Guido Pomidossi

Relationship of 24-hour Blood Pressure Mean and Variability to Severity of Target-organ Damage in Hypertension

Casual blood pressure (BP) can predict the development of cardiovascular morbidity and mortality, but the correlations between its values and the subsequent occurrence of such complications are low. This may depend on different individual resistance to the damage produced by hypertension. However, it may also depend on the recognized inability of causal BP to reflect accurately the 24-h mean and profile BP. In order to test the latter hypothesis, 24-h BP was recorded intra-arterially (Oxford method) in 108 hospitalized subjects with essential hypertension ranging from mild to severe. The 24-h means and standard deviations (i.e. variabilities) for systolic, mean and diastolic BP obtained by computer analysis of the BP tracing were related to the rate and severity of target-organ damage (TOD) assessed by clinical examination and quantified according to a predetermined score. The results confirmed that 24-h BP may be variably different from cuff BP among subjects. For nearly any value of cuff BP, subjects in whom the 24-h mean BP was low had a lower prevalence and severity of TOD than those in whom the 24-h mean BP was high (P less than 0.01). Furthermore, for nearly any level of 24-h mean BP, subjects in whom the 24-h BP variability was low had a lower prevalence and severity of TOD than those in whom the 24-h BP variability was high (P less than 0.05). These findings demonstrate that the severity of hypertension is more closely related to 24-h mean BP than to cuff BP values.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood pressure and heart rate variabilities in normotensive and hypertensive human beings.

Blood pressure and heart rate variabilities were studied in 89 ambulant normotensive or essential hypertensive subjects in whom blood pressure was recorded intra-arterially for 24 hours (Oxford method) under standardized living conditions. Data were analyzed beat to beat by a computer to provide mean values of the 48 half hours of the 24-hour period. Variabilities were assessed by the standard deviation and variation coefficients separately obtained for each half hour, as well as by the standard deviations and variation coefficients obtained by averaging the 48 mean values. In each subject, blood pressure and heart rate varied markedly either among or within half hours, indicating the existence of relatively long- and short-term variabilities during the 24 hours. When averaged for all subjects, the long-term variabilities showed only one systematic component, i.e., the marked reduction occurring during sleep. Sleep was further responsible for a marked reduction in the short-term blood pressure and heart rate variabilities. These variabilities showed marked (though nonsystematic) modifications, even outside sleep, which were positively related to the blood pressure and heart rate means. Modifications in blood pressure and heart rate means and short-term variabilities were also positively related to each other. All these features were common to normotensives and hypertensives. In hypertensives, the absolute long and short-term blood pressure variabilities were greater than in normotensives, but the percent blood pressure variabilities were similar. Heart rate variabilities (both absolute and percent) were similar in normotensive and hypertensive subjects. Heart rate variabilities were also similar whether the subjects had impaired or preserved baroreflex control of heart rate (vasoactive drug technique). These findings uncover a number of factors that are associated with and responsible for blood pressure and heart rate variabilities in human beings. The nature of these factors suggest a primary role of central nervous mechanisms in the production of these phenomena and in the overall cardiovascular modulation, with no substantial difference between conditions of normal and chronically elevated blood pressure.

EFFECTS OF BLOOD-PRESSURE MEASUREMENT BY THE DOCTOR ON PATIENT'S BLOOD PRESSURE AND HEART RATE

Changes in blood pressure in 10 or 15 min periods during which a doctor repeatedly measured blood pressure by the cuff method were monitored by a continuous intra-arterial recorder. In almost all the 48 normotensive and hypertensive subjects tested the doctors arrival at the bedside induced immediate rises in systolic and diastolic blood pressures peaking within 1 to 4 min (mean 26.7 +/- 2.3 mm Hg and 14.9 +/- 1.6 mm Hg above pre-visit values). There were large differences between individuals in the peak response (range, 4--75 mm Hg systolic and 1--36 mm Hg diastolic) unrelated to age, sex, baseline blood pressure, or blood-pressure variability. There was concomitant tachycardia (average peak response 15.9 +/- 1.5 beats/min, range 4--45 beats/min) which was only slightly correlated with the blood-pressure rise. After the peak response blood pressure declined and at the end of the visit was only slightly above the pre-visit level. A second visit by the same doctor did not change the average size of the early pressor response or the slope of its subsequent decline.

Evaluation of the baroreceptor-heart rate reflex by 24-hour intra-arterial blood pressure monitoring in humans.

The baroreceptor control of the sinus node was evaluated in 10 normotensive and 10 age-matched essential hypertensive subjects in whom ambulatory blood pressure was recorded intraarterially for 24 hours and scanned by a computer to identify the sequences of three or more consecutive beats hi which systolic blood pressure (SBP) and pulse interval (PI) progressively rose (+ PI/ + SBP) or fell (− PI/ −SBP) in a linear fashion, according to a method validated in cats. In normotensive subjects, several hundred +PI/+SBP and −PI/−SBP sequences of 3 beats were found whereas the number of sequences of 4,5, and more than 5 beats showed a progressive drastic reduction. The mean slopes of plus; PI/ + SBP (7.6 ± 2.0 msec/mm Hg) and − PI/− SBP (6.4 ± 1.5 msec/mm Hg) sequences were similar, but in both instances there was a large scattering of the values around the mean (variation coefficients: 64.2 ± 4.7 and 62.6 ± 2.4%). The slopes decreased as a function of the sequence length and baseline heart rate and increased to a marked extent during the night as compared with daytime values. All sequences were more rare (−33.2% for +PI/ + SBP and −31.7% for −PI/−SBP) and less steep in hypertensive subjects (−40.3 and −36.2%, respectively), who failed to show the marked nighttime increase in slope observed in normotensive subjects. To our knowledge, these observations provide the first description in humans of the baroreceptor-heart rate reflex in daily life. This reflex is characterized by marked within-subject variations hi sensitivity due in part to hemodynamic, temporal, and behavioral factors. All features of the baroreceptor-heart rate reflex are unpaired hi essential hypertension.

Alerting reaction and rise in blood pressure during measurement by physician and nurse

Blood pressure was monitored by a continuous intra-arterial recording in 46 subjects to investigate whether the alarm reaction and the blood pressure and heart rate increases that occur during cuff blood pressure measurement made by a physician 1) attenuate when the physicians visit is repeated several times and 2) are less pronounced if a nurse measures the blood pressure. In 16 subjects the peak mean blood pressure and heart rate rises that occurred in the early part of the physicians first visit (22.6 +/- 1.8 mm Hg and 17.7 +/- 1.7 beats/min) were virtually identical to those occurring during three subsequent visits by the same physician throughout a 2-day intra-arterial blood pressure monitoring. The less pronounced pressor and tachycardic responses observed in the last part of the physicians visit also were virtually identical among the four visits. In contrast, in 30 other subjects the blood pressure and heart rate rises that occurred during the nurses visit were 46.7% and 42.1% less (p less than 0.01) than those occurring during the physicians visit. The late and less pronounced pressor and tachycardic responses to the visit were also significantly less (p less than 0.01) in the former than in the latter condition. These results indicate that the error of overestimation of blood pressure inherent in cuff blood pressure measurement by a physician cannot be avoided by repeated visits by the physician over a short time span. It clearly can be reduced, however, if blood pressure measurements are performed by a nurse.

Arterial baroreflexes and blood pressure and heart rate variabilities in humans.

The factors responsible for 24-hour blood pressure and heart rate variabilities have never been clarified; however, studies performed in unanesthetized animals have shown an increase in blood pressure variability after sinoaortic denervation, and a negative relationship has been reported occasionally between blood pressure variability and baroreflex control of heart rate in humans. We have systematically investigated this issue in 82 ambulant hypertensive subjects using 24-hour intraarterial blood pressure recording (Oxford method) in which blood pressure and heart rate variabilities were measured by calculating the standard deviations of the values obtained throughout the 24 hours or during separate daytime and nighttime periods. Baroreflex sensitivity was assessed by the bradycardic or tachycardic responses to intravenous injections of phenylephrine or nitroglycerin and by the blood pressure response to changes in carotid transmural pressure obtained with a neck chamber. The sensitivity of the baroreceptor-heart rate reflex as Bssessed by the vasoactive drug technique showed a negative relationship with 24-hour blood pressure variability as well as with daytime and nighttime blood pressure variabilities measured separately (r = −0.28 to −0.50, p < 0.05). These Variabilities also correlated negatively with the sensitivity of the baroreceptor-blood pressure reflex as assessed by the neck chamber technique. By contrast, baroreflex sensitivity showed a positive correlation with heart rate variabilities (r = 0.32 to 0.47, p < 0.05). The relationship between baroreflex sensitivity and blood pressure and heart rate variabilities was confirmed when the data were analyzed by multiple regression to adjust for blood pressure and age differences among the 82 subjects. These results suggest that 1) arterial baroreflexes exert a buffering influence on the magnitude of daytime and nighttime blood pressure variabilities in humans; 2) these reflexes favor heart rate variability, which may represent one of the means by which baroreflex stabilization of blood pressure is accomplished; and 3) because of the low correlation indices between baroreflex sensitivity and blood pressure and heart rate variabilities, other factors (probably central in nature) are important in determining the size of these variations.

ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.

BackgroundIn humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however. Methods and ResultsIn nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPI caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7±3.2%, p<0.01), CBF did not change and CVR increased (+12.2±4.0%, p<0.05); diving caused an increase in mean arterial pressure and a reduction in heart rate. RPP increased (+14.3±3.5%, p<0.01), but despite this increase, there was a reduction in CBF and a marked increase in CVR (+37.3±7.4%, p<0.01). Captopril did not modify the blood pressure and heart rate responses to both stimuli except for a slight accentuation of the bradycardia to diving. Despite the unchanged or only slightly reduced RPP response, the increase in CVR was markedly and significantly attenuated (p<0.01). ConclusionsACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone.

Modification of arterial baroreflexes by captopril in essential hypertension

Captopril lowers blood pressure without increasing heart rate and plasma norepinephrine, which suggests that this drug may potentiate arterial baroreflexes. In eight subjects with untreated essential hypertension, blood pressure was monitored intraarterially and the effects of baroreceptor stimulation or deactivation were assessed by measuring (1) the slopes of the relations between increase or reduction in systolic pressure (intravenous phenylephrine or nitroglycerin) and the resulting lengthening or shortening in R-R interval, and (2) the increase or decrease in mean arterial pressure induced by increasing and decreasing carotid transmural pressure (neck chamber). The measurements were made before and after a hypotensive oral dose of captopril (50 mg). Before captopril, the slopes of the R-R interval changes with increase and reduction in systolic pressure were 8 and 4 ms/mm Hg, respectively. The slopes of the mean arterial pressure changes with increase and reduction in carotid transmural pressure were 0.51 and 0.40 mm Hg, respectively. After captopril, the responses to baroreceptor stimulation were unaltered but those to baroreceptor deactivation were augmented. The pressor and heart rate responses to hand-grip and cold exposure were unchanged by captopril. Administration of captopril is accompanied by a baroreflex potentiation which involves the lower portion of the stimulus-response curve of the reflex. This phenomenon (which may originate at the afferent baroreceptor fibers or centrally) may avoid a reduction in the tonic baroreflex influence during captopril-induced hypotension, thus contributing to the hemodynamic effects of the drug.

Control of blood pressure by carotid sinus baroreceptors in human beings

Abstract Most techniques available for studying arterial baroreflexes in man are unsuitable for analysis of the primary function of these reflexes, that is, arterial pressure control. Such control can be evaluated during increases and decreases in carotid baroreceptor activity obtained with a variable pressure neck chamber. This study reviews some technical aspects of the technique and describes the influence the carotid baroreceptors exert on arterial pressure in normotensive subjects and in those with essential hypertension. Major differences can be found in the two populations. In normotensive subjects the change in blood pressure is greater with a decrease than with an increase in baroreceptor activity. The former response becomes progressively less and the latter progressively greater with increasingly high blood pressure, so that in severe hypertension the reflex shows an asymmetry opposite to that in normotensive subjects, the change in blood pressure being greater with an increase than with a decrease in baroreceptor activity. These results imply that in human hypertension the carotid baroreflex mechanism controlling blood pressure undergoes a very marked resetting but shows no major reduction in sensitivity. In hypertensive subjects cardiac output and peripheral resistance were also measured. It was found that the depressor response to an increase in carotid baroreceptor activity depends on both a reduction in cardiac output and a systemic vasodilatation. However, peripheral vasoconstriction is the only factor accounting for the pressor response to reduced baroreceptor activity.

24-Hour blood pressure monitoring: Evaluation of Spacelabs 5300 monitor by comparison with intra-arterial blood pressure recording in ambulant subjects

The accuracy of 24-h blood pressure values obtained by ambulatory monitoring via the Spacelabs 5300 device was evaluated by comparison with simultaneous 24-h intra-arterial blood pressure recording from the contralateral arm. The comparison was made in eight essential hypertensive subjects in whom non-invasive blood pressure was measured every 15 (day) or 30 min (night). The measurements were automatically and visually edited to eliminate artefactual readings and hourly and 24-h means were calculated separately for systolic and diastolic blood pressure. The corresponding intra-arterial blood pressure means were also calculated. In the group as a whole, hourly means obtained by the non-invasive device were similar or only slightly different from those recorded intra-arterially. The 24-h systolic blood pressure mean obtained non-invasively was not significantly different from that obtained intra-arterially (138.4 +/- 9.1 and 142.9 +/- 9.2 mmHg, respectively), nor were the corresponding 24-h diastolic blood pressure means significantly different (83.5 +/- 4.5 and 80.6 +/- 3.5 mmHg, respectively). However, in spite of these similarities, there were contrasting and often large discrepancies between non-invasive and intra-arterial values in individual subjects. For the 24-h systolic blood pressure mean the discrepancies ranged from 7.6 +/- 1.1 to 16.1 +/- 2.2 mmHg and for the 24-h diastolic blood pressure mean, from 3.5 to 13.2 mmHg. Thus, the Spacelabs 5300 device has a limited ability to correctly estimate ambulatory blood pressure in individual subjects. It may be better suited for the estimation of group blood pressures, but only because errors are smoothed by the summation of individual errors of opposing signs.