Risk stratification of left ventricular hypertrophy in systemic hypertension using noninvasive ambulatory blood pressure monitoring

SYSTEMIC HYPEBTENSION

Risk Stratification of Left Ventricular Hypertrophy in Systemic Hypertension Using Noninvasive Ambulatory Blood Pressure Monitoring Paolo Verdecchia, MD, Giuseppe Schillaci, MD, Francesca Boldrini, MD, Massimo Guerrieri, MD, Camille Gatteschi, MD, Guglielmo Benemio, MD, and Carlo Porcellati, MD

Twenty-four-hour noninvasive ambulatory blood pressure (BP) monitoring and echocardiography were performed in 165 consecutive untreated hypertensive patients and in 92 healthy subjects. In the hypertensive group, left ventricular (LV) mass index showed closer correlations (all p
From the Division of Medicine, Civic Hospital “Beat0 G.Villa,” CittS della Pieve, Perugia, Italy. Manuscript received February 7. 1990: revised manuscript received and accepted April 26. 1990. Address for reprints: Paolo Verdecchia, MD, Civic Hospital “Beat0 G. Villa,” Division of Medicine, Hypertension Unit, 06062 Citta della Pieve, Perugia, Italy.

asual blood pressure (BP) 1.7 and electrocardiographic left ventricular (LV) hypertrophy’,” are well known independent predictors of cardiovascular morbidity and mortality. Recent evidence suggests that noninvasive ambulatory BP readings may be superior to casual BP readings in predicting future cardiovascular events.5,6 In fact, when comparing hypertensive patients with observed ambulatory BP above versus below a definite limit with respect to their predicted ambulatory BP levels (obtained by regressing ambulatory BP values on casual BP values), those with BP above a definite limit had a greater long-term incidence of fatal and nonfatal events.s.h These results have been substantially confirmed using intraarterial BP monitoring.7 Because ambulatory rather than casual BP is more closely related to LV mass,*-” one reason for the ability of ambulatory BP readings to discriminate between high- and low-risk subjects may be the identification of subsets of patients with different degrees of echocardiographic LV hypertrophy, an independent risk marker,12-I5 who would be in the same risk group if only casual BP and electrocardiography were used. To clarify the relations between casual BP, ambulatory BP and LV structure in the light of such epidemiologic findings, we studied a large group of hypertensive patients and control subjects using noninvasive ambulatory BP monitoring and echocardiography.

C

METHODS Patients: We studied 165 patients with essential hypertension (47% women) and 92 healthy normotensive subjects (50% women). They were consecutively chosen among patients with essential hypertension and healthy normotensive subjects examined in our laboratory from 1986 to 1989, partly included in a previous study on the effects of nocturnal BP reduction on LV mass,” and meeting all the following criteria: (1) no antihypertensive drugs for 24 weeks; (2) good quality echocardiographic tracings; (3) agreement within 5 mm Hg between BP recording unit and mercury sphygmomanometer in 13 consecutive measurements obtained simultaneously on the same arm before beginning ambulatory BP recording; and (4) absence of clinical, electrocardiographic or echocardiographic evidence of coronary or valvular disease, renal disease, transient cerebral ischemit attacks or stroke. In the hypertensive group, supine diastolic BP had to be 290 mm Hg in >-3 visits at

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TABLE

I Main

Findings

in the

Study

Population

Variables Age (wars) Height (cm) Weight (kg) BSA (m2) Casual BP (mm Hg) Systolic Diastolic Average 24hour BP (mm Hg) Systolic Diastolic Heart rate (beats/min) Casual Average 24hour Enddiastolic IVS thickness (cm) End-diastolic PW thickness (cm) LVenddiastolic diameter (cm) Shortening fraction (%) LV mass (g) LV mass index (g/mZ) Relative wall thickness Cross-sectional area (cma) Cross-sectional area index (cm2/mz) Data expressed as mean f standard deviation. BP = blood pressure; BSA = body surface area; IVS = lnterventrvzular

Normotensive Subjects (n = 92)

Hypertensive Patients (n = 165)

50(14) 168 (8) 73 (12) 1.80 (0.2)

52(12) 166 (9) 75 (14) 1.83 (0.2)

136 (13) 80 (7)

159(18) 98 (7)

119.1 411.2

<00001
123 (13) 79 (8)

142(16)

84.1 144.9


73 (10) 73 (6) 0.79 (0.2) 0.71(0.1) 5.29 (0.6) 4-O (7) 139 (46) 77 (23) 0.27 (0.07) 14.2 (3.6) 7.9(1.9)

76(12) 76 (8) 0.96 (0.3) 0.82 (0.2) 5.28 (0.7) 38 (7) 175 (69) 95 (34) 0.31 (0.08) 17.4(5.3) 9.5 (2.6)

septum;

LV = left ventricular;

pr0eedul-W

BLOOD

PRESSURE

MEASURE-

Clinical BP was measured after 10 minutes of supine rest by using a Hawksley Random Zero manometer (phase I and V) (Hawksley and Sons, Ltd, Lancing, West Sussex, England), with deflation rate fixed at 2 mm Hg/beat. Ambulatory BP was recorded by using the fully automatic units ICR 5200 and 90202 (Spacelabs, Redmond, Washington). In our laboratory, the ICR 5200 unit showed a correlation of 0.97 with both systolic and diastolic pressures measured simultaneously

II

Ventricular

Relations

of Casual

and

Average

24-Hour

0.2 0.6 0.4 0.3

5.8 11.4 22.8 25.8 0.001 3.5 20.4 21.6 18.4 25.3 25.8

0.016 0.0008
wall.

Blood

Pressure

to the

Echocardiographic

Indexes

of Left

Structure All Subjects

(n = 257)

SBP

End-diastolic IVS thickness End-diastolic PW thickness LV mass LV mass index Relative well thickness Cross-sectional area Cross-sectional area index “p
584

Ambulatory

P 1.8 0.2 0.8 1.0

on the same arm using a mercury sphygmomanometer.16 Other investigators have reported a similar correlation with the same unit. l7 Bladders of appropriate size (13 cm X 24 cm, 17 cm X 32 cm) were used. Mean arm circumference was 26.3 cm (standard deviation [SD] 3). The reading and analysis of data provided by the unit was done using the ABP5600 and ABP90204 interfaces (Spacelabs), with editing procedures described previously. * l The unit was set to take readings every 15 minutes through the 24 hours. The total number of ambulatory BP readings per patient was 107.4 (SD 12), and 89.6 (SD 11) readings per patient fulfilled editing criteria. Error percentage was 15.9% (SD 12). ECHOCARDIOGRAPHIC METHODS: M-Mode echocardiograms were recorded under cross-sectional control using ATL Ultramark 8 and 9 systems (Advanced Technology Laboratories, Bellevue, Washington). LV measure-

MENTS:

TABLE

PW = posterior

of Variance

F

92 (8)

l-week intervals, and all the 4 aforementioned criteria had to be fulfilled. Altogether, 114 hypertensive patients (69%) had never received antihypertensive drugs. Most normotensive subjects were healthy people referred to our center for a clinical checkup including echocardiography and ambulatory BP monitoring, and showing casual BP constantly <160/90 mm Hg. ExperilWlWlta~

Analysis

blood pressure:

THE AMERICAN

Normotensives DBP

SBP

Casual

24-h

Casual

24-h

0.40* 0.38* 0.38* 0.430 0.33* 0.41* 0.46*

0.509 0.53* 0.52* 0.51* 0.44’ 0.558 0.539

0.379 0.36* 0.34’ 0.34* 0.32* 0.37* 0.370

0.37* 0.43* 0.42* 0.39’ 0.34” 0.44* 0.399

IVS = interventncular

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LV = left ventricular;

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Hypertensives

DBP

(n = 165) DBP

SBP

Casual

24-h

Casual

24-h

Casual

24-h

Casual

24-h

0.20 0.28’ 0.23 0.32* 0.23 0.25* 0.34”

0.310 0.46* 0.349 0.36* 0.410 0.38* 0.40*

0.10 0.05 0.02 0.006 0.08 0.05 0.03

0.19 0.31* 0.23 0.20 0.28* 0.25’ 0.21

0.32* 0.26* 0.30* 0.35* 0.220 0.31* 0.38*

0.46’ 0.46* 0.41* 0.47* 0.36’ 0.510 0.47’

0.298 0.27’ 0.28* 0.28” 0.23. 0.308 0.30’

0.28* 0.344’ 0.37’ 0.33’ 0.22s 0.37’ 0.30’

PW = posterior

wdll: SBP = systohc blood pressure

ments were obtained at end-diastole and end-systole according to the recommendations of the American Society of Echocardiography (ASE).‘* LV mass was calculated using the following equation based on necropsy validation studiesi9: LV mass = 0.80 X [(ASEcube LV mass)] + 0.6 g, and ASE-cube LV mass = 1.04 X [(IVSd + LVIDd + PWTd)3 - LVIDd3], where IVSd = interventricular septal thickness at enddiastole, LVIDd = LV internal dimension at end-dias.

tole, and PWTd = posterior wall thickness at end-diastole. All echocardiographic examinations were performed by the same sonographer. Echocardiographic tracings were read in random order by 2 investigators who were unaware of the patients’ casual and ambulatory BP levels. Both investigators marked locations on stop frames on the screen of the ATL Ultrasound System, and the mean values from 15 measurements for each parame-

.

.

l

.

.

. l

.

.

. .

. .

.

I

..*.

.

.

I

l f

ID0

120

140

160

180

200

220

1. Relation of left ventricular for explanation.

I

, ..* 90

mass

index

to casual

.

., 100

120

110

(clinical)

and average

2. Relation of left ventricular for explanation.

mass

index

to casual

24-hour

.

1 70

CLINIC DIASTOLIC BLOOD PRESSURE.mmHg FIGURE See text

Ii0

1

140

160

180

200

AVERAGE 24-HSYSTOLIC BLOOD PRESSUREmmHg

CLINICSYSTOLIC BLOODPRESSURE .mmHg FIGURE See text

l :

100

(clinical)

.

.l

systolii

, .

. .

blood

pressure.

. 4

80 90 100 110 AVERAGE 24-H DIASTOLC BLOOD PRESSURE.mnHg

and average

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ter for observer were computed. Only frames with optimal visualization of LV interfaces and showing simultaneous visualization of IVS, PWT and LVID throughout the cardiac cycle were considered for reading. Relative wall thickness20 and cross-sectional area21 were calculated as previously described. Fractional shortening was calculated according to the formula [(LVIDd LVIDs)/LVIDd] X 100. STATISTICAL ANALYSIS: All data were stored by using the DBASE III software, and analyzed by using the SPSS/PC+ V2.0 package. 22 One-way analysis of variance, nonparametric tests and multiple comparisons according to Tukey’s test were used to compare the normotensive with the hypertensive group. The z statistics23 were used to test the significance of differences between correlation coefficients, and the t statistics24 to test parallelism of different regression lines. The 5% level of statistical significance was adopted for all tests. RESULTS Table I lists the statistical significance of differences between hypertensive patients and healthy normotensive subjects. Age, height, weight, sex prevalence and body surface area did not differ between the 2 groups. Casual and ambulatory heart rate were slightly higher in the hypertensive than in the normotensive group. Prevalence of LV hypertrophy (LV mass index > 120 g/ m2 25,26)was 7% in the normotensive and 17.6% in the hypertensive group. Within the latter group it was 14.8 and 30.0%, respectively, in patients with casual diastolic BP 90 to 104 mm Hg (n = 135) or 1105 mm Hg (n = 30). Rdations of casual and ambulatory blood pressure to left ventricular structure: Table II lists the correla-

tion coefficients of the echocardiographic indexes of LV structure to casual and ambulatory BP. In general,

there were weak correlations between casual or ambulatory BP readings and echocardiographic indexes of LV structure. However, all correlations in the normotensive and hypertensive groups were closer to the ambulatory than to the casual readings (all values p <0.05, with the exception of the correlations between diastolic BP and septal thickness, relative wall thickness and cross-sectional area index, which showed nonstatistically dissimilar correlation coefficients between casual and ambulatory readings). A plot of the relation of LV mass index to casual and average 24-hour systolic BP is shown in Figure 1. The relation of LV mass index to casual systolic BP was defined by the equation: LV mass index (g/m2) = 0.636 X casual systolic BP (mm Hg) - 5.74 (standard error of the b coefficient [SEb] = 0.134). The relation of LV mass index to average 24-hour systolic BP was defined by the equation: LV mass index (g/m2) = 1.01 X average 24-hour systolic BP (mm Hg) - 47.8 (SEb = 0.147). LV mass index increased more with average 24hour than with casual systolic BP (parallelism test24: p CO.05). A plot of the relation of LV mass index to casual and average 24-hour diastolic BP is shown in Figure 2. The relation of LV mass index to casual diastolic BP was defined by the equation: LV mass index (g/m*) = 1.405 X casual diastolic BP (mm Hg) - 41.78 (SEb = 0.375). The relation of LV mass index to average 24hour diastolic BP was defined by the equation: LV mass index (g/m2) = 1.319 X average 24-hour diastolic (mm Hg) - 25.23 (SEb = 0.297). LV mass index increased in a similar fashion to average 24-hour and casual diastolic BP (parallelism test24: p = difference not significant [NS]). Risk stratification

of kft ventricular

hypertrophy:

Figure 3 shows the scatter plot of the relation of average 24-hour ambulatory or casual systolic BP in the hy-

.

I

FIGURE 3. Relation of average 24how to casual (dinical) systolic bbed pressme.lhlimitof10mmttgabove a4dbebwtheregmmbnRnewasueed to generate groups of patienb with ambubteweystdkbbodpreuvedbproporllondly high (210 mm Hg) or bw (510 mm Hg) relative to casual --.

loo

120

140

160

180

200

CLINICSYSTOLIC BLOOD PRESSURE ,mmHg 586

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pertensive group. The relation was defined by the equation: Average 24-hour ambulatory systolic BP (mm Hg) = 54.16 + (0.55 X casual systolic BP [mm Hg]), SEb = 0.051, r = 0.64, p
higher in men than in women in the low ambulatory BP group defined by systolic (98 vs 75 g/m2, p <0.05) and diastolic (102 vs 83 g/m2, p <0.05) BP, but it did not differ between the genders in the high ambulatory BP group defined by systolic (116 vs 117 g/m?, p = NS) and diastolic (117 vs 98 g/m2, p = NS) BP. Electrocardiographic Romhilt-Estes score was 25 in 2 of 32, 5 of 102 and 5 of 31 patients, respectively, in the low, intermediate and high ambulatory BP groups defined by systolic BP, and in 2 of 38, 5 of 93 and 5 of 34 patients in the low, intermediate and high BP groups defined by diastolic BP, but none of the differences between the low and high BP groups yielded statistical significance (chi-square = 1.2 and 1.5, respectively, all p = NS). DISCUSSION

The findings of this study clarify some clinical implications of the superiority of ambulatory over casual BP readings in predicting the degree of cardiac involvement in a large population of untreated and unselected hypertensive patients. In these patients, prevalence of echocardiographic LV hypertrophy was rather low (14.8% in those with mild hypertension and 30% in patients with casual diastolic BP 2 105 mm Hg), as reported in comparable hypertensive populations.27%28 In agreement with previous studies using noninvasive8,9 or intraarteriallO BP monitoring, the correlation between LV mass and average 24-hour systolic or diastolic BP was closer than that between LV mass and casual BP. All correlations, however, were rather weak,

t

.

70 ,

.

90

l

120 CLINIC DIASTOLICBLOODPRESSURE, mmHg 100

110

FIGURE 4. Relation of average 24-hour to casual (clinical) The limit of 6 mm Hg above and bediastolic blood presswe. low the regre line was used to generate groups of patients with ambulatory diastolic blood pressure di!qnmpo&onally high (26 mm Hg) or low (56 mm Hg) relative to casual blood pressure.

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TABLE 111 Descriptive Findings, Casual and and in the “Low” (I), “Intermediate” (II) and Predicted Ambulatory Systolic Blood Pressure

Ambulatory Blood “High” (III) Blood

Pressure Pressure

and Echocardiographic Groups Defined by the

Data in the Normotensive Group Difference Between Observed and

Multiple

Hypertensive Normotensive Subjects (n = 92)

Variable Age (YW Weight (kg) Height (cm) BSA (m’) Casual SBP (mm Hg) Casual DBP (mm Hg) Casual HR (beats/min) Average 24-hour SBP (mm Hg) Average 24hour DBP (mm Hg) Average 24-hour HR (beats/min) End-diastolic VS thickness (cm) End-diastolic PW thickness (cm) LV end-diastolic diameter (cm) Shorteningfraction (%) LV mass (g) LV mass index (g/m’) Relative wall thickness Cross-sectional area (cm2) Cross-sectionat area index (cm2/m2)

50 73 168

Normotensives vs

(n = 165) ANOVA

I (n = 32) (14)

(12) (8) (0.2)

1.8 136 80 73 123 79 73 0.79 0.71 5.29 40 139 77 0.27 14.2 7.9

Patients

(13) (7) (10) (13)

(8) (6) (0.2) (0.1)

(0.6) (7) (4.6)

(23 (0.07)

(3.6) (1.9)

II (n = 102)

52 66 162 1.7 163 98 78 128 85 76 0.81 0.72 5.17 39 141 82 0.28 14.5 8.48

(13) (15)

03) c-J.2)

(15)

6) (13) (9) (7)

(8) Kw (0.2) (0.7)

(8) (51)

G-W (0.07) (3.9) (1.9)

52 76 167 1.8 157 97 77 140 92 76 0.95 0.82 5.26 39 172 93 0.32 17.2 9.36

(13)

(8) (0.2) (18) (6) (12) (11) (7)

(8) (0.3)

(0.2) (0.6) (7) (59)

(28) (0.08) (4.6)

(2.2)

54 80 169 1.9 163 100 76 161 99 78 1.10 0.95 5.46 37 223 117 0.35 20.9 11.06

II vs

I YS

--

III (n = 31)

(11)

Comparisons

(14) (13) (10)

(0.2) 122) (8) (13) (15)

(8) 63)

F

p

0.7 6.8 3.6 7.2 42.1 139.1 2.1 81.7 73.6

NS * * * * * NS * t

4.5 14.7 19.1 1.2 1.7 18.0 16.1 10.9 20.3 16.2

* * * NS NS * * * * *

(0.4)

(0.2) (0.7)

6) (87) (47) (0.10) (6.7)

(3.6)

I

II

Ill

II

III

III

NS NS NS * *

NS NS NS * *

* + * * *

* + * NS NS

* NS * NS NS

NS NS NS NS NS

NS I

* I

* *

* *

* *

* ri

NS NS NS

+ * *

+ * *

NS * *

NS * *

NS * *

NS NS NS NS NS

* * * * *

* * *NS” * NS * * * *

*

* * NS * *

* * *

Data expressed as mean f standard deviation. I = ambulatory systolic blood pressure 510 m m Hg than predicted: II = ambulatory systolic blood pressure wlthln 9 m m Hgof predlcted; III = ambulatory systolic blood pressure 210 m m Hg than predlcted. ANOVA = analysts of variance: BSA = body surface area; DBP = diastok blood pressure; HR = heart rate; LV = left ventricular; NS = not slgniflcant: PW = left ventrltular posterior wall; SBP = systolic blood pressure; VS = ventricular septum; * = p < 0 01: 7 p < 0.05.

TABLE

IV

Descriptive

Findings,

and in the “Low” (I), “Intermediate” Predicted Ambulatory Diastolic

Casual Blood

and (II) and Pressure

Ambulatory “High”

Blood (Ill)

Blood

Hypertensive Normotensive Subjects (n = 92)

Variable

Age Ws) Weight (kg) Height (cm) BSA (m*) Casual SBP (mm Hg) Casual DBP (mm Hg) Casual HR (beats/min) Average 24hour SBP (mm

Hg)

Average 24-hour DBP (mm Hg) Average 24-hour HR (beats/min) EnddiastolicVS thickness (cm) End-diastolic PW thickness (cm) LV enddiastolic diameter (cm) Shortening fraction (%) LV mass (g) LV mass index (g/m*) Relative wall thickness Cross-sectional area (cm’) Cross-sectional area index (cmZ/mZ)

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Patients

and

Echocardiographic

Groups

Defined

Data by the

in the

Difference

I (n = 38)

50 73 168 1.8 136 80 73 123

(14) (12)

79 73 0.79 0.71 5.29 40 139 77 0.27 14.2 7.9

(8)

82

(6)

(6) (0.2) (0.1) (0.6) (7) W)

75 0.90 0.79 5.14 39 158 90 0.29 15.0 8.67

(9) (0.2) (0.2) (0.6)

Q-9 (0.2) (13) (7) (10) (13)

(23) (0.07) (3.6) (1.9)

OF CARDIOLOGY

54 67 163 1.7 160

)I (n = 93)

98 76 131

(11) (13)

(8) (0.2)

(16) (6) (11) (11)

97 78 141 92 77 0.95 0.81 5.27

03)

38

(51) (26) (0.09) (4.1) (2.2)

172 92 0.31 17.1 9.20

II = ambulatory

VOLUME

51 77 168 1.9 157

66

diastolic

(6) (8) (0.3) (0.2) (0.6) (7) (64) (31) (0.08) (5.1) (2.5)

blood pressure

(1.3

55 78 168 1.9 164 98 76 156 101 77 1.03 0.90 5.46 2: 111 0.34 14.8 10.56

Group

Observed

Multiple

Comparisons

and

I

II

“S

“S

--

III (n = 34) (12) (14) (9) (0.2) (1% (7) (13) (14)

Normotensive Between

Normotensives vs

(n = 165) ANOVA

‘p<0.01;~p<0.05. Data expressed as mean f standard devlatton. I = ambulatory diastolic blood pressure 56 m m Hg than predlcted; 26 m m Hg than predlcted. Abbreviations as in Table Ill.

588

Pressure Pressure

(13) (7) (0.2) (1% (7) (13) (15) (5)

03)

(0.3) (0.2) (0.7) (5) @w (43) (0.09) (6.4) (3.3)

F

p

0.5 5.5 3.8 6.0 41.9 137.1 2.3 54.9

NS * * * * * NS *

123.3 4.0 9.4 11.9 1.6 2.0 12.3 11.5 6.9 13.0 11.8*

* * * * NS NS * * * *

within 5 m m Hg of predicted;

I

II

I11

II

II)

111

NS NS NS * *

NS NS NS * *

NS NS NS * *

+ + * NS NS

+ NS * NS NS

NS NS NS NS NS

t

*

*

*

0

*

NS * NS+ NS * NS *

* + * *

* NS NS NS

* NS + *

* NS NS *

NS NS NS NS NS’

* * * * *

NS * NS * NS + NS * NS*

* * * *

Ill = ambulatory

dustok

* * NS * *

blood pressure

and no more than 25% of variability in the echocardiographic indexes of LV structure could be accounted for by the relation with either ambulatory or clinical BP. The weakness of these correlations supports the view29,30 that several factors besides BP, including hemodynamic load and myocardial contractility,’ ’ are probably involved in the development of LV hypertrophy in human hypertension. Prediction

of the degree

of cardiac

hypertrophy:

Prevalence of LV hypertrophy by electrocardiography was low, as noted in comparable patient populations,34 and not enough to differentiate the high from the low ambulatory BP groups. This is probably due to the lower sensitity of electrocardiography in comparison with echocardiography in detecting LV hypertrophy proved at necropsy.35 The findings of this study suggest that one possible reason for the prognostic value of noninvasive ambulatory BP readings, as it has been reported,5,6may be the stratification of patients into subsetsat different risk of echocardiographically determined LV hypertrophy, an independent prognostic marker.i2m15 A practical clinical implication of our findings is that a thorough echographic examination of the left ventricle should be recommended in hypertensive patients with ambulatory BP disproportionally high relative to casual BP, and classified in the high ambulatory BP group. Conversely, echocardiography is probably of little clinical importance in hypertensive patients with ambulatory BP disproportionally low relative to casual BP and classified in the low ambulatory BP group. In these patients, LV massindex and other indexes of LV hypertrophy are likely to be within the normal range. These conclusions are supported by a recent study by White et al,36 who showed that in patients who were found to be hypertensive in the physician’s office, but normotensive on the basis of noninvasive ambulatory BP monitoring, LV massindex was not different from that of normotensive control subjects, and lower than in patients with higher ambulatory BP values.

Becausecorrelation coefficients measureonly the closenessof an associationbetween 2 variables, a significant difference between 2 correlation coefficients does not imply, in our case,that the echocardiographic measurements of LV structure are predicted differently by ambulatory than by casual BP. To clarify this point, we compared the slopeof the 2 regressionlines and found that the predicted value of LV mass index increased more with ambulatory than with casual systolic BP, and increasedto a comparable extent with ambulatory and casual diastolic BP. Thus, the same systolic BP level predicted a higher mean value of LV massif it was the average of about 90 noninvasive readings throughout the 24 hours, and predicted a lower mean value of LV massif it was a casual reading. By contrast, the same level of ambulatory or casual diastolic BP predicted comparablevalues of LV mass.Ambulatory systolic BP was thus superior to ambulatory diastolic BP in terms of advantage over casual BP in the prediction of the echocardiographic measurementsof LV structure in hypertension. Clinical implications: The high long-term morbidity and mortality in hypertensive patients with ambulatory Acknowledgment: We thank Maria Marchini for BP significantly higher than predicted5v6has been interher help in data handling. preted as an effect of greater cardiovascular load throughout 24 hours in these patients (thus producing higher long-term risk) than in patients with similar casual but lower ambulatory BP levels. These epidemio- REFERENCES 1. Sokolow M, Perloff D. The prognosis of essential h>pertens,on treated conserlogic findings suggestthat casual and ambulatory BP valivcly. Cin~ulation 1961;23:697-713. readingsare not alternative but complementary tools to 2. Kannel WB. Role of blood pressure in curduwascular morbidity and mortality. Prog Cardimwsc lk 1974, /7:5-24 assess the risk in an individual patient. 3. Kannel WB, Gordon T . Offuc D. Left ventricular hgperlrophy by elcctrocarIn this study, LV massand other echocardiographic diagram. Prevalence. mcidencc and mortalit) in the Framingham Study. ,&n indexes of cardiac hypertrophy were increased in pa- InternMrd 1969.71-89-105. Kannel WB, Gordon T . Castelli WI’, Margol~s JR Elrclrocardiographic left tient with disproportionally high ambulatory BP com- 4.ventricular hypertrophy and risk of coron;vq heart deeare The FramIngham pared with patients in the low ambulatory BP group. Study. Ann Intern Med 1970:72:R13-822. 5. Perloff D, Sokolow M. Couan K. The projgwsl~c \.dIuc of anbulatorq blood The prevalence of LV hypertrophy, which did not differ pressure. JAMA /983:249.2792-279X. between the normotensive and the low ambulatory BP 6. Perloff D, Sokolou M, Cowan RM. Juster RP. Prof.nostx value of ambulator> groups,increasedby more than fourfold from the low to blood preswrc mcasuremen& further analyses. J Hqwrrrm /989,7(,\upI,/ 3).S3the high ambulatory BP group. There were more wom- SIO. 7. Mann S. Mdler Craig MW. Raftcry EB. Superiority of ZJ-hour me3surcment en in the low than in the high ambulatory BP group, in of blood preaaurc over clinic wlue\ m determining prognws in hjpertension. <‘l/n agreement with the findings of Pickering et a13” who Exp IIyperrens 1985;,47-279 281 Drayer JIM, Weber MA, DeYoung JL. BP II\ a determmant of cardiac left showeda higher prevalence of women among subjects 8.!wmiculnr muscle mass. Arch Intern Med 1983;143:YO-Y2. with “white-coat hypertension” (i.e., normal daytime 9. Devereux RB. Pickering TG. Harshfield GA. Klemert HD. Dcnb) 1. Clark L, ambulatory BP despiteclinical hypertension); this could Prcgibon D. Jason M. Kleinert B, Borer JS. Laragh JH. Left ventricular hypertropb> m pdticnt\ with h)pertcnGon. m~portx~cc of blood prcshurc rcsponac tu explain part of the variation of LV massbetween the 3 regularl) recurring ctrex ~evwlation /983:68.470-476. ambulatory BP groups. In fact, LV massseemsto be 10. Ro\*landa DB. Cilover DR. Ireland MA. McLeay RAB. Stallard TJ. Watson lower in hypertensive women than in men,‘h at least be- RDS. Littler WA. Assessment of left ventricular mass and eta reap~nse to antihkpertensivr treatment. Lonwl 1982.1:4.(7 460. fore menopause. 33In our study, LV masswas lower in 11. Verdecchizr P. Schlllaci G, Gucrner~ M. Gatteschi C. Bcnemio G. Boldrlni t-. 1” women than in men in the group at lower risk of LV Porcellati C. Cwcadian blood pressure changes and left ventricular h)pertrophy h)perten\ion. C~rcularion / 990:8/:S?R 536 hypertrophy, but did not differ between the genders in essential 12. Casale PK. De\ereua RB, Miinrr M. Iullo G. Hanhfirld GA. Pickering TG. the group at higher risk of LV hypertrophy. LnrJgh JH Valur 01 echocardiographlc meazurrmcnt uf left ventricular mass in

THE AMERICAN

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OF CARDIOLOGY

SEPTEMBER

1, 1990

589

predicting

cardiovascular

morbid

events

in hypertensive

men. Ann

Inrem

Med

1986:105:173-178. 13. Levy D, Garrison

RJ, Savage DD, Kannel WB, Castelli WP. Left ventricular mass and incidence of coronary heart disease in an elderly cohort. The Framingham heart study. Ann Intern Med 1989;l lO:lOl-107. 14. Karen MJ, Casale PN, Savage DD, Laragh JH, Devereux RB. Relation of left ventricular mass to prognosis in essential hypertension. Circulation 1989; 8O(suppl IIj:II-538. 15. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli W. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham heart study. N Engl J Med 1990;322:1561-1566. 16. Verdecchia P, Gatteschi C, Benemio G, Boldrini F, Guerrieri M, Porcellati C. Home ambulatory blood pressure readings do not differ from clinic readings taken at the same time of day. J Hum Hypertem 1988:2:235-240. 17. Harshfield GA, Pickering TG, Blank S, Lindahl C, Stroud L, Laragh JH. Ambulatory blood pressure monitoring: recorders, applications and analyses. In: Weber MA, Drayer JIM, eds. Ambulatory Blood Pressure Monitoring. Darmstadt: Steinkopff Verlag, 1984:1-7. 18. Sahn DJ, DeMaria A, Kisslo J, Weyman A. The Committee on M-Mode Standardization of The American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echwardiographic measurements. Circulation 1978;58:1072-1083. 19. Devereux RB, Alonso DR. Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450-458. 20. Reichek N, Devereux RB. Reliable estimation of peak left ventricular systolic pressure by M-mode echographic determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients. Am Heart J 1982;103:202-209. 21. Ditchey RV, Schuler G, Peterson KL. Reliability of echocardiographic and electrocardiographic parameters in assessing serial changes in left ventricular mass. Am J Med 1981;70:1042-1050. 22. Norusis MJ/SPSS Inc. SPSS/PC+ V2.0. Base manual. Chicago, ILLSPSS Inc, 1988. 23. Snedecor GW, Cochran WG. Statistical methods. 7th ed. Ames, IA: The Iowa State Uniuersity Press, 1980:186-187. 24. Glantz SA. Primer of biostatistics. 2nd ed. New York: McGraw-Hill, 1987:211.

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25. Devereux RB, Pickering TG, Alderman MH, Chien S, Borer JS, Laragh JH. Left ventricular hypertrophy in hypertension. Prevalence and relationship to pathophysiologic variables. Hypertension 1987,9(supp/ II):II-53-H-60. 26. Devereux RB, Lutas EM, Casale PN, Kliglield P, Eisenberg RR, Hammond IW, Miller DH, Reis G, Alderman MH, Laragh JH. Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Co11 Cardiol 1984:4:1222-l 230. 27. Hammond IW, Devereux RB, Alderman MH, Lutas EM, Spitzer MC, Crowley JS, Laragh JH. The prevalence and correlates of echwardiographic left ventricular hyp-ertrophy among employed patients with uncomplicated hypertension. J Am Coil Cardiol 1986;7:639-650. 28. Kleinert HD, Harshfield GA, Pickering TG, Devereux RB, Sullivan PA, Marion RM, Mallory WK, Laragh JH. What is the value of home blood pressure measurement in patients with mild hypertension? Hypertemion 1984.6574-578. 29. Devereux RB. Echocardiographic insights into the pathophysiology and prognostic significance of hypertensive cardiac hypertrophy. Am J Hypertenr 1989; 2:186S-195s. 30. Frohlich ED. Physiologic considerations in left ventricular hypertrophy. In: Messerli FH, ed. The Heart and Hypertension. New York: Yorke Medical Books, 1987:87-98. 31. Ganau A, Devereux RB, Pickering TG, Roman MJ, Schnall PL, Santucci S, Spitzer MG, Laragh JH. Relation of left ventricular hemodynamic load and contractile performance to left ventricular mass in hypertension. Circulation 1990:81:25-i-36. 32. Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension? JAMA 1988;259:225-228. 33. Garavaglia GE, Messerli FH, Schmieder RE, Nunez BD, Oren S. Sex differences in cardiac adaptation to essential hypertension. Eur Heart J 1989; 10:1110-1114. 34. Carr AA, Prisant M, Watkins LO. Detection of hypertensive left ventricular hypertrophy. Hypertension 1985;7:948-954. 35. Devereux RB, Casale PN, Wallerson DC, Kligtield P, Hammond IW, Liebson PR, Campo E, Alonso DR. Laragh JH. Cost-effectiveness of echccardiography and electrocardiography for detection of left ventricular hypertrophy in patients with systemic hypertension. Hypertension 1987,9(suppl Il):II-69-11-76. 36. White WB, Schulman P, McCabe EJ, Dey HM. Average daily blood pressure, not office blood pressure, determines cardiac function in patients with hypertension. JAMA 1989;261:873-877.