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Reduced nocturnal fall in blood pressure, assessed by two ambulatory blood pressure monitorings and cardiac alterations in early phases of untreated essential hypertension


To investigate whether in recently diagnosed essential hypertensives a reduced nocturnal fall in blood pressure (BP), established on the basis of two 24-h ambulatory blood pressure monitorings (ABPM) is related to a greater cardiovascular damage. In all, 355 consecutive, recently diagnosed, never-treated essential hypertensives referred for the first time to our outpatient clinic were included in the study. Each patient underwent the following procedures: (1) two 24-h ABPMs performed within 3 weeks, (2) 24-h urinary collection for microalbuminuria, (3) nonmydriatic photography of ocular fundi, (4) echocardiography, (5) carotid ultrasonography. We defined nondipping profile as a night–day systolic and diastolic fall 10 % (mean of two ABPMs). A dipper BP profile was found in 238 patients, whereas in 117 patients a nondipper profile was present. The two groups were similar for age, gender, body mass index, smoking habit, clinic BP, 48-h BP and heart rate, while, by definition, night-time systolic and diastolic BP were significantly higher in nondippers than in dippers (130/81 vs 121/74 mmHg, P< 0.0001).The prevalence of left ventricular hypertrophy (LVH) defined by four different criteria: (a) LV mass index (LVMI) 125 g/m2 in both genders; (b) LVMI 134 gm2 in men and 110 in women; (c) LVMI125 g/m2 in men and 110 g/m2 in women; (d) LVMI51 g/m2.7 in men and 47 g/m2.7 in women was significantly higher in nondippers than in dippers (a: 12 vs 7%, P<0.05; b: 16 vs 7%, P<0.01; c: 20 vs 11%, P<0.01; d: 35 vs 23% P<0.02) and this finding was associated with a significant increase in aortic root and left atrium dimensions. There were no differences between the two groups in the prevalence of carotid and retinal changes and microalbuminuria. In conclusion our findings suggest that never-treated hypertensives with a reduced BP fall in the night time, defined on the basis of two ABPMs, have a higher prevalence of TOD than dippers, in terms of echocardiographic LVH. In this population setting, cardiac structural alterations are a more sensitive marker of the impact of the nocturnal BP load on cardiovascular system than other extracardiac signs of TOD.


In the last two decades, there has been an impres-sive growth in the use of 24-h ambulatory blood pressure monitoring (ABPM) for evaluation of subjects with suspected and established arterial hypertension, because the traditional measurements of BP are poorly representative of the daily BP load.1 ABPM, providing information about the diurnal BP changes associated with the sleep-wake cycle, has clearly documented that the majority of normotensive and hypertensive individuals have a marked nocturnal fall (dipping) in BP related to sleep.2,3 However, a noticeable fraction of subjects shows a blunted or even absent BP decrease at night and they have been defined as nondippers.4,5 The reduced or absent nocturnal fall has been reported in many different conditions, including essential and secondary hypertension, diabetes, renal diseases, sleep apnoea syndrome and diseases characterized by altered autonomic cardiovascular regulation.6,7,8,9 The suggestion that nondipping hypertensive patients have a higher prevalence of target organ damage (TOD) and an increased risk of cardiovascular events has been disputed. Many cross-sectional studies have demonstrated that individuals classified as nondippers show an increased frequency of different markers of TOD (left ventricular hypertrophy, carotid thickening and plaques, microalbuminuria, cerebral lacunae, cognitive deterioration)10,11,12,13,14 and of atherosclerotic cardiovascular complications.15 Other studies, however, have failed to demonstrate significant differences in cardiac and extracardiac involvement between dipper and nondipper hypertensives.16,17,18 A number of methodological problems appear to undermine the clinical significance of classifying hypertensive patients as dipper and nondipper on the basis of a single ABPM. One of the major reasons for the inability to confer an indisputable clinical value to a single quantification of the day–night difference in BP is represented by the limited reproducibility over time of this phenomenon.19,20 Therefore, the assumption that nocturnal BP profile can be defined as clinical trait on the basis of a single 24-h recording is not correct and this approximation represents a major confounding factor in evaluating TOD prevalence in dippers and nondippers. In the present study, we investigated, in a large group of never-treated essential hypertensive patients, the impact of a reduced nocturnal fall in BP, evaluated on the basis of two 24-h ABPMs, on cardiac and extracardiac TOD in the early phases of the natural history of arterial hypertension.


Patients and design

In all, 355 consecutive, never-treated hypertensive patients referred for the first time to our outpatient clinic were included in the study. They met the following inclusion criteria: (I) recent diagnosis of grade 1 or 2 hypertension (1 year ); (II) absence of secondary hypertension, congestive heart failure, previous myocardial infarction, cardiac valve diseases, of coronary bypass, diabetes mellitus, renal insufficiency and conditions preventing adequate ABPM; (III) good-quality echocardiographic and carotid ultrasonographic examinations; (IV) informed consent. All patients were subjected to the following procedures: (1) repeated clinic BP measurements; (2) blood sampling for routine chemistry examinations; (3) 24 h urine collection for microalbuminuria; (4) nonmydriatic retinography; (5) echocardiogram; (6) carotid ultrasonogram; (7) two ABPMs performed within a 3-week period (range: 7–21 days).

Clinical blood pressure measurement

BP was measured at two different visits in the outpatient clinic by a physician with a mercury sphygmomanometer (first and fifth phases of Koroktoff sounds taken as SBP and diastolic blood pressure (DBP), respectively) after the subjects had rested 5 min in the sitting position. Three measurements were taken at 1 min intervals, and the average used to define clinic systolic and diastolic BP.

Ambulatory blood pressure monitoring

The 24 h, ABPMs were carried out on the nondominant arm using a Spacelabs 90207 device (Spacelabs Inc, Richmond, WA, USA) after validation of its readings against those of a mercury sphygmomanometer by means of a Y tube. The device was set to obtain BP readings at 15 min intervals during the day (0.7:00–23:00 h) and at 20 min intervals during the night (23:00–0.7:00 h). In each patient, the time of application (+1 h), the daily activity and the type of device were the same for the two ABPMs. The patients were instructed to attend their usual day-to-day activities but to keep still at the time of measurements; all were asked to go to bed not later than 23:00 h and arise not before than 7:00 h. The BP monitorings were always performed over a working day (Monday to Friday). Each ABPM data set was first automatically scanned to remove artefactual readings according to preselected editing criteria. The recording was then analysed to obtain 24 h, daytime and night-time average SBP, DBP, heart rate and per cent nocturnal decrease of SBP and DBP. Dipping was defined as a reduction in average systolic and diastolic BP at night >10% of the average daytime BP, calculated as a mean of two ambulatory BP recordings.


M-mode, two-dimensional and Doppler echocardiographic examinations were performed using commercially available instruments (ATL HDI 3000 and 5000, Bothell, WA, USA) equipped with a 2.25 MHz imaging transducer. End-diastolic and end-systolic left ventricular internal diameter (LVIDd, LVIDs), interventricular septum thickness (IVST) and posterior wall thickness (PWT) were calculated from two-dimensionally guided M-mode tracing and measured during three to five consecutive cycles according to the Penn Convention.21 Left ventricular mass was estimated by Devereux's formula and normalized by body surface area (BSA) and by height2.7.22 LVH was defined according to four different criteria, that is when LVMI was equal or exceeded: (1) 125 g/m2 in both genders; (2) 134 g/m2 in men and 110 g/m2 in women; (3) 125 g/m2 in men and 110 g/m2 in women; (4) 51 g/m2.7 in men and 47 g/m2.7 in women.23 Patterns of left ventricular geometry were defined according to Ganau et al.24 Left ventricular systolic function was assessed by endocardial fractional shortening ((LVIDd-LVIDs)/LVIDd). Left ventricular filling was assessed by recording mitral flow by standard pulsed Doppler technique, and the following parameters were considered: early diastolic peak flow velocity (E), late diastolic peak flow velocity (A) and the ratio of the early-to-late flow velocity peaks (E/A ratio).25

Carotid ultrasonography

Images of the extracranial carotid artery walls (common, bifurcation, internal carotid arteries) were obtained in several projections by a high-resolution linear array 10 MHz probe, with the patient supine and the neck in slight hyperextension. End-diastolic intima-media thickness (IMT) of the far wall of both common carotid arteries was measured 5, 10 and 20 mm caudal to the bulb, using two-dimensional longitudinal sections of the vessel and the distance from the leading edge of the first echogenic line to the leading edge of the second echogenic line, as described by Pignoli et al26 and Salonen et al27 To obtain a mean value of common carotid IMT, all six measurements were averaged. A plaque was defined as a focal lesion 1.3 mm in any segment of either carotid artery.28 IM thickening was diagnosed when common IM thickness exceeded 0.8 mm.29 As previously reported in our laboratory, the intraobserver and the interobserver coefficients of variation for LV mass index are 7.4 and 8.6% respectively, and for common carotid IMT 9.2 and 10.1%.30,31


All subjects underwent a bilateral nonmydriatic retinography (Topcon TRC-NW3). Images were captured using an analogic camera (Topcon MT-1), set in order to obtain two photographs centred on the macula. The images, printed on professional film (Polaroid 779 High Speed Color Film ISO 640 29°), were immediately examined for quality (several photographs were taken if necessary) and were evaluated by two physicians, who had no knowledge of the patient's clinical characteristics, using the following simplified Keith–Wagener–Barker (KWB) classification:32 (I) diffuse arteriolar narrowing (an arteriovenous ratio of at least 1/2; (II) abnormal arteriovenous crossing (any degree of depression of the vein in a crossing situated at more than one papillar diameter from the papilla); (III) retinal haemorrhages or exudates.


At 24 h, urinary albumin concentration was measured by a commercially available radioimmunoassay kit (Sclavo SPA, Cinisello Balsamo, Italy). The detection limit of the method was 0.5 mg/l. Microalbuminuria was defined as a urinary albumin excretion 30 and <300 mg/24 h.

Statistical analysis

Statistical analysis was performed by the SAS System (version 6.12; SAS Institute Inc., Cary, NC, USA).Values have been expressed as means±s.d. or per cent. Mean values for dipper and nondipper patients were compared using Student's t-test for independent samples. χ2 statistics were used to compare categorical variables between groups. Correlations were obtained by using Pearson's equation. The limit of statistical significance was set at P<0.05.


On the basis of the mean nocturnal BP fall observed during two ABPMs, 238 subjects were classified as dippers (group I) and 117 as nondippers (group II). The former group included 193 patients with reproducible dipping profile and 45 variable dippers with average BP nocturnal fall >10%; the latter included 78 patients with concordant nondipping pattern and 39 variable nondippers with average BP fall <10%. Their demographic and clinical characteristics are indicated in Table 1. Age and sex distribution, heart rate, body mass index, known duration of hypertension, smoking habit, serum glucose, creatinine and total cholesterol did not differ significantly between the two groups. Clinic and ambulatory BP values are reported as the mean of two office measurements and two ABPMs, respectively. Clinic BP values were not significantly different in dippers and nondippers (147/97 vs 147/96 mmHg). Average 48 h SBP and DBP were superimposable in the two groups; however, daytime SBP and DBP were significantly higher in dippers than in nondippers, whereas night-time systolic and diastolic BP were significantly higher in nondippers.

Table 1 Demographic and clinical characteristics in dipper and nondipper hypertensives

Echocardiographic data

Left ventricular end-diastolic and systolic diameter, end-diastolic septal and posterior wall thickness, LV mass and LV mass indexed both for body surface area and height2.7 were slightly, but nonsignificantly higher in nondippers (Table 2). When LV echocardiographic data were analysed in a categorical way, as the presence or absence of altered patterns of LV structure and geometry, the prevalence of LVH was significantly higher in nondippers than in dippers. Depending on the method of LV mass indexation and the criteria used, LVH prevalence ranged from 12 to 35% in nondippers and from 7 to 23% in dippers. The lower prevalence was found in both groups using a nongender-specific partition value (>125 g/m2) and the higher prevalence was observed by using a gender-specific partition value indexed by height (>51/47 g/m2.7) (Figure 1). Regardless of the criteria used, eccentric hypertrophy was the most frequent type of LVH in nondippers and dippers. LV structural alterations in nondippers were associated with a significant increase in aortic root and left atrium dimensions. With regard to LV function, endocardial fractional shortening and early/late mitral flow velocity ratio were similar in the two groups.

Table 2 Left ventricular structure and function in dipper and nondipper hypertensives
Figure 1

Prevalence of left ventricular hypertrophy according to four different echocardiographic diagnostic criteria in dipper and nondipper hypertensive patients.

Carotid ultrasonographic data

Data of carotid studies are reported in Table 3 as means of measurements taken on both the right and the left side. The average of IM thickness of the far wall of the common carotid artery was slightly, but not significantly greater in nondippers than in dippers; the arterial lumen diameter, the relative wall thickness and the prevalence of carotid plaques were similar in both groups. A nonsignificantly higher prevalence of IM thickening was present in nondipper than in dipper hypertensives.

Table 3 Markers of extracardiac organ damage in dippers and nondippers

Retinal abnormalities and microalbuminuria

A high, similar rate of retinal vascular changes (narrowings and arteriovenous crossings) was observed in dippers and nondippers. In contrast, a low prevalence of microalbuminuria, if compared to other markers of TOD, was found in dippers and nondippers and mean urinary albumin excretion was substantially superimposable in the two groups ( Table 3).

Correlations between LV mass, clinic BP and ambulatory BP

In Table 4 are indicated the correlations between LV mass index, clinic and ambulatory BP values. Compared with clinic BP ambulatory BP was more closely related to LV mass index. The strengths of association of the LV mass index with 48 h, daytime and night-time BPs were similar.

Table 4 Correlations between LVMI, clinic and ambulatory BP in the whole population of the study

A weak but statistically significant inverse correlation was found between LV mass and the extent of the nocturnal fall in SBP (r=−0.19, P<0.01) and DBP (r=−0.16, P<0.01) LV mass index in the entire cohort of 355 hypertensives.


We have previously demonstrated in a small group of hypertensive patients that a reduced fall in BP at night persisting over time is associated with a more pronounced cardiovascular damage.33

The present study extends and refines those findings to a much larger sample of patients suggesting that a blunted nocturnal decrease in BP, diagnosed during the early phases of hypertension, is associated with a more pronounced cardiac involvement. Our results can be discussed as follows: first, absolute LV mass and LV mass index were slightly but not significantly higher in nondippers; however, when echocardiographic data were analysed in a categorical way the prevalence of LVH was significantly higher in nondippers, according to the four criteria used, this finding is probably related to the high rate of patients with normal LV mass and geometry found in our setting that may attenuate subtle, but clinically relevant differences in cardiac structure when analysed as continuous variables such as LV mass or LV mass index. The more pronounced LV damage was associated with an increased aortic root and left atrium dimensions but not with other markers of TOD, such as carotid structural changes, retinopathy and microalbuminuria. This evidence, besides showing the impact of reduced nocturnal fall in BP in the development of TOD in a selected population of young and middle-aged subjects with newly diagnosed essential hypertension, also gives some indications about the sensitivity and usefulness of different markers of TOD. Unlike LVH, an extremely high prevalence of grade 1–2 retinal alterations at nonmydriatic retinography, such as narrowings or arteriovenous crossing, was observed in dippers and nondippers. If considered a marker of TOD, these retinal abnormalities would identify almost two-thirds of patients as high-risk hypertensives. On the basis of these data, grade I and II alterations should not be considered among the criteria for a precise detection of TOD. On the other hand, the marginal prevalence of both common carotid IM thickening and microalbuminuria in this population suggests that these two markers, respectively, of vascular involvement and of intrarenal vascular dysfunction, may be less sensitive than echocardiography in this clinical setting. Secondly, the dipper and nondipper individuals did not differ with regard to age, gender, BMI, smoking habit, known duration of hypertension, clinic and average 24 and 48 h BP levels, and consequently, the more prominent cardiac alterations found in nondippers cannot be referred to higher overall BP load or to different confounding factors. Thirdly, the present study differed substantially from all previous studies investigating the relation between nocturnal BP profile and cardiovascular structure in that dipper and nondipper hypertensives were identified on the basis of two ABPMs consecutively carried-out over a short-term period (three weeks), using a definition of a fall <10% in SBP and DBP,34 calculated as a mean value of 48 h BP recording. Therefore, it is more likely, in these two particularly selected groups, including patients with reproducible nocturnal pattern, variable dippers with average BP fall >10% and variable nondippers with average fall <10%, that the more or less pronounced decrease in BP during the night time represents, with reasonable approximation, a true clinical trait. This latter point appears to be a fundamental issue, because the classification of hypertensive patients into dippers and nondippers on the basis of a single ambulatory BP monitoring has a limited reproducibility over time both in the absence and presence of drug treatment.19,20,35,36 In the present study, we found a different short-term variability in circadian BP according to the nocturnal profile observed in the first recording, being significantly greater in patients classified at first ABPM as nondippers (30%) than in dippers (9%). Accordingly to this finding the assumption that one single ABPM can provide a reliable classification of the patients into dippers or nondippers needs to be reconsidered. In fact, the increasing evidence for the poor reproducibility of nocturnal BP profile suggests that in a large fraction of patients the nondipping pattern cannot be considered as a definite clinical trait. Some other aspects of our study deserve mention. Several studies have investigated the potential impact of a reduced nocturnal fall in BP on cardiovascular structure and function in long-standing essential hypertensives, reaching controversial conclusions. Likewise, the few studies addressed to assess specifically both cardiac and extracardiac TOD in never-treated newly diagnosed patients showed discordant results. Some authors demonstrated that the nondipping status was associated with greater LVH or LV remodelling and LV diastolic abnormalities, increased carotid structural alterations, such as IM thickenings and carotid plaques,11,37 whereas other studies failed to demonstrate any significant difference in LV and carotid structure among dippers and nondippers.17,38 These conflicting results may be ascribed to many different factors. The classification into dippers and nondippers based on the single ABPM, used in all the above-mentioned studies, represents, probably, one of the major confounding factor, causing an inaccurate selection of nondippers. Furthermore, it has been suggested that the greater prevalence of cardiac structural and functional alterations found by some studies in nondippers may not be related to an abolished or reduced nocturnal fall in BP per se, but to higher BP values over 24 h; this observation may also be extended to carotid abnormalities. To avoid some of these potential confounding variables, we compared two homogenous groups, with similar demographic, metabolic, clinic, and 24 and 48 h BP values, that differ only by the extent of the nocturnal fall, assessed by two ambulatory BP recordings. Our results indicate that the nocturnal BP behaviour is relevant in the cardiovascular remodelling, and particularly in determining the early cardiac morphological changes, independent of the overall BP load, that was similar in dippers and nondippers. This finding was in part supported by the significant inverse correlation between LV mass and the extent of decrease in night-time BP in the whole population. A brief final comment regards the pathophysiological relation between a reduced nocturnal BP decline and TOD. In hypertensive patients, nondipping has been attributed to an imbalance between sympathetic and parasympathetic drive,39 that results in a predominance of pressor over depressor influences during the night. On the other hand, in long-standing hypertension, the presence of structural vascular alterations may contribute to a blunted BP nocturnal fall.40 Furthermore, some experimental data indicate that, in rats, LVH could be caused by elevating BP level only during sleep, and could be reduced by giving an ACE-inhibitor during the sleep period.41 Thus, it is reasonable to think that hypertensives who maintain over time a relatively elevated BP in the night develop more extensive cardiovascular damages than those who markedly reduce their BP during sleeping hours.

In conclusion, we suggest that: (1) a blunted nocturnal fall in BP, persisting over time, may have a relevant and independent role in the development of cardiac structural abnormalities during the early phase of essential hypertension, despite the fact that nondipper hypertensives have similar clinic and 48 h BP levels compared to dippers and (2) the nondipping status, in this clinical setting, can be considered a risk factor for LVH.


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Cuspidi, C., Michev, I., Meani, S. et al. Reduced nocturnal fall in blood pressure, assessed by two ambulatory blood pressure monitorings and cardiac alterations in early phases of untreated essential hypertension. J Hum Hypertens 17, 245–251 (2003).

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  • nondippers
  • ambulatory blood pressure monitoring
  • cardiac structure


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