Download Left Ventricular Hypertrophy in Hypertension

Left Ventricular Hypertrophy in Hypertension
Prevalence and Relationship to Pathophysiologic Variables
RICHARD B. DEVEREUX, THOMAS G. PICKERING, MICHAEL H. ALDERMAN, SHU CHIEN,
JEFFREY S. BORER, AND JOHN H.
LARAGH
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SUMMARY In less than a decade since development of echocardiographic measurement of left ventricular
muscle mass, studies using this technique have provided considerable information about the prevalence and
pathophysiology of left ventricular hypertrophy in human hypertension. Increased left ventricular mass has been
found in a significant minority of patients with systemic hypertension, with the exact prevalence dependent both
on how a population is selected and on the sex, race, and possibly age composition of its members. All published
studies have reported that left ventricular hypertrophy is more closely related to blood pressure recorded in the
patient's natural setting during normal activity or exercise — whether measured by portable recorder or home
manometer — than to blood pressure measured by the physician. In addition, studies indicate that the classic
hypertensive abnormalities of concentric left ventricular hypertrophy and increased peripheral resistance are
interrelated, while left ventricular hypertrophy is absent in a subgroup of patients with mild essential hypertension who exhibit high cardiac output and evidence of supernormal myocardial contractility. Conversely, the left
ventricular functional response to exercise is inversely related to the degree of hypertrophy. High levels of blood
viscosity, which would tend to blunt the reduction in peripheral resistance expected during sleep or exercise, have
also been associated with left ventricular hypertrophy in patients with essential hypertension. Echocardiographic
studies have provided evidence both for and against the hypothesis that activity of the sympathetic or reninangiotensin systems plays a direct role in causing hypertensive cardiac hypertrophy. These findings demonstrate
the useful role that echocardiographic assessment of left ventricular structure and function may play in hypertension research. (Hypertension 9 [Suppl II]: II-53-II-60, 1987)
KEY WORDS
•
echocardiography
• hypertension
• left ventricular hypertrophy
• blood pressure
blood viscosity
L
In this review, we summarize the available data to provide
preliminary answers to the following questions: Do all patients
with systemic hypertension exhibit cardiac involvement? Is hypertensive cardiac hypertrophy closely related to the level of
blood pressure, or does it convey independent information
about disease severity? Are cardiac findings related to cardiovascular dynamics in patients with hypertension? Do neural or
endocrine factors directly influence the heart — beyond their
influence on hemodynamics?
EFT ventricular hypertrophy (LVH) plays a dual role in
patients with systemic hypertension — being both a
J necessary adaptation to pump a normal amount of
blood against the increased pressure load and a pathologic manifestation of hypertensive cardiovascular disease. For many
years, knowledge of the complex status of the heart in human
hypertension advanced slowly because of the lack of suitable
means of measuring cardiac anatomy and function in unselected
hypertensive patients or of following their natural history. The
development over the last decade of accurate echocardiographic
methods for detection of LVH and characterization of ventricular contractile performance has catalyzed an explosion of information about the heart in hypertension.
Prevalence of Left Ventricular Hypertrophy in
Hypertension
Detection of LVH by echocardiogram depends not only on
the established accuracy of the method in reflecting anatomic
findings1'2 but also on use of correct normal limits. Although
considerable progress has been made in establishing statistically
reliable and reproducible normal limits,3' 4 no single criterion is
yet completely validated and universally accepted. Despite this,
tentative conclusions may be drawn about the prevalence of
LVH among patients with hypertension by examining the
results of studies in which hypertensive patients and normoten-
From the Department of Medicine, The New York Hospital-Cornell
Medical Center; the Department of Epidemiology and Social Medicine,
Albert Einstein College of Medicine; and the Department of Physiology,
Columbia University College of Physicians and Surgeons, New York, New
York.
Supported in part by Grant HL 18323 from the National Heart, Lung, and
Blood Institute.
Address for reprints: Richard B. Devereux, M.D., Division of Cardiology, Box 222, The New York Hospital-Cornell Medical Center, 525 East
68th Street, New York, NY 10021.
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FIGURE 1. Prevalence of left ventricular hypertrophy (LVH) in
four independent groups ofpatients with essential hypertension and
normotensive controls.5~s (Reprinted from Devereux el al.'° with
permission.)
sive controls were evaluated by identical echocardiographic
methods.
This approach can be applied in four available clinical studies
of patients with essential hypertension5"8 that include comparison groups of apparently normal subjects.6"9 In these studies the
overall prevalence of LVH was determined by applying identical cutoffs for left ventricular (LV) mass indexed for body size
(e.g., LV mass/body surface area > 120 g/m2) to both patients
and control populations. The prevalence of LVH was 23 to 48%
in hypertensive patients and 0 to 10% in normal subjects (Figure
1). Overall, 189 of 450 (42%) of hypertensive patients and 9 of
251 (3.6%) of controls exhibited LVH (chi square test = 117.1,
p< 10"6).10 These data establish that LVH occurs in a substantial minority of patients with mild to moderately severe essential
hypertension evaluated in a referral center. The finding that
LVH was detected by echocardiogram in a slightly higher percentage of apparently normal subjects than had been expected
statistically for upper 95% confidence limits (3.6% vs 2.5%)
may reflect a slight random fluctuation of results in a moderate
sized sample or admixture of a few individuals with clinically
undetected heart disease. A recent study" indicates that the
prevalence of LVH by the same echocardiographic criteria is
somewhat lower — 17% and 21%, respectively — among unselected patients with uncomplicated borderline or established
hypertension drawn from an employed population.
Further information about the prevalence of LVH in patients
with hypertension has been derived from more recent studies of
factors that influence normal LV mass or appear to modify the
cardiac response to hypertension. Of greatest importance in this
regard is recognition of demographic variables that should be
taken into account in determining statistically valid upper limits
of normal LV mass. All available studies agree that LV mass
should be indexed by body size, of which body surface area
appears to be the best measure by a narrow margin.4 Similarly,
the three largest echocardiographic studies of normal subjects3- *•' have found that LV mass indexed by body surface
area differs significantly between men and women, and the
primary LV measurements reported by Valdez et al.12. are in
accord with this conclusion. The tentative cutoff values we have
proposed for recognition of LVH, representing the 97th percentile of values in apparently normal subjects,4 are 2 111 g/m2 in
women and a 135 g/m2 in men.
2, FEBRUARY
1987
Effect of Sex
The prevalence of LVH found in men and women with essential hypertension is strikingly dependent on whether one uses
such sex-specific criteria or a single criterion of LV mass indexed for body surface area. When a single cutoff value for
hypertension is applied to both sexes, the prevalence of LVH is
consistently higher among men (26-56%) than women (1842%) in clinical studies 7 ' l3 ' 14 (Figure 2A). When sex-specific
criteria are used, however, a higher proportion of female
(43-61%) than male (18—41%) hypertensive subjects exhibit
LVH (Figure 2B). We have recently obtained similar results
(i.e., a higher prevalence of LVH in women by sex-specific
criteria and in men by unified criteria) in a study of patients with
hypertension in an employed population." The reasons for this
discrepancy between men and women with hypertension are not
clear but might include either a selective reduction in physical
activity among men with hypertension or a substantial prevalence of clinically inapparent heart disease, associated with mild
LVH, among apparently normal men. Longitudinal studies of
physical activity, cardiac status, and cardiovascular morbidity
will be needed to determine the cause.
Influence of Race
No difference has been detected between normal black and
white subjects in any echocardiographic measurement of LV
anatomy or function."' " In contrast, both Dunn etal. 16 and our
group"' 15 have reported that black patients with essential hypertension have a greater degree of LVH than white patients
with similar levels of clinically measured blood pressure, but
this was not found in a previous study.17 Our findings demonstrate a significant increase in relative wall thickness, an index
of concentric LVH, in black patients compared to white patients
of similar age, duration of hypertension, and prior treatment
status identified through the same worksite clinics (Table 1). In
the same group, the greater degree of concentric LVH among
black patients was associated with a modest elevation of peripheral resistance (Table 1), whereas white patients from the same
population exhibited an increased cardiac output without a significant increase in peripheral resistance.15 This evidence of
greater concentric LVH and a hemodynamic pattern felt to characterize more advanced hypertension in black as compared to
white patients makes an interesting parallel with the known
higher incidence of cardiovascular morbidity in black hypertensive persons,18 although it has not yet been established whether
the excess morbidity among blacks is accounted for by the
subset with concentric LVH.
Age and Hypertensive Cardiac Hypertrophy
Both increasing age and duration of hypertension would logically be expected to be associated with a higher prevalence and
greater severity of hypertensive cardiac hypertrophy, but we
have not been able to demonstrate this in cross-sectional studies
of large clinical6'7 or unselected" populations of patients with
systemic hypertension. Evidence does suggest, however, that a
small proportion of elderly hypertensive patients develop severe
LVH associated with symptoms of cardiac dysfunction. Topol
et al.19 recently reported 21 elderly patients with systemic hypertension, predominantly black women, with a mean age of 73
years, who exhibited severe concentric LVH, supernormal LV
systolic function, and severely impaired early diastolic LV filling. In an echocardiographic study of the original Framingham
cohort (mean age, 70 ± 7 years), Savage et al. 20 found that 27 of
1620 (1.7%) exhibited disproportionate thickness of the interventricular septum, associated in nearly all such subjects with a
history of at least mild hypertension as well as a high prevalence
of heart murmurs and cardiac symptoms. By their design, neither of these reports permits calculation of the prevalence of
cardiac hypertrophy among elderly patients in whom systemic
11-55
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FIGURE 2. Prevalence of left ventricular hypertrophy (LVH) in three independent groups of patients with essential
hypertension subdivided by sex.7' '*• '5 A. When the upper limit of normal for both sexes pooled (> 120 glm2) is used,
prevalence of LVH is higher in male patients. B. When sex-specific 97thpercentile upper limits of normal are used (males
2:135 glm2; females ^110 glm2), the prevalence of LVH is higher in female patients. (Reprinted from Devereux et al.10
with permission.)
hypertension has been diagnosed by conventional clinical criteria although the Framingham Study has an optimal data base in
which to do so.3
Hypertensive Cardiac Hypertrophy and Blood Pressure
Although early studies of highly selected patients suggested
that heart weight was closely related to the level of arterial blood
pressure,21 it is now clear that this is not normally the case. In
several groups of patients with uncomplicated essential hypertension, physician measurements of systolic blood pressure
have been only weakly related to echocardiographic LV mass,
with correlation coefficients of 0.24 to 0.45. 7 ' 1 3 2 2 - 2 3 Even
weaker correlations were observed in these studies between
diastolic arterial pressure and LV mass. A similarly modest
relationship (r = 0.43) was observed by Abi-Samra et al.24 in a
study of 74 patients with systemic hypertension.
Ambulatory Blood Pressure
Twenty years ago Sokolow et al.25 reported that evidence of
cardiovascular damage in patients with hypertension was more
closely related to blood pressure measured by a portable recorder than by physicians. More recently, the same group has reported that ambulatory blood pressure measurements were better
predictors than casual determinations of subsequent morbid
events in patients with hypertension.26 Both these studies, however, used an ambulatory recording system that was patient-
activated, thus precluding complete 24-hour recordings, and
also employed indirect means of detecting LVH, such as the
electrocardiogram.
Recording blood pressure through the entire 24-hour period
has been made possible by development of invasive27 and noninvasive28- M systems with acceptable accuracy. Because of
their greater acceptability and safety, noninvasive systems have
been most widely used and have provided important information about blood pressure variability30 with implications for
patient management.31 Three studies have compared the relationships between echocardiographically determined LV mass
and physician or 24-hour blood pressure measurement.7'32-33 In
each study average 24-hour systolic blood pressure was the
closest correlate of LV mass (Table 2). To gain further insight
into the relationship between cardiac hypertrophy and Blood
pressure during normal activity, we categorized.ambulatory
blood pressures by the setting in which they were recorded
(e.g., physician's office, occupational workplace, home, and
sleep).7 The closest relationships were observed between LV
mass index and average workplace systolic blood pressure
(r = 0.50, p<0.001) and between end-diastolic relative wall
thickness and average workplace diastolic blood pressure (r =
0.59, p<0.001). In this study LV mass was less closely related
to peak blood pressure than to the average workplace blood
pressure. These data suggest that the blood pressure response to
regularly recurring stress may have particular importance in the
pathogenesis of hypertensive cardiac hypertrophy.
TABLE 1. Cardiac Anatomy and Function in Black and White Normotensive and Hypertensive Subjects
Hypertensive
Narmotensive
Blacks
Whites
Blacks
(n = 30)
Measurement
(n = 62)
P
(n = 70)
P
207.2±56
NS
Left ventricular mass (g)
163.8±49.2
163.2 ±62.6
NS
0.43 ±0.11
<0.05
Relative wall thickness
NS
0.34±0.06
0.36±0.08
5.80±2.16
<0.01
Cardiac output (L/min)
NS
5.93 ±2.05
5.63 ±1.91
Total peripheral resistance
x 103 d y n c m s e c " 3
1.43 ±0.47
Data are means ± SD. NS - not significant.
Adapted from Hammond et al.13
NS
1.36±0.45
1.85±0.72
<0.01
Whites
(n = 45)
203.8 ±76.6
0.37 ±0.07
7 25±2.35
1.42 ±0.46
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ECHOCARDIOGRAPHY
TABLE 2.
SUPPL II HYPERTENSION, VOL 9, No 2, FEBRUARY
Correlation Between Blood Pressure Measurements and Left Ventricular Mass
Physician
Portable recorder
Casual
Self
Physician
24-hour
Workplace
Home
Exercise
Systolic Diastolic
Systolic Diastolic
Systolic Diastolic
Systolic Diastolic
n
Systolic
Diastolic
Devereux et al. 7
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86
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Drayer et al. 33
12
0.55
0.10
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0.56
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—
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Ren et al. 34
67
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-0.02
Reference
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1987
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—
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—
Data are correlation coefficients between left ventncular mass and the specified type of blood pressure measuring except for the study
of Kleinert et al.20 in which end-diastolic relative wall thickness was the index of left ventncular hypertrophy.
*= p < 0.001; t = p < 0.05; t= p < 0.01. Other correlations are not significant.
Other Blood Pressure Measurements
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Because obtaining precise 24-hour ambulatory blood pressure recordings is cumbersome and technically difficult, considerable attention has been devoted to finding other methods of
obtaining a reliable estimate of patients' average blood pressure. Two recent studies have yielded promising results. In the
first, we22 demonstrated that home blood pressure recordings by
trained patients not only provided a better estimate of average
24-hour blood pressure than did physician measurements but
also were more closely correlated to indices of LVH. The second study, by Ren et al., 34 reported a substantially closer relationship of LV mass to maximum systolic arterial pressure during treadmill exercise testing than to blood pressure at rest prior
to exercise (see Table 2).
Hypertensive Cardiac Hypertrophy and Cardiovascular
Dynamics
Because cardiac hypertrophy is felt to be an important adaptive response to hypertension, consideration must be given to
the degree to which LVH is matched to the hemodynamic load
and is successful in maintaining cardiac performance in hypertension. In the first studies in this regard, performed by Folkow35 in experimental animals, the severity of cardiac hypertropHy tended to parallel the severity of peripheral vascular
resistance. In a subsequent study by Shkhvatsabaya and coworkers,36 echocardiographically determined LV mass correlated significantly (r = 0.60, p<0.001) with vascular resistance
in the calf, measured by plethysmography during maximal
vasodilation.
Extending this line of investigation to 100 patients with essential hypertension, we examined the relationships between
systemic hemodynamics and the pattern of LV anatomy.13 A
significant positive correlation (r = 0.52, p<0.001) was observed between total peripheral resistance and end-diastolic LV
relative wall thickness (Figure 3A). Furthermore, cardiac index
was inversely related to relative wall thickness (r = —0.47,
p < 0.001) (Figure 3B). Taken together, these experimental and
clinical studies suggest that the cardiac pattern of concentric
LVH and the hemodynamic pattern of elevated peripheral resistance with low cardiac output are pathophysiologically interrelated.
Left Ventricular Performance
To investigate further the relationships between cardiac structure and function, we have performed an additional series of
studies. In order to exclude the possibility that excessive or
inadequate degrees of LVH in relation to blood pressure load
accounted for differences in LV function, we measured myocardial afterload by calculating end-systolic LV wall stress with a
catheterization-validated formula.37 As predicted from basic
principles of cardiac mechanics, a close inverse relationship
existed in 87 normotensive subjects between end-systolic stress
and LV fractional shortening, an echocardiographic index of
systolic ventricular performance (r = -0.83, /?<0.OOOl).38 A
significant inverse relationship between these variables was also
observed in 81 unmedicated patients with essential hypertension
(r = -0.78, p<0.001). When the data points from the hypertensive patients were superimposed on 95% confidence limits
derived from the normal subjects (Figure 4), a significant proportion of the hypertensive patients exhibited high fractional
shortening in relationship to wall stress (19 of 81 or 23%;
/><0.001 vs 1 of 87 normotensive subjects).
Subdivision of hypertensive patients into groups with normal
and increased LV performance based on this analysis of cardiac
mechanics revealed striking differences in both systemic hemodynamics and LVH (Table 3). Of note, the patients with increased ventricular performance exhibited substantially increased cardiac output, lower peripheral resistance, and an
absence of LVH compared to the hypertensive patients with
normal ventricular performance. In a more recent study from
our laboratory, hypertensive patients who had high fractional
shortening in relation to end-systolic stress on baseline measurements exhibited a significantly higher (p< 0.005) slope of the
end-systolic force-length line during nitroglycerin-induced reduction in hemodynamic load than hypertensive patients who
fell into the normal range of fractional shortening in relation to
end-systolic stress.39 Taken together, these studies suggest that
in the majority of mildly hypertensive patients the heart plays a
secondary role, undergoing adaptive hypertrophy in proportion
to the elevation of blood pressure. In a significant minority of
such patients, however, increased myocardial contractility may
have pathogenetic importance by allowing the heart to pump an
increased cardiac output without need for any hypertrophy.
Since an important capacity of the normal heart is the ability
to sustain a strikingly increased hemodynamic load during normal activity, assessment of the heart in hypertension is not
complete without evaluation of the cardiac responses to exercise. This has been directly evaluated by means of radionuclide
cineangiography at rest and during exercise in several recent
studies.40' 41 Among hypertensive patients with no evidence of
coronary artery disease, the prevalence of abnormal LV ejection
fraction responses to exercise has ranged from 9 of 37 patients
(24%)42 to 15 of 20 patients (75%).43 Our studies40'4I indicate
that a small proportion — approximately 10% — of the hypertensive patients who exhibit abnormal LV functional reserve
can be identified by evidence of impaired myocardial contractility (low echocardiographic fractional shortening in relation to
end-systolic stress) at rest; whereas in the remainder, LV dysfunction is only revealed by imposition of exercise stress. A
preliminary study from our laboratory44 suggests that LV dysfunction during exercise and LVH are closely linked, with an
inverse linear relationship (r = -0.50, p<0.0\) between echo-
HYPERTENSIVE CARDIAC HYPERTROPHY/Devfreu* et al.
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5
Total peripheral resistance (dyne-sec-cm" )
FIGURE 3. A. Left ventricular (LV) relative wall thickness at end diastole (vertical axis) is directly related to total
peripheral resistance (horizontal axis) in 100 unmedicated patients. B. Cardiac index (vertical axis) is inversely related
to LV relative wall thickness at end diastole (horizontal axis). (Reprinted from Devereux et al.'3 with permission.)
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cardiographically determined LV muscle mass and the change
in LV ejection fraction from rest to exercise observed among
hypertensive patients with LVH.
The ability of the left ventricle to sustain a normal or increased workload is also dependent on its diastolic performance
characteristics. Abnormalities of LV diastolic time intervals and
filling rates have been well documented in patients with systemic hypertension45' ** and may be a more sensitive marker of
hypertensive cardiac involvement than echocardiographic
LVH.47 These diastolic abnormalities appear to be manifestations of so-called pathologic LVH since subjects with a similar
degree of exercise-induced physiologic hypertrophy exhibited
normal LV diastolic properties in one study.48
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Blood Viscosity
Several lines of evidence suggest that altered blood rheology
may be importantly related to cardiac findings in hypertension.
Hematocrit and blood viscosity have been found to be higher in
hypertensive than normotensive individuals.49' w Recently we
reported a modest direct relationship between blood pressure
and whole blood viscosity in both hypertensive and normotensive subjects." We found that increased whole blood viscosity
in unselected patients with mild essential hypertension accounted for the entire increase in peripheral resistance in them as
compared with normotensive subjects drawn from the same
employed population.52 Finally, high rates of cardiovascular
morbidity have been reported in patients with hyperviscosity
due to hypertension53 or so-called pseudo-polycythemia.54 No
study, however, had related blood viscosity to objective cardiac
measurements in patients with hypertension.
Therefore, we recently undertook a study to examine the
relationships among arterial blood pressure, whole blood viscosity, and LVH in 24 patients with essential hypertension and
13 age- and sex-matched control subjects.23 A significant correlation was observed between mean arterial blood pressure and
whole blood viscosity in this study population (r = 0.52,
p<0.005). Similarly, mean blood pressure was modestly related to LV mass in the hypertensive patients (r = 0.47, p<0.02)
and in the normotensive subjects (r = 0.44, p = NS; Figure
TABLE 3. Hemodynamics and Left Ventricular Hypertrophy in Hypcrtensive Patients with Normal and Increased Left Ventricular Performance
Variable
Patients
with
normal LV
performance
p
Age (yr)
53±9
NS
55 + 13
111±13
NS
112±15
Cardiac index (L/min/m2)
3.39±1.00
<0.005
4.25±1.33
Total peripheral resistance
(dyncmsec" 5 )
Relative wall thickness
1,582 ±584
0 42±0.10
<0.05
<0.005
l,257±5O2
0.34±0.06
End systolic stress (»K3 dynes/cm 2 )
FIGURE 4. Data points for left ventricularfractionalshortening
and end-systolic stress in 81 untreated patients with essential hypertension are superimposed on the solid regression line and
dashed 95% confidence interval of this relationship in 87 normal
subjecfs. A close inverse relation is observed (T = —0.78, p <
0.001), and 19 of 81 hypertensive patients exhibit increased ventricular function in relation to wall stress (compared to 1 of 87
normotensive subjects, p<0.0001). (Reprintedfrom Lulas et al.3S
with permission of the American Heart Association.)
Mean blood pressure (mm Hg)
LV = left ventricular, NS = not significant.
Adapted from Lutas et al. 3 *
Patients
with
increased LV
performance
11-58
ECHOCARDIOGRAPHY
SUPPL II HYPERTENSION, VOL 9, No 2, FEBRUARY
1987
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FIGURE 5. A. Mean blood pressure and left ventricular (LV) mass in patients with essential hypertension (r = 0.47,
p < 0.02) and in normotensive control subjects (r = 0.44, NS). B. Relationship between blood viscosity at a shear rate of
104 sec'1 (T\B 104) and LV mass. A close relation exists between these variables in the hypertensive patients (r = 0.80,
p < 0.001), and the points for hypertensive patients without LV hypertrophy (below dotted line) tend to overlap those of
the normotensive control subjects. (Reprinted from Devereux et al.23 with permission.)
5A). A close correlation was observed (Figure 5B) between
whole blood viscosity at the high shear rate of 104 sec ~' and LV
mass in the hypertensive patients (r = 0.80, p< 0.001), which
was significantly closer than the correlation between mean
blood pressure and LV mass (p<0.02). Furthermore, as shown
in Figure 5B, the relationship between viscosity and LV mass in
normotensive subjects closely resembled that in the hypertensive patients with normal whole blood viscosity.
Neurohumoral Factors and Hypertensive Cardiac
Hypertrophy
Although hemodynamic factors have received the most attention in studies of the pathogenesis of hypertensive cardiac hypertrophy, considerable scatter clearly exists in the relationships
between the best available measures of blood pressure and LV
muscle mass. The search for nonhemodynamic causes of LVH
in hypertensive patients has focused mostly on neurohumoral
factors, principally the sympathetic and renin-angiotensin
systems.
Evidence in favor of the so-called catecholamine hypothesis
of LVH was originally derived from studies using sympathetic
agonists33 and antagonists56 in intact animals. More recently,
Simpson and co-workers37' 38 have provided evidence that induction of protein synthesis by norepinephrine in tissue-cultured cardiac myocytes is an a,-receptor-mediated phenomenon. Limited studies in patients with essential hypertension
have suggested a positive relationship between plasma norepinephrine concentration and LV mass59 and a greater reduction in
LV mass than blood pressure during treatment with sympatholytic drugs. 60 ' 6I These results have not been consistently observed,62 however, and recent observations in patients with
pheochromocytoma63 suggest that applicability of the catecholamine hypothesis to clinical hypertension may be limited.
The suggestion that renin-angiotensin system activity directly stimulates myocardial hypertrophy is also based primarily on
experimental observations. Thus, Robertson et al.6* reported
that radiolabeled angiotensin II rapidly localized in nuclei of
cardiac and smooth muscle cells, while Khairallah and Kanabus65 have documented a significant increase in ventricular
weight after 6 days of angiotensin II infusion at a mildly pressor
dose. Some studies of patients treated with angiotensin converting enzyme inhibitors have suggested that echocardiographic
LV mass may decrease more than expected for the induced
reduction in blood pressure,6* but this finding has not been
consistent.67' M
Our studies suggest that the renin-angiotensin system may
have more important effects on LV function than on its structure. Thus, patients with low-renin essential hypertension had
higher LV fractional shortening and cardiac index than those in
normal and high-renin subgroups,6 while relief of vasoconstriction by captopril in those with high-renin essential hypertension
was associated with an increase in cardiac index.68 In a separate
study,69 we observed an inverse relation between plasma renin
activity and LV fractional shortening, an index of systolic performance. We have subsequently documented that patients with
renovascular hypertension, the overwhelming majority of
whom have high plasma renin levels, have significantly poorer
LV systolic function than age-, sex- and blood pressurematched patients with essential hypertension.70
Acknowledgment
We thank Miss Virginia Bums for her assistance in preparation of this
manuscript.
References
1. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation
1977^5:613-618
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Left ventricular hypertrophy in hypertension. Prevalence and relationship to
pathophysiologic variables.
R B Devereux, T G Pickering, M H Alderman, S Chien, J S Borer and J H Laragh
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Hypertension. 1987;9:II53
doi: 10.1161/01.HYP.9.2_Pt_2.II53
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