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Left Ventricular Changes in Isolated Office Hypertension
A Blood Pressure–Matched Comparison With Normotension and Sustained Hypertension
Anna M. Grandi, MD;
Roberta Broggi, MD;
Sara Colombo, MD;
Rosa Santillo, MD;
Daniela Imperiale, MD;
Andrea Bertolini, MD;
Luigina Guasti, MD;
Achille Venco, MD
Arch Intern Med. 2001;161:2677-2681.
ABSTRACT
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Background Isolated office (IO) hypertension is a benign condition according to
some researchers, whereas others believe it is associated with cardiovascular
abnormalities and increased cardiovascular risk. The aim of this study is
to compare morphofunctional characteristics of the left ventricle (LV) in
IO hypertensive subjects, normotensive subjects (hereafter, hypertensives
and normotensives), and never-treated sustained hypertensives. The 3 groups
were matched not only by age, sex, and body mass index but also by clinic
blood pressure (BP) (IO hypertensives and sustained hypertensives) and daytime
BP (IO hypertensives and normotensives).
Methods We enrolled 42 IO hypertensives (clinic BP >140 and/or 90 mm Hg and
daytime BP  130/80 mm Hg), 42 sustained hypertensives (clinic BP >140 and/or
90 mm Hg and daytime BP  140 and/or 90 mm Hg) and 42 normotensives (clinic
BP <135 and/or 85 mm Hg and daytime BP 130/80 mm Hg). Left ventricular
morphologic features and function were assessed using digitized M-mode echocardiography.
Results Compared with normotensives, IO hypertensives had significantly thicker
LV walls, increased LV mass, reduced diastolic function, increased prevalence
of LV hypertrophy, and preclinical diastolic dysfunction. Sustained hypertensives,
compared with IO hypertensives, had significantly thicker LV wall, higher
LV mass, and lower diastolic function, whereas the prevalence of LV hypertrophy
and preclinical diastolic dysfunction was greater than in IO hypertensives,
but the difference did not reach statistical significance (P = .29).
Conclusions Comparing matched BP groups, IO hypertensives have LV morphofunctional
characteristics considerably different from normotensives and qualitatively
similar to sustained hypertensives. Therefore, our results support the hypothesis
that IO hypertension should not be considered as simply a benign condition.
INTRODUCTION
ISOLATED OFFICE (IO) hypertension, also defined as "white-coat" hypertension,
is a frequently diagnosed condition characterized by persistently elevated
office blood pressure (BP) combined with normal daytime ambulatory BP.1-2 The incidence of this condition is
12% to 50%, depending on the definition of IO hypertension used and the population
studied.3-4 The literature remains
inconclusive on the issue of whether IO hypertension carries a pathological
risk: it is considered an essentially benign condition by some researchers5-10
and a pathological situation, potentially associated with cardiovascular risk,
by others.11-19
There is general agreement that compared with sustained hypertensives, IO
hypertensives have substantially less target organ damage and cardiovascular
risk.7-9,14, 17, 20-21
However, compared with normotensives, IO hypertensives show some degree of
cardiovascular abnormality, as in many,12-19,22
but not all,5-6,8-9
similar studies.
Many factors can account for the discrepancies between results. Besides
differences in age and body mass index (BMI) in the groups compared, a major
role is played by the use of different daytime BP criteria for defining IO
hypertension and by the enrollment of hypertensives previously treated with
antihypertensive drugs that can, per se, modify cardiovascular characteristics.
Moreover, an important source of bias is the limited BP comparability among
groups: often, IO hypertensives have clinic BPs lower than sustained hypertensives
and ambulatory BPs within the reference range but substantially higher than
normotensives.
Therefore, we compared the morphofunctional characteristics of the left
ventricle (LV) in IO hypertension, normotension, and never-treated sustained
hypertension, selecting 3 groups of individuals carefully matched not only
by age, sex, and BMI but also by clinic BP (IO hypertensives and sustained
hypertensives) and daytime BP (IO hypertensives and normotensives).
PARTICIPANTS AND METHODS
PARTICIPANTS
The patients enrolled had been selected from among 438 hypertensives
never treated with antihypertensive drugs, referred in 2 years (1997-1999)
to our outpatient hypertension clinic (Division of Internal Medicine, University
of Insubria, Varese, Italy) because of office BPs repeatedly (>4 visits in
4 months) higher than 140 and/or 90 mm Hg. We enrolled 42 IO hypertensives
(18 men and 24 women; mean ± SD age, 42 ± 6 years; mean ±
SD BMI [calculated as weight in kilograms divided by the square of height
in meters], 25.3 ± 2.7) and 42 sustained hypertensives individually
matched by sex, age (within 1 year), BMI (within 1.0 kg/m2), and
mean clinic BP (within 3 mm Hg). The major selection criteria were an LV M-mode
echocardiogram of good quality; no clinical, electrocardiographic, or echocardiographic
evidence of heart failure, myocardial infarction, angina pectoris, or congenital
or valvular heart diseases; and no systemic diseases, such as diabetes mellitus
or connective tissue disorders, which could induce changes in LV structure
and function. From a survey of the hospital staff, we recruited 42 normotensives,
individually matched with IO hypertensives by sex, age, BMI, and mean daytime
BP. None of the participants were receiving any medications.
Mean clinic BP for the matching was obtained by averaging BP values
taken during 2 visits that were 1 week apart. During each visit, the same
operator, using a mercury sphygmomanometer, measured BP 3 times at 10-minute
intervals with patients in the sitting position after a 20-minute rest. We
defined patients as IO hypertensive when clinic BP was greater than 140 and/or
90 mm Hg and daytime BP was 130/80 mm Hg or less; as sustained hypertensive
when clinic BP was greater than 140 and/or 90 mm Hg and daytime BP was 140
and/or 90 mm Hg or higher; and as normotensive when clinic BP was less than
135/85 mm Hg and daytime BP was 130/80 mm Hg or less.
This study was approved by the ethical committee of the Department of
Clinical and Biological Sciences, University of Insubria, and all the participants
gave informed consent.
ECHOCARDIOGRAPHIC EXAMINATION
Echocardiographic examination was performed using a Hewlett-Packard
Sonos 1500 echograph (Hewlett-Packard, Andover, Mass) with a 2.0/2.5-MHz transducer.
Left ventricular M-mode echocardiograms were recorded under 2-dimensional
control, at a paper speed of 100 mm/s, and an electrocardiogram was performed
simultaneously. The M-mode tracings were evaluated by a single masked operator
(A.M.G.) who digitized 4 consecutive cardiac cycles of each echocardiogram,
as originally described by Upton and Gibson,23
using a Numonics 2205 graphic tablet (Numonics, Montgomeryville, Pa). A personal
computer was used to process digitized data, averaging the 4 cardiac cycles.
We evaluated LV end-diastolic diameter, end-diastolic thickness of the interventricular
septum and posterior wall, LV mass according to the Penn convention,24 LV mass index (LV mass normalized for body surface
area), percentage fractional shortening of LV diameter, peak shortening rate
of LV diameter, peak lengthening rate of LV diameter, and peak thinning rate
of the LV posterior wall.
The reference ranges of the laboratory variables were derived from the
evaluation of 200 healthy adults; the upper reference limits for LV mass index
were 130 g/m2 for men and 110 g/m2 for women. The reproducibility
of the echocardiographic measurements have been tested on 20 healthy individuals
(each examined 3 times by using the same ultrasonic technique); the same operator
digitized 4 consecutive cardiac cycles of each echocardiogram. The coefficients
of variation were as follows: LV end-diastolic diameter, 0.4%; septal thickness,
3.2%; posterior wall thickness, 3.4%; peak shortening rate, 1.1%; peak lengthening
rate, 4.7%; and peak thinning rate, 7.3%.
24-HOUR AMBULATORY BP MONITORING
Noninvasive ambulatory BP monitoring was performed using a portable
automated Takeda TM 2421 ambulatory BP monitor (Takeda, Osaka, Japan), and
24-hour heart rate monitoring was performed simultaneously. The unit was set
to take readings every 15 minutes throughout the 24 hours. The following variables
were evaluated: mean 24-hour, daytime (7 AM to 10 PM), and nighttime (10 PM
to 7 AM) systolic and diastolic BP and heart rate and nocturnal decline (percentage)
in systolic and diastolic BP.
STATISTICAL ANALYSIS
Statistical evaluation of the results was performed using analysis of
variance, followed by the Scheffé test. The  2 test
was used to compare differences in prevalence among groups. Values are expressed
as mean ± SD; P<.05 was considered statistically
significant.
RESULTS
As a consequence of selection criteria, the 3 groups were comparable
in age, sex, waist-hip ratio, and BMI; clinic BP was nearly identical in IO
hypertensives and sustained hypertensives and significantly higher than in
normotensives (P<.001). Ambulatory BP was nearly
identical in IO hypertensives and normotensives and significantly lower than
in sustained hypertensives (P<.001) (Table 1). The 3 groups were of comparable
socioeconomic status.
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Table 1. Clinical Characteristics of Study Participants*
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Left ventricular end-diastolic diameter was normal (<56 mm) in all
participants and was not significantly different among the 3 groups, whereas
septal and posterior wall thickness increased significantly from normotensives
to IO hypertensives to sustained hypertensives (Table 2) (P<.001). Left ventricular
hypertrophy (LV mass index >130 g/m2 in men and >110 g/m2 in women) was found in 7 IO hypertensives (17%; P = .03 vs normotensives) and in 17 sustained hypertensives (40%; P = .12 vs IO hypertensives); mean LV mass index increased
significantly from normotensives to IO hypertensives to sustained hypertensives
(Table 2) (P<.001). Percentage fractional shortening and peak shortening rate
of LV diameter—indices of LV systolic function—were normal (>30%
and >1.9 s-1, respectively) in all participants and similar
among the 3 groups (Table 2).
Left ventricular diastolic function was impaired (peak lengthening rate of
LV diameter <3.6 s-1and/or peak thinning rate of the LV
posterior wall <8.4 cm/s) in 11 IO hypertensives (26%; P = .005 vs normotensives) and in 19 sustained hypertensives (45%; P = .29 vs IO hypertensives). Mean values of both diastolic
indices decreased significantly from normotensives to IO hypertensives to
sustained hypertensives (Table 2)
(P<.001).
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Table 2. Comparison of LV Morphofunctional Variables Among the 3 Study
Groups*
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COMMENT
To our knowledge, this is the first study on LV characteristics in IO
hypertension that compares IO hypertensives with normotensives and sustained
hypertensives matched not only by sex, age, and BMI but also by mean clinic
BP (IO hypertensives and sustained hypertensives) and mean daytime BP (IO
hypertensives and normotensives). By using this design, we avoid important
sources of bias, represented by IO hypertensives having clinic BPs higher
than normal but substantially lower than those of sustained hypertensives
and, above all, daytime BPs within the reference range but substantially higher
than those of normotensive controls. In the latter condition, because a BP
even slightly higher than normal may result in a severe increase in the hemodynamic
load of the heart,25 differences in LV characteristics
between IO hypertensives and normotensives could be related to differences
in daytime ambulatory BP rather than to IO hypertension. Another factor that
affects the outcome of studies of IO hypertension is the cutoff BP value selected
for daytime BP normality: higher daytime values lead to higher prevalence
of IO hypertension and greater prevalence of LV changes in this condition.
Many studies that found cardiovascular changes in IO hypertensives similar
to those in sustained hypertensives and significantly different from those
in normotensives used a daytime BP cutoff value of 140/90 mm Hg or higher.
This criterion has been questioned recently: this value is probably too high,
leading to sustained hypertensives being defined as IO hypertensives, and
it has been suggested that a restrictive definition (daytime BP 130/80
mm Hg) is more reliable for diagnosing IO hypertension.26-27
In our study, to reliably compare true IO hypertensives and true sustained
hypertensives, we chose the restrictive cutoff value of 130/80 mm Hg as the
upper normal daytime BP for defining IO hypertension and the value of 140/90
mm Hg as the lower daytime BP for sustained hypertension. Finally, we enrolled
only individuals never treated with antihypertensive drugs to avoid the possible
effect of previous treatments on LV characteristics.28-29
Following the previously mentioned criteria, we studied 3 groups that
were almost identical in age, sex, BMI, mean clinic BP, and mean daytime BP.
Our main finding is that IO hypertensives have LV morphofunctional changes
qualitatively similar to sustained hypertensives but of lesser extent. In
fact, compared with normotensives, IO hypertensives had significantly thicker
LV walls, increased LV mass, a higher prevalence of LV hypertrophy, decreased
diastolic function, and a higher prevalence of preclinical diastolic dysfunction.
Sustained hypertensives, compared with IO hypertensives, had significantly
thicker LV wall, higher LV mass, and lower diastolic function, whereas the
prevalence of LV hypertrophy and preclinical diastolic dysfunction was greater
than in IO hypertensives, but the difference did not reach statistical significance
(P = .29). Left ventricular end-diastolic diameter
was normal in all participants and almost identical in the 3 groups; therefore,
the difference in LV mass index was due to the progressively increased thickness
of the interventricular septum and the posterior wall from normotensives to
IO hypertensives to sustained hypertensives, indicating a predominant concentric
pattern of hypertrophy. As a consequence of selection criteria, the differences
in LV characteristics among normotensives, IO hypertensives, and sustained
hypertensives were not accounted for by differences in age, sex, BMI, clinic
BP, or ambulatory BP.
Considering the data from the literature, our finding of increased LV
mass in IO hypertension is in agreement with many,12, 14, 17-18,30
but not all,5-6,8-10,31
studies, whereas all authors12, 14, 17-18,31
agree in reporting a normal LV systolic function, as we have found in our
group of IO hypertensives. Left ventricular diastolic function in IO hypertension
has been evaluated in few studies, using different methods and reaching different
conclusions: compared with normotensives, diastolic function has been found
to be normal,17-18 reduced but
not significantly12 or significantly decreased.14-16,31 We
evaluated LV diastolic function by means of peak lengthening rate and peak
wall thinning rate, both derived from digitized M-mode echocardiograms. These
indices, less used than Doppler-derived variables, are more sensitive in discriminating
between normal and impaired diastolic function in the presence of myocardial
hypertrophy; they are also less affected by heart rate and events occurring
during isovolumic relaxation.32 As noted previously,
IO hypertensives had diastolic indices significantly lower than normotensives
and higher than sustained hypertensives; moreover, the prevalence of preclinical
diastolic dysfunction, significantly higher in IO hypertensives than in normotensives,
was greater in sustained hypertensives, but the difference between sustained
hypertensives and IO hypertensives did not reach statistical significance.
It is well known that in hypertension, LV diastolic dysfunction is an early
finding, often preceding the development of detectable LV hypertrophy33-34: the same pattern is followed in
IO hypertension, as demonstrated by our finding of a prevalence of diastolic
dysfunction greater than the prevalence of LV hypertrophy in IO hypertensives
and sustained hypertensives.
Our study does not explain the underlying mechanism leading to the development
of LV changes in IO hypertension, but it may be speculated that transient
BP increases, caused by exaggerated responses to mild stress, such as during
medical evaluation, may have an effect on cardiac growth, leading to hypertrophy.
One study35 in dogs showed that concentric
LV hypertrophy can be produced by intermittent compression of the dogs' limbs
to increase BP. Furthermore, experimental studies have shown that brief episodes
of cardiac pressure overload are sufficient to induce growth-related genes
and protein synthesis in the heart.36
Left ventricular hypertrophy is an independent risk factor for cardiovascular
morbidity and mortality37; therefore, taken
together, the findings of increased LV mass and decreased diastolic function
indicate that IO hypertension confers an increased cardiovascular risk, also
when the diagnosis of IO hypertension is based on a restrictive cutoff value
for normal daytime BP.
Recently, Muldoon et al,19 matching individuals
on the basis of clinical and daytime BP, reached similar results regarding
carotid artery changes: carotid artery involvement (increased intima media
thickness and plaque index) was greater in IO hypertensives than in normotensives
and was similar to that in sustained hypertensives.
In conclusion, IO hypertension, defined on the basis of a restrictive
value for normal daytime BP, is associated with LV morphofunctional changes
similar, at least qualitatively, to those found in never-treated sustained
hypertensives. In fact, in strictly BP-matched groups, IO hypertensives have
increased LV mass and decreased LV diastolic indices compared with normotensives,
with sustained hypertensives having higher LV mass and lower diastolic function
compared with IO hypertensives. These differences are not accounted for by
differences in age, sex, BMI, clinic BP, or ambulatory BP. Therefore, the
results of this study support the hypothesis that IO hypertension should not
be simply considered a benign condition; further studies are needed to determine
whether longitudinal monitoring and nonpharmacological interventions are enough
or whether IO hypertensives with demonstrated cardiovascular remodeling also
need drug treatment.
AUTHOR INFORMATION
Accepted for publication April 19, 2001.
Corresponding author and reprints: Anna M. Grandi, MD, via Bagaini
15, 21100 Varese, Italy (e-mail: amgrandi{at}libero.it).
From the Department of Clinical and Biological Sciences, Faculty of
Medicine, University of Insubria, Varese, Italy.
REFERENCES
| |
1. Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension? JAMA. 1988;259:225-228.
FREE FULL TEXT
2. 1999 World Health Organization–International Society of Hypertension
Guidelines for the Management of Hypertension. J Hypertens. 1999;17:151-183.
ISI
| PUBMED
3. Verdecchia P, Schillaci G, Boldrini F, Zampi I, Porcellati C. Variability between current definitions of "normal" ambulatory blood
pressure: implications for the assessment of white-coat hypertension. Hypertension. 1992;20:555-562.
FREE FULL TEXT
4. Pickering TG, Coats A, Mallion JM, Mancia G, Verdecchia P. Blood pressure monitoring, task force V: white-coat hypertension. Blood Press Monit. 1999;4:333-341.
PUBMED
5. 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.
FREE FULL TEXT
6. Gosse P, Promax H, Durandet P, Clementy J. "White coat" hypertension: no harm for the heart. Hypertension. 1993;22:766-777.
FREE FULL TEXT
7. Verdecchia P, Porcellati C, Schillaci G, et al. Ambulatory blood pressure: an independent predictor of prognosis in
essential hypertension. Hypertension. 1994;24:793-801.
FREE FULL TEXT
8. Cavallini MC, Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Is white coat hypertension associated with arterial disease or left
ventricular hypertrophy? Hypertension. 1995;26:413-419.
FREE FULL TEXT
9. Pierdomenico SD, Lapenna D, Guglielmi MD, et al. Target organ status and serum lipids in patients with white coat hypertension. Hypertension. 1995;26:801-807.
FREE FULL TEXT
10. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Zampi I, Gattobigio R. White-coat hypertension and white-coat effect: similarities and differences. Am J Hypertens. 1995;8:790-798.
FULL TEXT
|
ISI
| PUBMED
11. Julius S, Mejia A, Jones K, et al. "White coat" versus "sustained" borderline hypertension in Tecumseh,
Michigan. Hypertension. 1990;16:617-623.
FREE FULL TEXT
12. Kuwajima I, Suzuki Y, Fujisawa A, Kuramoto K. Is white coat hypertension innocent? structure and function of the
heart in the elderly. Hypertension. 1993;22:826-831.
FREE FULL TEXT
13. Hoegholm A, Bang LE, Kristensen KS, Nielsen JW, Holm J. Microalbuminuria in 411 untreated individuals with established hypertension,
white coat hypertension and normotension. Hypertension. 1994;24:101-105.
FREE FULL TEXT
14. Cerasola G, Cottone S, Nardi E, et al. White-coat hypertension and cardiovascular risk. J Cardiovasc Risk. 1995;2:545-549.
FULL TEXT
| PUBMED
15. Glen SK, Elliot HL, Curzio JL, Lees KR, Reid JL. White-coat hypertension as a cause of cardiovascular dysfunction. Lancet. 1996;348:654-657.
FULL TEXT
|
ISI
| PUBMED
16. Chang NC, Lai ZY, Chan P, Wang TC. Left ventricular filling profiles in young white coat hypertensive
patients without hypertrophy. Hypertension. 1997;30:746-752.
FREE FULL TEXT
17. Palatini P, Mormini P, Santonastaso M, et al for the HARVEST Study Investigators. Target organ damage in stage I hypertensive subjects with white coat
and sustained hypertension: results from the HARVEST Study. Hypertension. 1998;31:57-63.
FREE FULL TEXT
18. Muscholl MW, Hense HW, Brockel U, Doring A, Riegger GAJ, Schunkert H. Changes in left ventricular structure and function in patients with
white coat hypertension: cross sectional survey. BMJ. 1998;317:565-570.
FREE FULL TEXT
19. Muldoon MF, Nazzaro P, Sutton-Tyrrell K, Manuck SB. White-coat hypertension and carotid artery atherosclerosis: a matching
study. Arch Intern Med. 2000;160:1507-1512.
FREE FULL TEXT
20. Cuspidi C, Marabini M, Lonati L, et al. Cardiac and carotid structure in patients with established hypertension
and white-coat hypertension. J Hypertens. 1995;13:1707-1711.
ISI
| PUBMED
21. Khattar RS, Senior R, Lahiri A. Cardiovascular outcome in white-coat versus sustained mild hypertension:
a 10-year follow-up study. Circulation. 1998;98:1892-1897.
FREE FULL TEXT
22. Zakopoulos N, Papamichael C, Papaconstantinou H, et al. Isolated clinic hypertension is not an innocent phenomenon: effect
on the carotid artery structure. Am J Hypertens. 1999;12:245-250.
FULL TEXT
|
ISI
| PUBMED
23. Upton MT, Gibson DG. The study of left ventricular function from digitized echocardiograms. Prog Cardiovasc Dis. 1978;20:359-384.
FULL TEXT
|
ISI
| PUBMED
24. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: validation
of the method. Circulation. 1977;55:613-618.
FREE FULL TEXT
25. Hammond IW, Devereux RB, Alderman MH, Laragh JH. Relation of blood pressure and body build to left ventricular mass
in normotensives and hypertensive employed adults. J Am Coll Cardiol. 1988;12:996-1004.
ABSTRACT
26. Mancia G, Sega R, Bravi C, et al. Ambulatory blood pressure normality: results from the PAMELA study. J Hypertens. 1995;13:1377-1390.
ISI
| PUBMED
27. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Porcellati C. White-coat hypertension: not guilty when correctly defined. Blood Press Monit. 1998;3:147-152.
PUBMED
28. Dahlof B, Pennert K, Hansson L. Reversal of left ventricular hypertrophy in hypertensive patients:
a meta-analysis of 109 treatment studies. Am J Hypertens. 1992;5:95-110.
ISI
| PUBMED
29. Grandi AM, Venco A, Bertolini A, et al. Left ventricular function after reversal of myocardial hypertrophy
in systemic hypertension and response to acute increase of afterload by cold
pressor test. Am J Cardiol. 1992;69:1439-1441.
FULL TEXT
|
ISI
| PUBMED
30. Owens PE, Lyons SP, Rodriguez SA, O'Brien ET. Is elevation of clinic blood pressure in patients with white coat hypertension
who have normal ambulatory blood pressure associated with target organ changes? J Hum Hypertens. 1998;12:743-748.
FULL TEXT
|
ISI
| PUBMED
31. Soma J, Wideroe TE, Dahl K, Rossvoll O, Skjaerpe T. Left ventricular systolic and diastolic function assessed with two-dimensional
and Doppler echocardiography in "white coat" hypertension. J Am Coll Cardiol. 1996;28:190-196.
ABSTRACT
32. Lee CH, Hogan JC, Gibson DG. Diastolic disease in left ventricular hypertrophy: comparison of M-mode
and Doppler echocardiography for the assessment of rapid ventricular filling. Br Heart J. 1991;65:194-200.
FREE FULL TEXT
33. Philips RA, Goldman ME, Ardeljan M, et al. Determinants of abnormal left ventricular filling in early hypertension. J Am Coll Cardiol. 1989;14:977-985.
ISI
| PUBMED
34. Kapuku GK, Seto S, Mori H, et al. Impaired left ventricular filling in borderline hypertensive patients
without cardiac structural changes. Am Heart J. 1993;125:1710-1716.
FULL TEXT
|
ISI
| PUBMED
35. Kingwell BA, Krause L, Julius S. The effect of hypertensive episodes and cardiac hypertrophy on the
canine cardiac baroreflex. Clin Exp Pharmacol Physiol. 1994;21:31-39.
ISI
| PUBMED
36. Schunkert H, Sandoshima JI, Kagaya Y, Weinberg EO, Izumo S, Riegger G. Angiotensin II induced growth responses in isolated adult rat hearts:
evidence for load independent induction of cardiac protein synthesis by angiotensin
II. Circ Res. 1995;76:489-497.
FREE FULL TEXT
37. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular
mass in the Framingham Heart Study. N Engl J Med. 1990;322:1561-1566.
ABSTRACT
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