high negative pleural pressure) and 2) bound abdomen and open chest (high positive abdominal pressure). During sustained contractions, diaphragmatic blood flow at maximum levels of activation was significantly higher with negative pleural pressure (P less than 0.05). In contrast with this, intermittent diaphragmatic contractions did not yield a significant difference between diaphragmatic blood flow with negative pleural pressure and with positive abdominal pressure at maximal levels of transdiaphragmatic pressure. During both sustained and intermittent contractions, blood pressure, as measured from the carotid artery, did not vary significantly between negative pleural pressure and positive abdominal pressure. We conclude that during sustained tetanic diaphragmatic contractions, diaphragmatic blood flow is obstructed by high positive abdominal pressures, but during intermittent diaphragmatic contractions, high positive abdominal pressures do not affect total blood flow, since any inhibition of blood flow during the contractile period can be compensated for during the relaxation period between contractions.

Abdomen↗
PubMed1991

Effect of alveolar and pleural pressures on interstitial pressures in isolated dog lungs.

We report the first direct measurements of perialveolar interstitial pressures in lungs inflated with negative pleural pressure. In eight experiments, we varied surrounding (pleural) pressure in a dog lung lobe to maintain constant inflation with either positive alveolar and ambient atmospheric pleural pressures (positive inflation) or ambient atmospheric alveolar and negative pleural pressures (negative inflation). Throughout, vascular pressure was approximately 4 cmH2O above pleural pressure. By the micropuncture servo-null technique we recorded interstitial pressures at alveolar junctions (Pjct) and in the perimicrovascular adventitia (Padv). At transpulmonary pressure of 7 cmH2O (n = 4), the difference of Pjct and Pady from pleural pressure of 0.9 +/- 0.4 and -1.1 +/- 0.2 cmH2O, respectively, during positive inflation did not significantly change (P less than 0.05) after negative inflation. After increase of transpulmonary pressure from 7 to 15 cmH2O (n = 4), the decrease of Pjct by 3.3 +/- 0.3 cmH2O and Pady by 2.0 +/- 0.4 cmH2O during positive inflation did not change during negative inflation. The Pjct-Pady gradient was not affected by the mode of inflation. Our measurements indicate that, in lung, when all pressures are referred to pleural or alveolar pressure, the mode of inflation does not affect perialveolar interstitial pressures.

Animals↗
PubMed1989

Lability of arterial pressure after baroreceptor denervation is not pressure dependent.

The mechanisms of increased arterial pressure lability after sinoaortic deafferentation remain unknown. We have shown previously in rats with chronic sinoaortic deafferentation (7-14 days after sinoaortic deafferentation) that ganglionic blockade significantly reduced mean arterial pressure and arterial pressure lability. The present study investigated the possibility that lability is related to the level of arterial pressure. Rats were instrumented chronically and heart rate and mean arterial pressure were sampled every 5 seconds in the conscious, freely moving state. Graded sustained increases in pressure (+10 to +82 mm Hg) produced by constant infusion of angiotensin II, phenylephrine, or vasopressin did not affect lability (standard deviation of 30-minute sampling period); whereas, graded hypotension (-10 to -70 mm Hg) produced by infusions of adenosine, nitroprusside, or nisoldipine appeared to reduce lability. Analysis of covariance and orthogonal polynomial curve fitting demonstrated a significant correlation between the decrease in mean arterial pressure and the decrease in lability produced by nisoldipine but not by adenosine or nitroprusside. Lability does not appear to be solely dependent on the level of arterial pressure because lability was reduced by adenosine when pressure was maintained at control levels by simultaneous infusion of phenylephrine. We conclude that 1) arterial pressure lability is not influenced by elevation of arterial pressure but can be reduced when pressure is lowered by certain vasodilators and 2) pressure alone does not appear to be the major determinant of lability because it can be attenuated by vascular smooth muscle relaxants even when pressure is maintained.

Adenosine↗
PubMed2001

Pressure-altering agents affect central aortic pressures more than is apparent from upper limb measurements in hypertensive patients: the role of arterial wave reflections.

The pressure pulse does not have the same amplitude in central and peripheral arteries, but it is amplified toward the periphery; the degree of this amplification depends principally on wave reflection. Despite the conventional clinical and epidemiological focus on peripheral pressures, the most physiologically relevant pressures for both cardiac and vascular effects are central pressures. The reflected wave contributes differently in the configuration of the peripheral and central pressure waveform. Therefore, we hypothesized that agents that alter wave reflections could have an unequal effect on central and peripheral pressures in hypertensive patients. Thus, the effect of caffeine was investigated in 10 hypertensive subjects according to a randomized, placebo-controlled, double-blind, crossover design. Central aortic pressures and wave reflection were assessed with applanation tonometry and pulse wave analysis. After caffeine, augmentation index and augmented pressure increased by 4.6%, (P<0.005) and 5.7 mm Hg (P<0.001), respectively, indicating increased effect of wave reflection from the periphery. The increase in aortic systolic pressure was greater compared with that in radial artery pressure at 30 minutes (25%) and marginally greater at 60 minutes (21%). Furthermore, the increase in aortic pulse pressure was greater at 30 and 60 minutes (34% and 40%, respectively). The intensified reflected wave after caffeine was largely responsible for the disparate effect between central and peripheral pressures by boosting the peak of the central and not of the peripheral waveform. This study shows that pressure-altering agents might affect central pressures more than is apparent from the corresponding upper limb values because of the concomitant changes in wave reflection.

Aorta↗
PubMed1998

A comparison between systolic aortic root pressure and finger blood pressure.

BACKGROUND: Digital photoplethysmography is used to assess hemodynamic variability and baroreflex sensitivity. Numerous studies have critically evaluated the accuracy of the photoplethysmographic device against peripheral pressure. The aim of our study was to compare finger blood and aortic root pressure. METHODS: We prospectively compared simultaneous recordings of systolic pressure at the aortic root and finger level over three consecutive respiratory cycles in 15 patients (56+/-11 years) undergoing routine cardiac catheterization. Data were obtained at baseline, during deep breathing maneuver (0.1 Hz), and after left ventricular cineangiography. RESULTS: At baseline, systolic finger pressure overestimated systolic aortic pressure (145.2+/-22.5 vs 115.0+/-20.1 mm Hg; p<0.001). The pressure difference (30.2+/-17.0 mm Hg) was not influenced by systolic aortic pressure. There was no relationship between pressure difference and the main determinants of the pulse wave amplification phenomenon. There was a beat-to-beat relationship between finger and aortic pressure in 14 of 15 subjects (slope ranging from 0.37 to 1.70; ordinate: from -56 to +98 mm Hg). During the deep breathing maneuver and after left ventricular cineangiography, finger pressure still overestimated aortic pressure by 32.3+/-15.0 mm Hg and 38.3 13.9 mm Hg, respectively (each p<0.001). There was a beat-to-beat relationship between systolic aortic root pressure (IAoBP) and systolic finger (FBP) in 13 of 15 patients, with major scattering of both slopes and ordinates. Throughout the study, there was no predictable relationship between the level of IAoBP and pressure bias. CONCLUSIONS: As expected, FBP was almost always higher than IAoBP. Importantly, the differences in systolic pressure did not correlate with known determinants of the pulse wave amplification phenomenon. The device must be used cautiously if one wants to noninvasively track spontaneous or induced changes in IAoBP.

Aorta↗
PubMed1995

Circadian blood pressure rhythm and atrial natriuretic peptide in prednisolone-induced blood pressure elevation.

The effect of prednisolone, given as a 4-day oral treatment, on 24-h ambulatory blood pressure rhythm, vasoactive hormones and correlation between blood pressure and vasoactive hormones were studied in 11 healthy men. Blood pressure was monitored at intervals of 15 min during the day and of 30 min during the night. Plasma concentrations of angiotensin II, aldosterone, atrial natriuretic peptide (ANP) and arginine vasopressin and serum concentration of insulin were measured in the morning during basal conditions. The 24-h systolic, diastolic and mean blood pressures were significantly higher after prednisolone treatment. Waking blood pressure was not significantly changed, but sleeping systolic and mean blood pressures were significantly elevated after treatment. The nocturnal systolic blood pressure fall was less pronounced after treatment (before 22%, and after 16%, p<0.01), whereas the nocturnal, mean and diastolic dips were preserved. ANP was significantly increased by prednisolone treatment, from 10.1 to 14.6 pmol l-1, p<0.005. The changes in concentration of ANP were significantly correlated to the changes in 24-h diastolic blood pressure (r = -0.63, p<0.05), 24-h mean blood pressure (r = -0.68, p<0.05), waking diastolic blood pressure (r = 0.83, p<0.01) and waking mean blood pressure (r = -0.67, p<0.01). We found that short-term prednisolone treatment elevated the overall 24-h blood pressure, reduced systolic blood pressure fall during sleep, and increased plasma concentration of ANP, and that the increase in ANP was inversely correlated to the increase in blood pressure. We suggest that the increase in ANP is a secondary and compensatory phenomenon which at least to some extent counteracts the hypertensive and sodium retaining effect of prednisolone.

Adult↗
PubMed1993

Ambulatory blood pressure monitoring and blood pressure self-measurement in the diagnosis and management of hypertension.

OBJECTIVE: To review published evidence on the use of ambulatory and self-measurement devices in the diagnosis and management of hypertension. DATA SOURCES: Computerized literature searches and manual review of bibliographies. STUDY SELECTION: Articles documenting original research pertaining to the diagnosis, treatment, or prognosis of hypertension using ambulatory or self-measurement devices. RESULTS: Studies that have compared office, self-measured, and ambulatory blood pressures have documented substantial, but nonsystematic, differences. Such findings have raised concern over the appropriateness of diagnosing hypertension and initiating drug therapy in individuals with high office blood pressure but comparatively low self-measured or ambulatory blood pressure ("office" or "white coat" hypertension). Evidence from a large number of cross-sectional studies and a single prospective study suggests that blood pressure- related end-organ damage is more closely associated with ambulatory than with office blood pressure. Less evidence supports self-measured blood pressure in this regard, and data are insufficient to compare ambulatory and self-measured blood pressure in terms of cardiovascular disease risk prediction. The estimated resource cost of an ambulatory blood pressure test is approximately $120, whereas charges range from $100 to $450. The annualized resource cost of blood pressure self-measurement is $50 or less. On a national level, the annual direct costs of ambulatory blood pressure monitoring could be as high as $6 billion, if this technique were used routinely to diagnose and monitor hypertensive patients. The extent to which direct costs would be offset by savings from less frequent or more efficient treatment for hypertension cannot be estimated reliably. Several practical and technical issues also detract from the potential usefulness of ambulatory and self-measurement devices. Finally, there is some evidence that office blood pressures measured by well-trained nonphysicians may serve as an alternative to ambulatory and self-measurement techniques in estimating usual blood pressure. CONCLUSION: Limited clinical applications of ambulatory blood pressure monitoring and blood pressure self-measurement in the diagnosis and management of hypertension appear to be warranted. Endorsement of these technologies for routine clinical use, however, will require more convincing evidence of their clinical effectiveness.

Ambulatory Care↗