ORIGINAL ARTICLE. Introduction. Materials and methods

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1 Journal of Human Hypertension (1999) 13, Stockton Press. All rights reserved /99 $ ORIGINAL ARTICLE Value of ambulatory intra-arterial blood pressure monitoring in the long term prediction of left ventricular hypertrophy and carotid atherosclerosis in essential hypertension RS Khattar, R Senior, JD Swales and A Lahiri Department of Cardiac Research, Northwick Park and St. Mark s Hospital NHS Trust and Institute for Medical Research, Harrow, Middlesex, UK The aim of this study was to compare the abilities of clinic and ambulatory blood pressure (BP) to predict the long term occurrence of left ventricular hypertrophy and carotid atherosclerosis in uncomplicated hypertensive patients. Two hundred and ninety-five patients who had undergone 24-h ambulatory intra-arterial BP monitoring on the basis of an elevated clinic BP, attended followup at a mean of 10.2 (±3.5) years later. This consisted of a history, physical examination, risk factor profile and serum cholesterol level. Echocardiography and carotid ultrasonography were also performed to determine left ventricular mass index and maximal intima-media thickness (IMTmax), a measure of carotid atherosclerosis severity. The factors most strongly correlated with both left ventricular mass index and IMTmax were age, 24-h mean pulse pressure and 24-h mean. Age, 24-h mean and body mass index were independent correlates of left ventricular hypertrophy (R 2 = 17%), whereas age, 24-h mean pulse pressure and pack years were independent predictors of carotid atherosclerosis (R 2 = 34%). Clinic BP did not feature in the final model for the long term prediction of cardiovascular end-organ damage. These findings promote a role for ambulatory BP monitoring in guiding aggressiveness of drug therapy in an attempt to limit potential target organ damage. Keywords: ambulatory blood pressure; left ventricular hypertrophy; carotid atherosclerosis Introduction The importance of clinic-based measurements of systolic and diastolic pressure (SBP/DBP) as determinants of cardiovascular morbidity and mortality 1,2 has long been recognised, but the relationship with target organ damage is less consistent. 3 Twenty-four hour ambulatory blood pressure (BP) monitoring offers a more valid assessment of an individual s true BP by taking frequent readings during routine daily activities. 4 Consequently, cross-sectional studies have generally shown ambulatory BP to be a better indicator of target organ damage than clinic BP measurements. 5 However, longitudinal data comparing the abilities of clinic and ambulatory BP to predict subsequent cardiovascular end-organ damage are limited. In a preliminary study by our group, ambulatory pulse pressure was found to be strongly correlated with the long term hypertrophic changes of the left ventricular myocardium (left ventricular mass index) and carotid arteries. 6 However, the pres- Correspondence: Dr A Lahiri, Cardiology Department, Northwick Park Hospital, Watford Road, Harrow, Middlesex, HA1 3UJ, UK Received 20 February 1998; revised 15 July 1998; accepted 17 July 1998 ence or absence of manifest left ventricular hypertrophy was not assessed and atherosclerotic changes of the carotid arteries were not evaluated. Left ventricular hypertrophy and carotid atherosclerosis are important forms of target organ damage as they both confer an increased risk of subsequent cardiovascular events. 7,8 In otherwise uncomplicated patients, they may therefore be considered surrogate end-points of overt cardiovascular disease. In the present study on a larger group of patients, we hypothesised that ambulatory BP monitoring may be better able to predict the long term occurrence of left ventricular hypertrophy and carotid atherosclerosis compared to isolated clinic BP measurements, in hypertensive patients without manifest cardiovascular disease. A comparison of demographic characteristics, ambulatory and clinic BP data and BP control in those with and without left ventricular hypertrophy and carotid atherosclerosis was also made. Materials and methods The hypertension database in our institution consists of 723 patients who had undergone 24-h intraarterial BP monitoring within the period 1st January 1979 to 1st January All were originally

2 112 referred for the management of hypertension based on a persistently elevated clinic SBP 140 mm Hg and/or a clinic DBP 90 mm Hg taken over a period of weeks to months in a primary care setting. At the initial hospital visit, BP was measured by a nurse or technician with the patient resting for 5 10 min in the supine position. Those in whom clinic BP was elevated were requested to undergo 24-h intraarterial ambulatory BP monitoring within 2 months thereafter, to aid diagnostic evaluation. Antihypertensive medication had either not been started or had been withdrawn in the 8 weeks preceding intraarterial BP monitoring. Baseline clinic BP was taken as the mean of two or more readings at separate visits, in the 4 weeks prior to or after the intra-arterial study. Secondary causes of hypertension were excluded, as far as possible, in all patients by measurement of serum urea, creatinine and electrolytes, urinary catecholamines, chest X-ray and more recently intravenous renal digital subtraction angiography. Patients with secondary hypertension or a history of overt cardiovascular disease manifesting as coronary heart disease, peripheral vascular disease or cerebrovascular disease were excluded. Written informed consent was obtained prior to ambulatory intra-arterial BP monitoring. General practitioners were informed of the results of the test and antihypertensive therapy was commenced if considered appropriate on clinical grounds. Subsequent assessment of BP control and treatment was largely left to the individual general practitioners and based on clinic BP measurements in keeping with standard clinical practice. Follow-up Active follow-up was performed during an 18- month period from 1994 to Of the 723 patients, 96 patients had died (data from the National Health Service Central Register, Southport, UK), 226 patients failed to respond to two written communications and the remaining 401 patients attended for follow-up re-evaluation. This consisted of a full history, physical examination, clinic BP measurement on usual medication, risk factor profile, blood urea, serum electrolytes and creatinine estimation, total cholesterol level, echocardiography and carotid ultrasonography. Of these 401 patients, 106 were excluded from the analysis as follows: 70 gave a history of interim ischaemic heart disease, heart failure or cerebrovascular disease and two had significant valvular disease, factors that may have confounded the relationships between baseline BP measurements and subsequent left ventricular mass and carotid artery structure; 11 had wall motion abnormality suggestive of underlying ischaemic heart disease and 23 had inadequate echocardiographic or carotid ultrasound images. Therefore, data from a total of 295 patients was obtained in this study. Intra-arterial blood pressure monitoring The technique of intra-arterial BP recording used in this laboratory has been well documented 10 as has the method of analysis. 11 BP was recorded from a fine brachial artery cannula using a specially designed transducer/perfusion unit and an Oxford Medilog Mark I tape recorder. The equipment was designed so that patients were fully ambulant and able to carry out their normal daily activities. The 24-h tape recordings were analysed on a custombuilt hybrid computer, using a program which calculated mean hourly BP and heart rate. Mean systolic and diastolic intra-arterial BPs were calculated by averaging the 24-hourly systolic and diastolic readings. The daytime period was defined as the time interval between 6 am and 10 pm and the night-time period as that between 10 pm and 6 am. Non-dippers were arbitrarily defined as those who did not exhibit a reduction in mean systolic and by at least 10% from day to night, and the remaining subjects were classified as dippers. Echocardiography All subjects underwent M-mode and two-dimensional echocardiography performed by the same investigator using a commercially available machine (ATL Ultramark 9 HDI CV, Bothell, WA, USA) with a 2 3 MHz broad band transducer. Left ventricular dimensions were obtained from two-dimensionally guided M-mode tracings according to the recommendations of the American Society of Echocardiography 12 and left ventricular mass index (LVMI) was calculated using the anatomically validated formula below. 13 LVMI = 0.8 {1.04 [(LVEDD + PWT + IVST) 3 LVEDD 3 ] 13.6} body surface area g/m 2 where LVEDD is the left ventricular end-diastolic diameter, PWT the end-diastolic posterior wall thickness and IVST the end-diastolic interventricular septal thickness. Left ventricular hypertrophy was considered present if LVMI was at least 125 g/m 2 for men and 110 g/m 2 for women. Carotid ultrasonography Both carotid arteries were imaged in all subjects using the high resolution Kontron Sigma 44 ultrasound system equipped with a mechanical sector probe with a 7.5 Mhz annular imaging transducer providing an axial resolution of 0.15 mm. The scan converter enabled freezing of the images during scanning and distance measurements were made using software-driven cursors with digital display to 0.1 mm. The mid- and distal common carotid artery, carotid bulb and proximal portions of the internal and external carotid arteries were systematically interrogated in short axis and long axis views for the detection of atherosclerotic plaque formation. A plaque was defined as a distinct area with an intimamedia thickness at least 50% greater than that of the adjacent wall 14 and the maximal intima-media thickness measurement (IMTmax) was used as a

3 semi-quantitative score for carotid atherosclerosis severity. In the absence of atheroma, the intimamedia thickness of the far wall of the distal common carotid artery was taken as IMTmax. Analysis and reproducibility of left ventricular and carotid artery measurements Carotid artery measurements were performed online by a single operator (RSK), blinded to the BP findings. Left ventricular measurements were obtained by off-line analysis of the echocardiographic images by the same observer on a separate day. The echocardiographic studies were similarly performed without prior knowledge of the BP data and analysed in random order of patients. To assess serial intra-observer reproducibility of LVMI and IMTmax measurements, 30 patients underwent echocardiography and carotid ultrasonography on two separate occasions within a period of 2 weeks. The single determination standard deviation (s.d.) method was used for this purpose 15 and revealed co-efficients of variation of 14% and 11% for LVMI and IMTmax, respectively. Statistical analysis The clinical variables analysed included age, gender, body mass index, serum cholesterol and pack years of smoking. BP data consisted of initial clinic systolic, diastolic and pulse pressure, 24-h mean, daytime mean and night-time mean systolic and diastolic intra-arterial BP, 24-h mean pulse pressure and non-dipper status. Hourly standard deviations of ambulatory systolic and reflecting long term BP variability were also included in the analysis. Echocardiographic and carotid ultrasound parameters included LVMI and IMTmax, respectively. Spearman s rank correlation coefficients relating clinical and BP variables to LVMI and IMTmax were calculated, with respective P values testing whether there was a significant difference from zero. A comparison of those with and without manifest left ventricular hypertrophy and carotid atherosclerosis was performed using two sample t-tests. Stepwise logistic regression analysis using both forward and backward variable selection was performed to determine the independent predictors of left ventricular hypertrophy and IMTmax. Continuous variables were expressed as mean (±s.d.) and a P value 0.01 was considered statistically significant. Results A total of 295 patients were investigated of whom 161 were male and 134 female, with a mean age of 58.2 (±11.1) years and a mean follow-up period of 10.2 (±3.5) years. The group consisted of 220 Caucasians, 53 Asians and 22 Afro-Caribbean subjects with body mass index of 26.5 (±4.4) kg/m 2 and serum total cholesterol of 5.6 (±1.0) mmol/l. A positive smoking history was given by 129 patients (35 were current smokers) and 15 patients had diabetes mellitus. Antihypertensive medication was being taken by 90% of the study group, of whom 54% were on monotherapy and 46% were taking at least two drugs. One hundred and twenty-one patients were being treated with calcium antagonists, 105 were on ACE-inhibitors and 88 were taking betablockers; diuretics were administered to 87 patients and 12 patients were prescribed other classes of antihypertensive drugs. Haemodynamic data Table 1 summarises the initial and follow-up clinic BP measurements and results of 24-h intra-arterial BP monitoring for the study population. These support the general rule that clinic BP measurements tend to be higher than those during ambulatory BP monitoring. 16 In addition, follow-up clinic systolic and s were significantly lower than the initial clinic readings (P 0.001). Notably, 248 patients were classified as dippers and 47 as nondippers. Blood pressure control and target organ damage BP control was assessed by comparing baseline and follow-up clinic BPs of the study patients. Table 2 summarises the reductions in clinic BP from baseline to follow-up in those with and without left ventricular hypertrophy and carotid atherosclerosis, respectively. Table 3 compares the amount of antihypertensive treatment being taken by these four groups of patients at follow-up. Notably, there were significant reductions in clinic systolic and diastolic BPs from baseline to follow-up in all four groups of patients with and without left ventricular hypertrophy and carotid atherosclerosis (P 0.001). The reductions in clinic systolic and in the groups with and without left ventricular hypertrophy were similar despite more intensive antihypertensive treatment in the group with left ventricular hypertrophy. With respect to carotid atherosclerosis, there was a similar decrease in clinic in those with and without carotid atherosclerosis (15 ± 33 mm Hg vs 14 ± 20 mm Hg, respectively; P = NS), but a significantly greater reduction in DBP in the Table 1 Summary of ambulatory BP parameters Variable Mean ± s.d.(mm Hg) Initial clinic 166 ± 20 Initial clinic 101 ± h mean ± 19.7 Daytime ± 19.9 Night-time ± h mean 90.0 ± 13.0 Daytime 95.3 ± 13.3 Night-time 78.3 ± h mean pulse pressure 62.5 ± 12.2 Standard deviation of hourly mean 17.8 ± 5.8 Standard deviation of hourly mean 12.5 ± 4.1 Follow-up clinic 152 ± 23 Follow-up clinic 92 ± 11 BP = blood pressure. 113

4 114 Table 2 Reductions in clinic BP, from baseline to follow-up, in those with and without left ventricular hypertrophy and carotid atherosclerosis LVH No LVH P value (n = 95) (n = 200) Systolic BP reduction (mm Hg) 11 ± ± 26 NS Diastolic BP reduction (mm Hg) 10 ± 16 9 ± 16 NS Atheroma No atheroma P value (n = 134) (n = 161) Systolic BP reduction (mm Hg) 15 ± ± 20 NS Diastolic BP reduction (mm Hg) 12 ± 18 7 ± LVH = left ventricular hypertrophy; BP = blood pressure; NS = not significant. Table 3 Antihypertensive treatment in those with and without left ventricular hypertrophy and carotid atherosclerosis Antihypertensive treatment (%) Nil Monotherapy Multiple therapy Left ventricular hypertrophy No left ventricular hypertrophy Carotid atherosclerosis No carotid atherosclerosis group with carotid atherosclerosis (12 ± 18 mm Hg vs 7 ± 13 mm Hg, respectively; P = 0.003). A greater proportion of patients with carotid atherosclerosis were taking multiple antihypertensive drugs compared to those without carotid atherosclerosis. Relationship between clinical and haemodynamic parameters, left ventricular hypertrophy and carotid atherosclerosis Correlation coefficients, relating clinical data, clinic BP measurements and ambulatory BP parameters to LVMI and IMTmax are listed in Table 4. The factors most strongly correlated with both LVMI and IMTmax were age, 24-h mean pulse pressure and 24- h mean, daytime mean and night-time mean SBP. Initial clinic SBP also had a significant, but weaker positive association with LVMI and IMTmax. Gender, body mass index, serum cholesterol, initial clinic and ambulatory diastolic pressures and non- Table 4 Spearman s rank correlation coefficients relating clinical and haemodynamic data to left ventricular mass index and IMTmax* Clinical variables LVMI IMTmax Age Pack years of smoking Initial h mean Daytime Night-time Initial pulse pressure h mean pulse pressure LVMI = left ventricular mass index, BP = blood pressure. *P except correlation between pack years of smoking and LVMI (P = NS). dipper status were not significantly correlated with either left ventricular mass index or IMTmax. Left ventricular hypertrophy was present in 95 patients and carotid atherosclerotic plaques were detected in 134; 52 patients had evidence of both left ventricular hypertrophy and carotid atherosclerosis, and 118 patients had neither. Age, body mass index and all measures of baseline clinic and ambulatory BP, particularly systolic and pulse pressure were significantly greater in those with left ventricular hypertrophy compared to those without left ventricular hypertrophy (Table 5). With respect to carotid atherosclerosis, age, pack years of smoking and baseline clinic and ambulatory systolic and pulse pressures were significantly greater in the group of patients with carotid atherosclerosis (Table 6). In contrast to the relationship with left ventricular hypertrophy, there were no significant differences in clinic or ambulatory s between those with and those without carotid atherosclerosis. Table 5 Clinical and haemodynamic data comparing those with and without manifest left ventricular hypertrophy with respective P values LVH present LVH absent P value (n = 95) (n = 200) Age (years) 64.8 ± ± Body mass index 27.2 ± ± (kg/m 2 ) Cholesterol (mmol/l) 5.7 ± ± 0.9 NS Pack years of smoking 8.1 ± ± 12.1 NS Initial ± ± Initial ± ± Initial pulse pressure 68.8 ± ± h mean ± ± Daytime mean ± ± Night-time mean ± ± h mean diastolic 92.7 ± ± BP Daytime mean 97.9 ± ± Night-time mean 80.5 ± ± h mean pulse 69.0 ± ± pressure BP = blood pressure, LVH = left ventricular hypertrophy, NS = not significant.

5 Table 6 Clinical and haemodynamic data comparing those with and without carotid atherosclerosis with respective P values Atherosclerosis Atherosclerosis P value present absent (n = 134) (n = 161) Age (years) 63.4 ± ± Body mass index 26.1 ± ± 4.4 NS (kg/m 2 ) Cholesterol (mmol/l) 5.7 ± ± 1.0 NS Pack years of smoking 10.7 ± ± Initial ± ± Initial ± ± 10.3 NS Initial pulse pressure 68.9 ± ± h mean ± ± Daytime mean ± ± Night-time mean ± ± h mean diastolic 90.0 ± ± 12.4 NS BP Daytime mean 95.2 ± ± 12.9 NS Night-time mean 78.2 ± ± 13.4 NS 24-h mean pulse 66.8 ± ± pressure BP = blood pressure, NS = not significant. Multivariate analysis The variables analysed included clinical parameters and BP data, initially using systolic and diastolic BPs and then replacing DBP with pulse pressure. In this setting, age, 24-h mean SBP and body mass index were independent correlates of left ventricular hypertrophy (R 2 = 17%), whereas age, 24-h mean pulse pressure and pack years were independent predictors of carotid atherosclerosis (R 2 = 34%). It is, therefore, notable that the average BP level over a 24-h period was a better predictor of target organ damage than either daytime or night-time BP. Furthermore, clinic BP was not an independent predictor of either left ventricular hypertrophy or carotid atherosclerosis. Discussion The results of our study showed that age, ambulatory SBP and body mass index were independent predictors of left ventricular hypertrophy, whereas age, ambulatory pulse pressure and pack years of smoking were independently associated with carotid atherosclerosis. Notably baseline clinic BP bore no independent relationship with either of these surrogate end-points. It is perhaps not surprising that the systolic component of BP was the only independent haemodynamic predictor of left ventricular hypertrophy, as end-systolic stress is the principal factor which raises left ventricular mass and is largely governed by SBP. However, haemodynamic and clinical parameters could only account for 17% of the variability of left ventricular hypertrophy in our model and this suggests that other independent mechanisms may also influence cardiac structure. Notably, genetic and hormonal factors appear to be important in determining cardiac and vascular hypertrophy in humans. 20 The pulsatile component of BP was the major haemodynamic determinant of carotid atherosclerosis severity. An increase in pulse pressure is common with advancing age as a result of increased aortic stiffening and this latter manifestation raises systolic pressure and reduces diastolic pressure at any given mean arterial pressure. 21 It is possible that the greater reduction in clinic DBP in the group with carotid atherosclerosis was not only an effect of antihypertensive treatment, but also a manifestation of stiffened atherosclerotic arteries. A previous report showed pulse pressure to be independently related to carotid intima-media thickness; 22 abnormalities of carotid artery structure and differences in distending pressure between hypertensives and control subjects that may account for alterations in vascular stiffness have also been demonstrated. 23 Although it is not clear whether elevated pulse pressure is a causative factor or merely a manifestation of atherosclerotic disease, recent studies have shown that a wide pulse pressure may be associated with left ventricular hypertrophy, 24 carotid artery stenosis 25 and an increased incidence of cardiovascular events, 26 particularly myocardial infarction. 27 Other variables that have been shown to contribute to carotid atherosclerosis include plasma concentrations of high density lipoprotein cholesterol, uric acid and fibrinogen. 28,29 The intra-arterial method of ambulatory BP monitoring was adopted not only because it provides the most authentic measurement of BP, but also because of a lack of properly validated automated non-invasive monitors for 24-h BP assessment at the commencement of the study. Indeed, this direct method of BP measurement has since been used as the reference standard by which non-invasive monitors have been validated. 30 Aside from its invasive nature, intra-arterial BP monitoring has the advantage of providing continuous beat to beat BP recordings in truly ambulant patients. In contrast, non-invasive auscultatory and oscillometric monitors rely on intermittent recordings at predetermined time intervals; these may not be accurate during unrestricted physical activity as they require the cuff arm to be completely still during measurement. For ethical reasons, intra-arterial ambulatory BP monitoring was not repeated in the study population to assess BP control or influence further management. BP management during the follow-up period was largely based on clinic BP readings as part of standard clinical practice, BP reductions from baseline to follow-up were relatively similar in those with and without target organ damage. Given the independent longitudinal association of pre-treatment ambulatory BP parameters to cardiovascular complications (which was not seen with clinic BP), greater attention to ambulatory BP data may prove more effective in the long term management of hypertension. These findings promote a role for ambulatory BP monitoring in identifying those patients who may be in need of closer supervision and possibly more aggressive medical therapy in an attempt to reduce the risk of future cardiovascular 115

6 116 complications. Interestingly, the independent relationship between ambulatory BP and target organ damage was present despite interim drug therapy in the majority of patients. Since antihypertensive treatment could only have served to weaken this relationship, it is possible that the true association may have been even stronger and therefore its value in the management of high risk patients conceivably even greater. Given the lack of widespread availability of ultrasound technology at the beginning of this study, echocardiography and carotid ultrasonography were not performed when intra-arterial BP monitoring was undertaken at the initial evaluation. Therefore it is not possible to know with certainty how LVMI and maximal carotid intima-media thickness may have altered between the initial and follow-up examinations. Nonetheless, since age is an established and strong determinant of both left ventricular mass and carotid intima-media thickness, it is very likely that these parameters increased with time. Acknowledgements This study was supported by an educational grant from the Northwick Park Hospital Cardiac Research Fund. We gratefully acknowledge the advice and support of the late Dr EB Raftery and the statistical services of Caroline Dore. References 1 Breslin DC, Gifford RW, Fairbairn JF II. Essential hypertension. A 20 year follow-up study. Circulation 1996; 33: Kannel WB. Role of blood pressure in cardiovascular morbidity and mortality. Progr Cardiovasc Dis 1974; XVII(1): Bauwens FR et al. Influence of the arterial blood pressure and nonhemodynamic factors on left ventricular hypertrophy in moderate essential hypertension. Am J Cardiol 1991; 68: Pickering TG. Blood pressure measurement and detection of hypertension. Lancet 1994; 344: Clement DL, De Buyzere M, Duprez D. Prognostic value of ambulatory blood pressure monitoring. J Hypertens 1994; 12: Khattar RS et al. Longitudinal association of ambulatory pulse pressure with left ventricular mass and vascular hypertrophy in essential hypertension. J Hypertens 1997; 15: Koren MJ et al. Relation of left ventricular mass and geometry to morbidity and mortality in men and women with uncomplicated essential hypertension. Ann Intern Med 1991; 114: Salonen JT, Salonen R. Ultrasound B-mode imaging in observational studies of atherosclerotic progession. Circulation 1993; 87 (Suppl 3): Acharya DU, Heber ME, Dore CJ, Raftery EB. Ambulatory intra-arterial blood pressure in essential hyppertension: effects of age, sex race and body mass The Northwick Park Hospital Database Study. Am J Hypertens 1996; 9: Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood pressure. Lancet 1978; 1: Cashman PM, Stott FD, Millar-Craig MW. Hybrid system for fast data reduction of long-term blood pressure recordings. Med Biol Eng Comput 1979; 17: Sahn DJ, DeMaria A, Kisslo J, Weymen A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978; 58: Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass index in man: anatomic validation of the method. Circulation 1977; 55: Salonen R, Seppanen K, Ravramara R, Salonen JT. Prevalence of carotid atherosclerosis and serum cholesterol levels in Eastern Finland. Arteriosclerosis 1988; 8: Chinn S. Repeatibility and method comparison. Thorax 1991; 46: Harshfield GA, Pickering TG, James GD, Blank SG. Blood pressure variability and reactivity in the natural environment. In: Meyer-Sabellek W, Anlauf M, Gotzen R, Steinfeld L (eds). Blood pressure measurements: new techniques in automatic and 24 hour indirect monitoring. Springer-Verlag: New York, 1990; pp Verhaaren HA et al. Bivariate genetic analysis of left ventricular mass and weight in pubertal twins (The Medical College of Virginia Study). Am J Cardiol 1991; 68: Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Circulation 1991; 83: Bohm RO et al. A long term study of catecholamine levels and plasma renin activity in borderline hypertension. J Hypertens 1987; 5: Castellano M et al. Angiotensin converting enzyme I/D polymorphism and arterial wall thickness in a general population. Circulation 1995; 91: Safar ME. Pulse pressure in essential hypertension: clinical and therapeutical implications. J Hypertens 1989; 7: Suurkula A et al. Ultrasound evaluation of atherosclerotic manifestations in the carotid artery in high-risk hypertensive patients. Risk Intervention Study (RIS) group. Arteriosclerosis and Thrombosis 1994; 14(8): Roman MJ et al. Parallel cardiac and vascular adaptation in hypertension. Circulation 1992; 86: Pannier B et al. Pulse pressure and echocardiographic findings in essential hypertension. J Hypertens 1989; 7: Sutton-Tyrell K et al. Predictors of carotid stenosis in older adults with and without isolated systolic hypertension. Stroke 1993; 24: Darne B et al. Pulsatile versus steady component of blood pressure: a cross-sectional analysisand a prospective analysis on cardiovascular mortality. Hypertension 1989; 13: Madhavan S, Ooi W, Cohen H, Alderman MH. Relation of pulse pressure and blood pressure reduction to the incidence of myocardial infarction. Hypertension 1994; 23: Crouse JR et al. Risk factors for extracranial carotid artery atherosclerosis. Stroke 1987; 18: Joensuu T et al. Determinants of femoral and carotid artery atherosclerosis. J Int Med 1994; 236: Casadei R et al. 24 hour blood pressure monitoring: evaluation of Spacelabs 5300 monitor by comparison with intra-arterial blood pressure recording in ambulant subjects. J Hypertens 1988; 6:

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