International Journal of Cardiology, 36 (1992) 135-149 0 1992 Elsevier Science Publishers B.V. All rights reserved
CARD10
135 0167-5273/92/$05.00
01497
Review
Ambulatory blood pressure monitoring and circadian variation of cardiovascular disease; clinical and research applications Henry J. Purcell, J. Simon R. Gibbs, Andrew J.S. Coats and Kim M. Fox Royal Brompton National Heart and Lung Hospital, London, UK (Received
6 March
1992: accepted
25 March
1992)
Purcell HJ, Gibbs JSR, Coats AJS, Fox KM. Ambulatory blood pressure monitoring and circadian variation of cardiovascular disease; clinical and research applications. Int J Cardiol 1992;36:135-149. Ambulatory blood pressure monitoring is an evolving technology. It has an established role in the diagnosis of hypertension, the clinical management of selected patients, and in the evaluation of new medication. From continuous recording much has been learned about the circadian nature of blood pressure and heart rate. Future research holds promise for a greater understanding of the mechanisms and treatment of cardiovascular disease. The purpose of this short review is to describe the development of ambulatory blood pressure monitoring, and outline some of its important contributions to date; and also to explore the research potential and clinical utility of advanced intravascular monitoring techniques, such as the continuous recording of pulmonary artery pressure in ambulant patients. Key words: Ambulatory blood pressure monitoring; Circadian variation; Pulmonary artery pressure.
Introduction The concept of continuous recording of physiological variables in unrestricted man was pioneered by Holter, who in the mid-1950’s developed the portable magnetic tape “electrocardiocorder”, with a capability of recording the electrocardiogram directly from chest surface electrodes for periods of up to 10 h [l]. Holter envisaged a future where human beings would be “wired for research, with numerous little boxes piling-up information about body function” [2].
Correspondence to: Dr H.J. Purcell, Dept. of Cardiology, Level 3 (Chelsea), Room 386, Royal Brompton National Heart and Lung Hospital, Sydney Street, London SW3 6NP, UK.
Such activities were complemented by clinical workers such as Sokolow and colleagues who were interested in the level of blood pressure measured with portable recorders and the correlation with severity of complications in hypertension [3]. The subsequent development of a portable system incorporating a perfusion pump, transducer and miniature analogue tape recorder [4,5] enabled workers to record blood pressure data in the ambulatory setting for up to 24 h. Thus it became possible to characterise the circadian variability of heart rate and blood pressure in normal subjects and various patient groups. Early studies were conducted using an indwelling brachial artery catheter, while workers particularly in the field of aerospace medicine were
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developing simple and reliable techniques and equipment for automatic, indirect measurement of systolic and diastolic blood pressures [6]. Various devices were developed including a non-invasive System which utilised a small nitrogen cylinder to inflate an arm cuff. Korotkoff sounds were identified with a crystal microphone and amplifier, and these frequencies were then demodulated into DC voltages and recorded on magnetic tape [7]. Now there is a proliferation of non-invasive measurement systems, and this wide availability demands a standardised protocol for the validation of such systems which is both practicable and generally acceptable [8]. Two protocols have recently been proposed [9,10] with revisions of each imminent [ill.
Circadian variation of systemic arterial blood pressure One of the earliest studies on the effects of rest, sleep and work on blood pressure were conducted by Hill [12] who, using the Hill-Barnard sphygmometer, consisting of a manually inflated cuff and pressure gauge system, confirmed that during sleep the “arterial pressure falls very decidedly”. The subsequent availability of an automatic oscillographic recorder which periodically inflated a pneumatic cuff, enabled the investigation of blood pressure variation for 24-h periods in the absence of an observer. Recordings by Oxford workers from 8 “normal” subjects and 30 ‘hypertensive’ patients showed that all had striking variability in systolic and diastolic pressures. This variability was similar in males and females. There was a tendency for pressure to peak in the early evening and to fall profoundly during sleep. Sometimes this correlated with electroencephalographic measurement of depth of sleep. In 3 subjects who woke enough to speak to a nurse or void, elevations of systolic pressures of between 20-50 mmHg occurred, which gradually returned to baseline in the succeeding 20-40 min. In a study of 22 subjects, 8 of whom were medical staff or patients with medical problems unrelated to high blood pressure, using direct, continuous arterial pressure recordings, blood pressures fell in both normotensives and hypertensives during
sleep, and varied less than during waking h. Pressure falls were greatest in those sleeping at home [4]. Littler et al. demonstrated a fall of some 20% of the waking pressure in subjects during sleep D31. The effects of sleep on the cardiovascular system have been extensively reviewed [14,108]. Rapid eye motion (REM) sleep is characterised by increase in the variability of blood pressure and heart rate. In general a fall in blood pressure occurs during non-REM sleep. Modifications in cardiac function during sleep appear to be dependent on a balance between the sympathetic and parasympathetic nervous system. During nonREM phases there is a tendency to a relative increase in parasympathetic activity with slowing of heart rate and lowering of blood pressure. Using continuous intra-arterial recordings, Millar-Craig described the circadian variation of blood pressure in a study of 20 untreated hypertensive and five normotensive patients [15]. Among the hypertensives blood pressure was highest at 10 am, and progressively fell throughout the day. It was lowest during sleep at 3 a.m., and then began to rise again. By 6 a.m. this rise had increased rapidly, and the rate of increase was accentuated after waking at 7 a.m. Normotensives did not exhibit the 10 a.m. peak in pressure. Their pressures began to fall in the late afternoon and onwards until they reached a nadir at 3 a.m. They began to rise again at 5 a.m. prior to waking, and the rate of rise was similar to that seen in hypertensives. This pre-waking rise in blood pressure has been the subject of some controversy. Floras et al. maintained that it was artifactual and due to arousal and physical activity [16], a view supported by Littler [17] who maintained that there was no appreciable blood pressure rise before awakening, and that sleep and physical activity were the predominant influences on arterial pressure. Re-analysis of the original work, which included re-plotting the data “normalised” to time of awakening, confirmed the initial findings [181. An inherent problem with analysis of this kind is the difficulty in determining waking time, invariably this is unreliable and does not necessarily occur at a fixed time each day. As Pickering has
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pointed out also, the effects of physical (and mental) activity on blood pressure are pervasive [19]; and a wide range of commonly occurring activities could account for a substantial proportion of overall blood pressure variance [20]. Further insight into this phenomenon has come from a recent study by Broadhurst et al. [21] who performed 24-h intra-arterial ambulatory blood pressure monitoring in 30 male and 20 female volunteers. The familiar diurnal pattern of blood pressure, qualitatively similar to that of hypertensives, was seen as was the prewaking rise in pressure which occurred at relatively fixed heart rates. This was of the order of 6.3 mmHg systolic and 3.9 mmHg diastolic in the 2 h prior to waking, and was similar to that observed by Floras [16]. As the data from Broadhurst were realigned to the time of waking, the rise in pressure is less likely to be attributable to arousal, unless arousal occurs in a stuttering prolonged fashion. Broadhurst et al. suggest that the pre-waking pressure rise may be mediated by selective alpha-vasoconstriction. Circumstantial evidence to support this view comes from observations that betaadrenoceptor blocking drugs have little effect on the rise in blood pressure between 6-10 a.m., whereas the combined alpha- and beta-blocking drug labetalol almost completely abolishes this early morning rise [22]. The precise mechanisms of the morning rise in pressure are unknown. Since there is an increase in the incidence of stroke and myocardial infarction in the early morning time [231 it might be beneficial to abolish the pressure rise. Muller et al. [23] have postulated that the increase in arterial pressure on rising may increase the haemodynamic forces leading to rupture of atherosclerotic plaque, thrombus formation and ultimately myocardial infraction. Alternatively a plaque waiting to rupture is more likely to do so as the sympathetic surge of wakening occurs. In this case an early morning excess may be a middle of the night “deficit” of events. Circadian rhythms have also been demonstrated for fibrinolytic and clotting factors [24,25]. Furlan and co-workers [261 have used spectral analysis of systolic arterial pressure and RR interval variabilities as markers of sympathetic and
vagal control, to demonstrate an early morning rise in sympathetic activity and a reduction of vagal tone, which may act as a trigger to a cascade of activities resulting in a cardiovascular event. There has been dispute regarding whether the diurnal pattern of blood pressure variation is indeed a “genuine” intrinsic circadian rhythm or is determined by activity. A recent overview by Quyyumi [27], is probably representative of the current view. He suggests that factors such as heart rate, blood pressure, noradrenaline levels and plasma renin activity have an endogenous circadian rhythm, which is exaggerated by awakening and exercise. Studies conducted among shift workers have shown evidence for an endogenous rhythm for heart rate, but not for blood pressure [28]. Seasonal
influences
on blood pressure
A further extension of circadian research has been to investigate the effects of seasonal change in haemodynamics and blood pressure. In the summer, peripheral vasodilatation is associated with proportional increases in stroke volume and cardiac output whereas in winter peripheral vasoconstriction is associated with proportional decreases in cardiac output and stroke volume. Similarly significant increases in systemic vascular resistance and plasma noradrenaline are seen in winter time [29]. A recent study in hypertensives confirms that arterial blood pressure may be strongly influenced by environmental temperatures and that clear seasonal influences can be detected in small scale studies especially when integrated with ambulatory monitoring [30]. Such findings may have profound importance for the diagnosis and treatment of hypertensives. These data are interesting also in terms of the observed variations in monthly death ratios from cardiovascular disease in England and Wales. Death from coronary heart disease, stroke and other circulatory diseases account for more than half of the winter excess in Britain (bronchitis and pneumonia accounting for most of the remainder) (Fig. 1). Experimentally it has been shown that exposure to mild cold causes increases
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in platelet and red cell counts and blood viscosity, as well as blood pressure, and it is suggested that normal thermoregulatory adjustments to mild surface cooling may account for increases in coronary and cerebral thrombosis in Britain as air temperatures fall from summer to winter [311.
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,.. p which was synchronised with pressure by an event button connected to both of the recorders. These three systems had some important drawbacks. The principle difficulty with fluidfilled catheters is ascertaining the zero reference point for levelling the external pressure transducer [96]. In practice the difficulties and inaccuracies in estimating the zero reference point in ambulant patients warrant the use of a micromanometer tipped catheter since its tip is also its zero reference point. In addition, micromanometer-tipped catheters do not suffer from the data loss encountered with fluid-filled catheters and do not require anticoagulation. Micromanometertipped catheters do suffer from unpredictable zero drift [97], making most unsuitable for longterm pressure measurement. The frequency response of 8 Hz of two of these systems has been too low for accurate pulmonary artery pressure measurement during tachycardia. The characteristic features of pulmonary artery pressure and more than 95% of their energy are present in the first 6 harmonics [98], although measurable components extend up to the 11th harmonic [99]. Since the fundamental harmonic is the same as the heart rate, a frequency range of O-12 Hz is required for physiological investigations at heart rates up to 120 beats/min. These limitations have been overcome by developing a fourth system which features a new pulmonary artery catheter. This is a 7F micromanometer tipped catheter (Gaeltec Ltd) which incorporates an in vivo calibration system to allow correction for zero drift 1971.This is connected to a commercially available digital ambulatory
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recorder in which the pressure wave is sampled at 16 Hz and stored in semiconductor memory. On completion of a recording, data are transferred from the ambulatory recorder via a serial data link to an Acorn Archimedes desktop computer for further data processing using custom written software [ 1191.
Results from ambulatory pulmonary artery pressure studies Pulmonary artery diastolic pressure has been used as a measure of left ventricular filling pressure to investigate coronary artery disease. This has shown that in patients with coronary artery disease during exercise and ambulatory monitoring the magnitude of ST-segment depression correlated with the rise in pulmonary artery diastolic pressure [loo]. In patients with syndrome X, pulmonary artery diastolic pressure did not rise despite ST-segment depression suggesting that syndrome X is not associated with abnormal left ventricular function [loll. Depression of ST segments during silent myocardial ischaemia was shown to be associated with a rise in diastolic pressure [102] and ambulatory pulmonary artery pressure was also used to investigate variant angina [103]. It was suggested that the pulmonary
artery diastolic pressure rose at night both in patients with normal and abnormal coronary arteries [104]. The system using a fluid filled catheter [94] has been adapted to include measurement of blood pressure and has been used to study normal subjects [ 1051. Although this study investigated only 6 subjects and does not meet the stringent criteria for normality applied by others [92], it is the only normal ambulatory study reported. During an 8 to 10-h period the subjects, mean age 28.6 yr, had an average resting pulmonary artery pressure (in mmHg (SD)) of 13.9 (1.1)/5.5 (0.9) and on submaximum exercise of 33.3 (1.7)/12.0 (0.9). These data have been compared with a study of pulmonary hypertensive patients [106]. Ambulatory pulmonary artery pressure monitoring has also been used in a small number of patients with valve disease and heart failure to guide clinical management [93]. In the only circadian study of ambulatory pulmonary artery pressure, diurnal variation of pulmonary artery pressure has been observed in patients with chronic heart failure [107]. In this study pulmonary artery pressure rose at night in all but the most severely symptomatic patients (Fig. 4). The nocturnal rise may be largely a consequence of lying down although this does not
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Fig. 4. Diurnal
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appear to be the only mechanism. Nocturnal elevation of pulmonary artery pressure probably also occurs in normal subjects [log]. These nocturnal pulmonary artery pressure changes are in contrast to the behaviour of systemic arterial pressure. Further studies in heart failure have examined pulmonary artery pressure changes during normal daily activities and different types of exercise testing [109]. Important differences in haemodynamic changes were observed and used to challenge the value of maximum exercise testing in chronic heart failure. Similar investigations have demonstrated a lack of effect of catheterisation itself on the pulmonary artery pressure [llOl. Reliable assessment of pulmonary artery pressure requires catheterisation. It appears to be safe and well tolerated. The principal application of long-term continuous ambulatory pulmonary artery pressure monitoring is as a research tool to investigate the natural history and pathophysiology of diseases such as coronary artery disease, heart failure, pulmonary hypertension and chronic respiratory disease. It may be used to investigate physiological and pathological variations and to assess the effects of drug therapy on central haemodynamics.
pressure has been described as “the Sunrise industry” [112]. Reference values for ambulatory blood pressures are accumulating [ 113,114] and large community-based investigations such as the PAMELA Study, planned to obtain an epidemiological evaluation of 24-h ambulatory blood pressure values, are currently underway 11151;and the technique will enable identification of patients with elevated blood pressures in the work place, during routine activity and in sleep. Although we are aware of technical limitations, in selected patients it is undoubtedly helpful in diagnosis of hypertension, and in determining progress and the therapeutic response to non-pharmacologic and drug therapies. While ambulatory monitoring should not at present be used as a routine for diagnosis of hypertension [ 1161, epidemiological studies will undoubtedly clarify whether ambulatory blood pressure and/or blood pressure may be more valuable than clinic blood pressure in predicting or revealing early blood pressure elevation. No doubt too, ambulatory blood pressure monitoring will have an increasing role as an adjunct to a number of research areas [117,118]. References
Conclusions There is much to learn about the circadian pattern of heart rate and blood pressure in normal individuals and patients with cardiovascular disease. Of particular interest is whether by drug therapy we can alter the pattern of increased myocardial ischaemia, heart attack and stroke, seen in the early morning period and whether reduction of ischaemia and better control of blood pressure will affect prognosis. Ambulatory blood pressure monitoring will no doubt play a significant role in such investigations. While intraarterial blood pressure measurement remains the “gold standard” and an important research tool with which to study pathophysiology, its use is limited. Noninvasive devices, although not entirely devoid of adverse effects, are comparatively safe [llll. Because of its increasing popularity non-invasive ambulatory monitoring of blood
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rial pressures in humans: relationship to arterial pressure and hormones. Am J Physiol 1986;25:HlOl-H108. Richards AM, Ikram H, Crozier IG, Nicholls MCI. Jans S. Ambulatory pulmonary arterial pressure in primary pulmonary hypertension: variability, relation to systemic arterial pressure, and plasma catecholamines. Br Heart J 1990;63:103-108. Gibbs JSR, Cunningham AD, Shapiro LM, Park A, Poole-Wilson PA, Fox KM. Diurnal variation of pulmonary artery pressure in chronic heart failure. Br Heart J 1989;62:30-35. Lugaresi E, Coccagna G. Cirignotta F et al. Breathing during sleep in man in normal and pathological conditions. In: Fitzgerald RS, Gautier H, Lahiri S. eds. The regulation of respiration during sleep and anesthesia. New York and London: Plenum Press, 1978;35-45. Gibbs JSR. Keegan J. Wright. Fox KM, Poole-Wilson PA. Pulmonary artery pressure changes during exercise and daily activities in chronic heart failure. J Am Call Cardiol 1990:15:52-61. Gibbs JSR. Ferrari R. Keegan J. et al. The intluence of right-heart catheterisation on pulmonary arterial pressure in chronic heart failure: relationship to neuroendocrinal changes. Int J Cardiol 1991;33:365-376. Bottini. PB, Zhoades RB. Carr AA, Prisant LM. Mechanical trauma and acute neuralgia associated with automated ambulatory blood pressure monitoring (letter). Am J Hypertens 1991;4:283. Hunyor SN, Cejnar M. Blood pressure machines and measurement. In: Hunyor S, Whitworth J, eds. Hypertens Management. ch. 1. Sydney: MacLennan and Petty Publishers 1990:3-10. Cox J., O’Malley K., Atkins N., O’Brien E. A comparing of the twenty-four-hour blood presure profile in normotensive and hypertensive subjects. J Hypertens 19Y1;9tsuppl 11:53-56. Staessen J., Celis H., De Cort P.. Thijs L.. Amery A. An inventory of studies on ambulatory blood pressure in large groups of subjects. J Hypertens 1991:9(suppl 8I:S48-s50. Cesana G., De Vito G.. Ferrario M. Ambulatory blood pressure normalcy: the PAMELA Study. J Hypertens 19Y1,9tsuppl 3l:S17-S23. 1991 Guidelines for the Prevention of Hypertens and Associated Cardiovascular Disease. Summary prepared by WHO/ISH Guidelines Committee. J Hypertens 1992:10:97-99. Sideris DA, Kontoyannis DA, Michalis L, Adractas A. Moulopoulos SD. Acute changes in blood pressure as a cause of cardiac arrhythmias. Eur Heart J 1987;8:45-52. Fredrikson M, Blumenthal JA. Serum lipid levels and ambulatory blood pressure. J Ambulatory Monitoring 1990:2:113-11X. Gibbs JSR, MacLachlan D. Fox KM. A new system for ambulatory pulmonary artery pressure recording. Br Heart J 1992:in press.
CARD10
135 0167-5273/92/$05.00
01497
Review
Ambulatory blood pressure monitoring and circadian variation of cardiovascular disease; clinical and research applications Henry J. Purcell, J. Simon R. Gibbs, Andrew J.S. Coats and Kim M. Fox Royal Brompton National Heart and Lung Hospital, London, UK (Received
6 March
1992: accepted
25 March
1992)
Purcell HJ, Gibbs JSR, Coats AJS, Fox KM. Ambulatory blood pressure monitoring and circadian variation of cardiovascular disease; clinical and research applications. Int J Cardiol 1992;36:135-149. Ambulatory blood pressure monitoring is an evolving technology. It has an established role in the diagnosis of hypertension, the clinical management of selected patients, and in the evaluation of new medication. From continuous recording much has been learned about the circadian nature of blood pressure and heart rate. Future research holds promise for a greater understanding of the mechanisms and treatment of cardiovascular disease. The purpose of this short review is to describe the development of ambulatory blood pressure monitoring, and outline some of its important contributions to date; and also to explore the research potential and clinical utility of advanced intravascular monitoring techniques, such as the continuous recording of pulmonary artery pressure in ambulant patients. Key words: Ambulatory blood pressure monitoring; Circadian variation; Pulmonary artery pressure.
Introduction The concept of continuous recording of physiological variables in unrestricted man was pioneered by Holter, who in the mid-1950’s developed the portable magnetic tape “electrocardiocorder”, with a capability of recording the electrocardiogram directly from chest surface electrodes for periods of up to 10 h [l]. Holter envisaged a future where human beings would be “wired for research, with numerous little boxes piling-up information about body function” [2].
Correspondence to: Dr H.J. Purcell, Dept. of Cardiology, Level 3 (Chelsea), Room 386, Royal Brompton National Heart and Lung Hospital, Sydney Street, London SW3 6NP, UK.
Such activities were complemented by clinical workers such as Sokolow and colleagues who were interested in the level of blood pressure measured with portable recorders and the correlation with severity of complications in hypertension [3]. The subsequent development of a portable system incorporating a perfusion pump, transducer and miniature analogue tape recorder [4,5] enabled workers to record blood pressure data in the ambulatory setting for up to 24 h. Thus it became possible to characterise the circadian variability of heart rate and blood pressure in normal subjects and various patient groups. Early studies were conducted using an indwelling brachial artery catheter, while workers particularly in the field of aerospace medicine were
136
developing simple and reliable techniques and equipment for automatic, indirect measurement of systolic and diastolic blood pressures [6]. Various devices were developed including a non-invasive System which utilised a small nitrogen cylinder to inflate an arm cuff. Korotkoff sounds were identified with a crystal microphone and amplifier, and these frequencies were then demodulated into DC voltages and recorded on magnetic tape [7]. Now there is a proliferation of non-invasive measurement systems, and this wide availability demands a standardised protocol for the validation of such systems which is both practicable and generally acceptable [8]. Two protocols have recently been proposed [9,10] with revisions of each imminent [ill.
Circadian variation of systemic arterial blood pressure One of the earliest studies on the effects of rest, sleep and work on blood pressure were conducted by Hill [12] who, using the Hill-Barnard sphygmometer, consisting of a manually inflated cuff and pressure gauge system, confirmed that during sleep the “arterial pressure falls very decidedly”. The subsequent availability of an automatic oscillographic recorder which periodically inflated a pneumatic cuff, enabled the investigation of blood pressure variation for 24-h periods in the absence of an observer. Recordings by Oxford workers from 8 “normal” subjects and 30 ‘hypertensive’ patients showed that all had striking variability in systolic and diastolic pressures. This variability was similar in males and females. There was a tendency for pressure to peak in the early evening and to fall profoundly during sleep. Sometimes this correlated with electroencephalographic measurement of depth of sleep. In 3 subjects who woke enough to speak to a nurse or void, elevations of systolic pressures of between 20-50 mmHg occurred, which gradually returned to baseline in the succeeding 20-40 min. In a study of 22 subjects, 8 of whom were medical staff or patients with medical problems unrelated to high blood pressure, using direct, continuous arterial pressure recordings, blood pressures fell in both normotensives and hypertensives during
sleep, and varied less than during waking h. Pressure falls were greatest in those sleeping at home [4]. Littler et al. demonstrated a fall of some 20% of the waking pressure in subjects during sleep D31. The effects of sleep on the cardiovascular system have been extensively reviewed [14,108]. Rapid eye motion (REM) sleep is characterised by increase in the variability of blood pressure and heart rate. In general a fall in blood pressure occurs during non-REM sleep. Modifications in cardiac function during sleep appear to be dependent on a balance between the sympathetic and parasympathetic nervous system. During nonREM phases there is a tendency to a relative increase in parasympathetic activity with slowing of heart rate and lowering of blood pressure. Using continuous intra-arterial recordings, Millar-Craig described the circadian variation of blood pressure in a study of 20 untreated hypertensive and five normotensive patients [15]. Among the hypertensives blood pressure was highest at 10 am, and progressively fell throughout the day. It was lowest during sleep at 3 a.m., and then began to rise again. By 6 a.m. this rise had increased rapidly, and the rate of increase was accentuated after waking at 7 a.m. Normotensives did not exhibit the 10 a.m. peak in pressure. Their pressures began to fall in the late afternoon and onwards until they reached a nadir at 3 a.m. They began to rise again at 5 a.m. prior to waking, and the rate of rise was similar to that seen in hypertensives. This pre-waking rise in blood pressure has been the subject of some controversy. Floras et al. maintained that it was artifactual and due to arousal and physical activity [16], a view supported by Littler [17] who maintained that there was no appreciable blood pressure rise before awakening, and that sleep and physical activity were the predominant influences on arterial pressure. Re-analysis of the original work, which included re-plotting the data “normalised” to time of awakening, confirmed the initial findings [181. An inherent problem with analysis of this kind is the difficulty in determining waking time, invariably this is unreliable and does not necessarily occur at a fixed time each day. As Pickering has
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pointed out also, the effects of physical (and mental) activity on blood pressure are pervasive [19]; and a wide range of commonly occurring activities could account for a substantial proportion of overall blood pressure variance [20]. Further insight into this phenomenon has come from a recent study by Broadhurst et al. [21] who performed 24-h intra-arterial ambulatory blood pressure monitoring in 30 male and 20 female volunteers. The familiar diurnal pattern of blood pressure, qualitatively similar to that of hypertensives, was seen as was the prewaking rise in pressure which occurred at relatively fixed heart rates. This was of the order of 6.3 mmHg systolic and 3.9 mmHg diastolic in the 2 h prior to waking, and was similar to that observed by Floras [16]. As the data from Broadhurst were realigned to the time of waking, the rise in pressure is less likely to be attributable to arousal, unless arousal occurs in a stuttering prolonged fashion. Broadhurst et al. suggest that the pre-waking pressure rise may be mediated by selective alpha-vasoconstriction. Circumstantial evidence to support this view comes from observations that betaadrenoceptor blocking drugs have little effect on the rise in blood pressure between 6-10 a.m., whereas the combined alpha- and beta-blocking drug labetalol almost completely abolishes this early morning rise [22]. The precise mechanisms of the morning rise in pressure are unknown. Since there is an increase in the incidence of stroke and myocardial infarction in the early morning time [231 it might be beneficial to abolish the pressure rise. Muller et al. [23] have postulated that the increase in arterial pressure on rising may increase the haemodynamic forces leading to rupture of atherosclerotic plaque, thrombus formation and ultimately myocardial infraction. Alternatively a plaque waiting to rupture is more likely to do so as the sympathetic surge of wakening occurs. In this case an early morning excess may be a middle of the night “deficit” of events. Circadian rhythms have also been demonstrated for fibrinolytic and clotting factors [24,25]. Furlan and co-workers [261 have used spectral analysis of systolic arterial pressure and RR interval variabilities as markers of sympathetic and
vagal control, to demonstrate an early morning rise in sympathetic activity and a reduction of vagal tone, which may act as a trigger to a cascade of activities resulting in a cardiovascular event. There has been dispute regarding whether the diurnal pattern of blood pressure variation is indeed a “genuine” intrinsic circadian rhythm or is determined by activity. A recent overview by Quyyumi [27], is probably representative of the current view. He suggests that factors such as heart rate, blood pressure, noradrenaline levels and plasma renin activity have an endogenous circadian rhythm, which is exaggerated by awakening and exercise. Studies conducted among shift workers have shown evidence for an endogenous rhythm for heart rate, but not for blood pressure [28]. Seasonal
influences
on blood pressure
A further extension of circadian research has been to investigate the effects of seasonal change in haemodynamics and blood pressure. In the summer, peripheral vasodilatation is associated with proportional increases in stroke volume and cardiac output whereas in winter peripheral vasoconstriction is associated with proportional decreases in cardiac output and stroke volume. Similarly significant increases in systemic vascular resistance and plasma noradrenaline are seen in winter time [29]. A recent study in hypertensives confirms that arterial blood pressure may be strongly influenced by environmental temperatures and that clear seasonal influences can be detected in small scale studies especially when integrated with ambulatory monitoring [30]. Such findings may have profound importance for the diagnosis and treatment of hypertensives. These data are interesting also in terms of the observed variations in monthly death ratios from cardiovascular disease in England and Wales. Death from coronary heart disease, stroke and other circulatory diseases account for more than half of the winter excess in Britain (bronchitis and pneumonia accounting for most of the remainder) (Fig. 1). Experimentally it has been shown that exposure to mild cold causes increases
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in platelet and red cell counts and blood viscosity, as well as blood pressure, and it is suggested that normal thermoregulatory adjustments to mild surface cooling may account for increases in coronary and cerebral thrombosis in Britain as air temperatures fall from summer to winter [311.
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,.. p which was synchronised with pressure by an event button connected to both of the recorders. These three systems had some important drawbacks. The principle difficulty with fluidfilled catheters is ascertaining the zero reference point for levelling the external pressure transducer [96]. In practice the difficulties and inaccuracies in estimating the zero reference point in ambulant patients warrant the use of a micromanometer tipped catheter since its tip is also its zero reference point. In addition, micromanometer-tipped catheters do not suffer from the data loss encountered with fluid-filled catheters and do not require anticoagulation. Micromanometertipped catheters do suffer from unpredictable zero drift [97], making most unsuitable for longterm pressure measurement. The frequency response of 8 Hz of two of these systems has been too low for accurate pulmonary artery pressure measurement during tachycardia. The characteristic features of pulmonary artery pressure and more than 95% of their energy are present in the first 6 harmonics [98], although measurable components extend up to the 11th harmonic [99]. Since the fundamental harmonic is the same as the heart rate, a frequency range of O-12 Hz is required for physiological investigations at heart rates up to 120 beats/min. These limitations have been overcome by developing a fourth system which features a new pulmonary artery catheter. This is a 7F micromanometer tipped catheter (Gaeltec Ltd) which incorporates an in vivo calibration system to allow correction for zero drift 1971.This is connected to a commercially available digital ambulatory
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recorder in which the pressure wave is sampled at 16 Hz and stored in semiconductor memory. On completion of a recording, data are transferred from the ambulatory recorder via a serial data link to an Acorn Archimedes desktop computer for further data processing using custom written software [ 1191.
Results from ambulatory pulmonary artery pressure studies Pulmonary artery diastolic pressure has been used as a measure of left ventricular filling pressure to investigate coronary artery disease. This has shown that in patients with coronary artery disease during exercise and ambulatory monitoring the magnitude of ST-segment depression correlated with the rise in pulmonary artery diastolic pressure [loo]. In patients with syndrome X, pulmonary artery diastolic pressure did not rise despite ST-segment depression suggesting that syndrome X is not associated with abnormal left ventricular function [loll. Depression of ST segments during silent myocardial ischaemia was shown to be associated with a rise in diastolic pressure [102] and ambulatory pulmonary artery pressure was also used to investigate variant angina [103]. It was suggested that the pulmonary
artery diastolic pressure rose at night both in patients with normal and abnormal coronary arteries [104]. The system using a fluid filled catheter [94] has been adapted to include measurement of blood pressure and has been used to study normal subjects [ 1051. Although this study investigated only 6 subjects and does not meet the stringent criteria for normality applied by others [92], it is the only normal ambulatory study reported. During an 8 to 10-h period the subjects, mean age 28.6 yr, had an average resting pulmonary artery pressure (in mmHg (SD)) of 13.9 (1.1)/5.5 (0.9) and on submaximum exercise of 33.3 (1.7)/12.0 (0.9). These data have been compared with a study of pulmonary hypertensive patients [106]. Ambulatory pulmonary artery pressure monitoring has also been used in a small number of patients with valve disease and heart failure to guide clinical management [93]. In the only circadian study of ambulatory pulmonary artery pressure, diurnal variation of pulmonary artery pressure has been observed in patients with chronic heart failure [107]. In this study pulmonary artery pressure rose at night in all but the most severely symptomatic patients (Fig. 4). The nocturnal rise may be largely a consequence of lying down although this does not
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appear to be the only mechanism. Nocturnal elevation of pulmonary artery pressure probably also occurs in normal subjects [log]. These nocturnal pulmonary artery pressure changes are in contrast to the behaviour of systemic arterial pressure. Further studies in heart failure have examined pulmonary artery pressure changes during normal daily activities and different types of exercise testing [109]. Important differences in haemodynamic changes were observed and used to challenge the value of maximum exercise testing in chronic heart failure. Similar investigations have demonstrated a lack of effect of catheterisation itself on the pulmonary artery pressure [llOl. Reliable assessment of pulmonary artery pressure requires catheterisation. It appears to be safe and well tolerated. The principal application of long-term continuous ambulatory pulmonary artery pressure monitoring is as a research tool to investigate the natural history and pathophysiology of diseases such as coronary artery disease, heart failure, pulmonary hypertension and chronic respiratory disease. It may be used to investigate physiological and pathological variations and to assess the effects of drug therapy on central haemodynamics.
pressure has been described as “the Sunrise industry” [112]. Reference values for ambulatory blood pressures are accumulating [ 113,114] and large community-based investigations such as the PAMELA Study, planned to obtain an epidemiological evaluation of 24-h ambulatory blood pressure values, are currently underway 11151;and the technique will enable identification of patients with elevated blood pressures in the work place, during routine activity and in sleep. Although we are aware of technical limitations, in selected patients it is undoubtedly helpful in diagnosis of hypertension, and in determining progress and the therapeutic response to non-pharmacologic and drug therapies. While ambulatory monitoring should not at present be used as a routine for diagnosis of hypertension [ 1161, epidemiological studies will undoubtedly clarify whether ambulatory blood pressure and/or blood pressure may be more valuable than clinic blood pressure in predicting or revealing early blood pressure elevation. No doubt too, ambulatory blood pressure monitoring will have an increasing role as an adjunct to a number of research areas [117,118]. References
Conclusions There is much to learn about the circadian pattern of heart rate and blood pressure in normal individuals and patients with cardiovascular disease. Of particular interest is whether by drug therapy we can alter the pattern of increased myocardial ischaemia, heart attack and stroke, seen in the early morning period and whether reduction of ischaemia and better control of blood pressure will affect prognosis. Ambulatory blood pressure monitoring will no doubt play a significant role in such investigations. While intraarterial blood pressure measurement remains the “gold standard” and an important research tool with which to study pathophysiology, its use is limited. Noninvasive devices, although not entirely devoid of adverse effects, are comparatively safe [llll. Because of its increasing popularity non-invasive ambulatory monitoring of blood
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71 Delea CS. Chronobiology of blood pressure. Nephron 1979;23:91-97. 72 Raftery EB. Ambulatory blood pressure: methodological considerations. J Ambulatory Monitoring 1989;2;123-133. 73 Mancia G, Parati G. Experience with 24-hour ambulatory blood pressure monitoring in hypertension. Am Heart J 1988;116:1134-1140. 74 Hope SL, Alun-Jones E, Sleight P. Validation of the accuracy of the Medilog ABP non-invasive blood pressure monitor. J Ambulatory Monitoring 1988;1:1:39-51. 75 O’Brien E., Mee F., Atkins N., O’Malley K. Validation requirements for ambulatory blood pressure measuring systems. J Hypertens 1991;9(suppl 8):S13-S15. 76 Zachariah PK. Sheps SG, Smith RL. Clinical use of home and ambulatory blood pressure monitoring. Mayo Clin Proc 1989;63:1436-1446. 77 Zachariah PK et al. Blood pressure load - a better determinant of hypertension. Mayo Clin Proc 1989;63: 1085-1091. 78 White WB, Schulman P, McCabe EJ. Holley M, Dey MD. Average daily blood pressure monitoring. JAMA 1989;261:873-877, 79 Broadhurst P, Hughes LO, Raftery EB, Non-invasive ambulatory blood pressure monitors: a cautionary note. J Hypertension 1990;8:595-597. 80 White WB. Ambulatory blood pressure monitoring during exercise and physical activity. J Hypertens 1991;9 (suppl 8kS22-S24. 81 Weber MA. Application of ambulatory blood pressure monitoring J Ambulatory Monititoring 1989;2:1/2:135142. 82 Meyer-Sabellek W., Schulte K-L., Gotzen R. Non-invasive ambulatory blood pressure monitoring: Technical possibilities and problems. J Hypertension 1990:8(suppl 6):S3-SlO. 83 Tarazi RC. The heart in hypertension. N Engl J Med 1985;312:308-9. 84 Egger M. Bianchetti MG, Gnldinger M, Kobelt R, Oethker 0. Twenty four hour intermittent ambulatory blood pressure monitoring. Arch Dis Child 1987;62:1130-1135. 85 Fixler DE, Wallace JM, Thornton WE, Dimmitt P. Ambulatory blood pressure monitoring in hypertensive adolescents. Am J Hypertens 1990;3:288-292. 86 Brown SJ. A comparative study of hypertension in black and non-black adolescents (abstract). J Human Hypertens 1990;4;2;195. 87 Imai Y et al. Circadian blood pressure variations under different pathophysiological conditions. J Hypertens 90;8(suppl 7):S125-S132. 88 Halligan A., O’Brien E., O’Malley K. Darling M. Walshe J. Clinical application of ambulatory blood pressure measurement in pregnancy. J Hypertens 1991;9(suppl 8J:S75s77. 89 Padfield PL, Stewart MJ. Ambulatory blood pressure monitoring in secondary hypertension. J Hypertens 1991;9(suppl 8):S69-S71. 90 Cornelissen G et al. From various kinds of heart rate
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