Diminished nocturnal decline in blood pressure in elderly hypertensive patients left ventricular hypertrophy
with
To assess the circadian blood pressure (BP) changes in elderly hypertensive patients with left ventricular hypertrophy (LVH), the ambulatory BP was measured noninvasively every 30 minutes for 24 hours in those patients with LVH (n = 15) and without LVH (n = 23), and in normotensive elderly subjects (n = 11). Although the daytime systolic BP (SBP) was comparable in the two hypertensive groups, the nighttime SBP in patients with LVH tended to be higher than in patients without LVH (149.0 f 15.1 versus 138.4 + 20.1 mm Hg, p < 0.10). The LV mass index correlated significantly with the nighttime SBP (r = 0.43, p < O.Ol), but not with the daytime SBP (r = 0.24, ns), with clinic SBP (I = 0.14, p = ns) or the SBP after handgrip exercise (r = 0.31, p = ns). The difference in the systolic BP between daytime and nighttime (D-N SBP) in patients with LVH (2.8 -t 9.4 mm Hg) was significantly less than that in patients without LVH (12.8 k 18.0 mm Hg) (p < 0.02). In addition, the D-N SBP correlated inversely with the left ventricular mass index (r = -0.33, p < 0.05). It was concluded that hypertension in the elderly with LVH was associated with a diminished nocturnal decline in blood pressure. (AM HEART J 1992;87:1307.)
Iwao Kuwajima, MD, Yasuko Suzuki, MD, Tatsuo Shimosawa, MD, Akiko Kanemaru, MD, Satoshi Hoshino, MD, and Kizuku Kuramoto, MD. Tokyo, Japan
Left ventricular hypertrophy (LVH) is an inevitable outcome of long-term high blood pressure (BP), and is an important predictor of cardiovascular morbidity and mortality. l, 2Although a considerable number of studies have indicated that the LV mass,estimated by echocardiography, is more closely related to the 24-hour average BP3>4 than to the clinic BP, it is still controversial whether the daytime or nighttime BP has more pathogenic significance for the development of LVH. Some investigators5)6 insist that a better correlation exists between LV mass and BP after stress or exercise, while others79I5 recognize a higher correlation with BP measured during the nighttime. Recently, it has been recognized that there are some conditions associated with diminished or lost nocturnal decline in the BP.‘-ila 20~21 Although the blood pressure rises during the daytime and declines at nighttime in the normal population, the decline in From
the Division
Received Reprint ropolitan 411135827
of Cardiology,
for publication requests: Geriatric
May
Tokyo 28, 1991;
Metropolitan accepted
Geriatric Nov.
Hospital.
1, 1991.
Iwao Kuwajima, MD, Division of Cardiology, Hospital, 35-2, Sakaecho, Itabasiku, Tokyo
Tokyo Met173, Japan.
the nighttime BP is lost in many conditions associated with autonomic dysfunction.8-11, 20+21It is surprising that a nocturnal BP decline was not seen in one third of elderly hypertensive patients22 in whom the prevalence of autonomic dysfunction is known to be high. Recent studies by us12and by Grassi et alI3 have demonstrated that the baroreceptor reflex function, which plays an important role in the maintenance of physiologic blood flow to the vital organs, is impaired in hypertensive patients with LVH. Based on these considerations, we hypothesized that hypertensive patients with LVH have a diminished or lost decline in nighttime BP. In the present study, we examined the circadian BP pattern in elderly hypertensive patients with and without LVH to test this hypothesis and to clarify whether the daytime or nighttime BP correlates more closely with the LV mass. METHODS Thirty-eight elderly hypertensive patients and 11 normotensive elderly subjects (NT) over 60 years old were recruited for the study. Hypertension was defined as a sitting office BP of more than 160 mm Hg systolic or 90 mm Hg diastolic on three measurements at Z-week intervals. All
1307
May 1992
1308
Kuwajim
Table 1. Clinical
et al.
American
background
of subjects HT-1 (I)
No. WF) Age (yr) Office SBP (mm Hg) Office DBP (mm Hg) LVMI (gm/i#) WT HT-1,
Hypertensive
group
1; HT-2,
NT
HT.2
(21
15 (l/14) 76.7 i 5.1 179.2 f 19.4 90.3 f 12.2 197.4 _t 58.8
(10:313, 72.3 + 6.1 177.7 ? 16.0 88.5 i 14.3 103.5 + 15.7
28.2 + 2.3
18.9 -c 2.2
(mm)
blood pressure; LVMI, *p < 0.05.
Heart Journal
hypertensive
left ventricular
group
mass index;
2, NT,
normotensive
WC!‘, wall thickness
(3) 11 cm) 74.7 z!I 134.3 t 72.8 + 90.6 f
I us 2
I us 3
2 L’S 3
NS t t t
NS t t t
NS NS NS *
t
t
NS
5.3 14.4 10.0 15.0
17.3 I 2.0
group; M/F, male-to-female (septal + posterior wall).
ratio; SBP, systolic blood pressure; DBP, diastolic
tp < 0.01.
Table II. Analysis
of ambulatory
blood pressure HT-1
Whole-day DBP (mm Hg) Hg) SBP (mm Daytime SBP (mm Hg) Daytime DBP (mm Hg) Nighttime
SBP
(mm
80.4 151.2 151.7 82.0 149.0 77.5 2.8 188.7
Hg)
Nighttime DBP (mm Hg) D-N difference of SBP (mm Hg) SBP after
HG
(mm
Hg)
DBP
HG
(mm
Hg)
after
HG,
(I)
ff * f -c + k +
HT-2
80.4 146.6 151.0 83.2 138.4 74.5 12.8 191.6
8.1 14.8 13.7 6.4 15.1 8.2 9.4 22.1
85.0 k 18.6
handgrip
exercise;
other
NT
(2)
+* * t + f f i
8.7 15.4 15.1 9.0 20.1 10.6 16.0 24.5
67.5 123.1 126.1 69.5 116.6 64.3 8.0 145.3
86.8 +- 18.6 33.3 i- 20.2
36.9 + 21.4 12.8 + 9.8
ASBP after HG (mm Hg) ADBP after HG (mm Hg) D-N, Daytime-nighttime; *p < 0.1
monitoring
9.2 _t 11.4
abbreviations
as in Table
(3)
++ -+ + k k + f
1 us 2
5.0 12.8 11.5 5.5 15.6 9.5 10.5 16.0
NS NS NS NS * NS t NS
70.0 + 9.9 22.3 i- 10.1 8.9 + 7.7
2 us 3
1 us 3
: : $ NS NS
: $ I !: NS NS
NS NS NS
: t NS
: NS NS
HG
ABP
I.
tp < 0.02. $p < 0.01.
Table III. Correlation
between
0fiL-e SBP
Daytime
Nighttime
mass index D-N
SBP
BP after
after
HG
SBP
DBP
SBP
DBP
Difference
SBP
DBP
SBP
DBP
0.24 0.26
0.19 0.21
0.43t 0.44t
0.28 0.32
-0.33* -0.34*
0.31 0.32
0.19 0.20
0.19 0.19
0.10 0.12
LVMI
0.14
0.13
0.26
0.16
as in Tables
and left ventricular
DBP
WT Abbreviations *p < 0.05. tp < 0.01.
blood pressure
I and
II.
patients had either never been treated with or had discontinued antihypertensive drugs at least 2 weeks before ambulatory BP monitoring. Secondary hypertension was ruled out by routine clinical and laboratory examinations. Histories or clinical signs of coronary or valvular heart disease, congestive heart failure, cerebrovascular disease, diabetes mellitus, or autonomic nervous dysfunction were all negative. The hypertensive patients were divided into two groups based on the finding of LVH, which was estimated by M-mode echocardiography. Group 1 (HT-1) consisted of 15 cases with LVH (mean age 76.7 years). Group 2 consisted of 23 cases without LVH (mean age 72.8 years). LVH
was defined as a left ventricular mass index (LVMI) of more than 130 gm/m2 calculated with the formula validated by Devereux et a1.14 M-mode echocardiograms (Hewlett-Packard Co., Medical Products Group, Andover, Mass.) were recorded under the guidance of two-dimensional echocardiographic imaging following 10 minutes rest by the patients in a supine position. The BP and pulse rate were measured before and after an isometric handgrip exercise, which was conducted for 3 minutes at 30 % of maximal voluntary contraction of the right hand. The ambulatory BP was measured noninvasively every 30 minutes for 24 hours using an ABPM630
Volume Number
123 5
Circadian BP in elderly hypertensives 1309 Night SBP mmHg
Day SBP mmHg
0
175
l
l
l
0
150
.
l
150
g+-/
l %.* %
l
l
l
125
l e
l
I.
100
ns
’
100
y==O.156X+116.9 rs0.431 p