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Journal of the American College of Cardiology
© 2001 by the American College of Cardiology
Published by Elsevier Science Inc.
Vol. 38, No. 7, 2001
ISSN 0735-1097/01/$20.00
PII S0735-1097(01)01663-1
Left Ventricular Mass and
Cardiovascular Morbidity in Essential
Hypertension: The MAVI Study
Paolo Verdecchia, MD, FACC, Giancarlo Carini, MD, Antonio Circo, MD, Emilio Dovellini, MD,
Ezio Giovannini, MD, Michele Lombardo, MD, Pasquale Solinas, MD, Marco Gorini, MD,
Aldo Pietro Maggioni, MD, and the MAVI Study Group
Firenze, Italy
This study investigated the prognostic value of left ventricular (LV) mass at echocardiography
in uncomplicated subjects with essential hypertension.
BACKGROUND Only a few single-center studies support the prognostic value of LV mass in uncomplicated
hypertension.
METHODS
The MAssa Ventricolare sinistra nell’Ipertensione study was a multicenter (45 centers)
prospective study. The prespecified aim was to explore the prognostic value of LV mass in
hypertension. Admission criteria included essential hypertension, no previous cardiovascular
events, and age ⱖ50. There was central reading of echocardiographic tracings. Treatment was
tailored to the single subject.
RESULTS
Overall, 1,033 subjects (396 men) were followed for 0 to 4 years (median, 3 years). Mean age
at entry was 60 years, and systolic/diastolic blood pressure was 154/92 mm Hg. The rate of
cardiovascular events (⫻100 patient-years) was 1.3 in the group with normal LV mass and 3.2
in the group (28.5% of total sample) with LV mass ⱖ125 g/body surface area (p ⫽ 0.005).
After adjustment for age (p ⬍ 0.01), diabetes (p ⬍ 0.01), cigarette smoking (p ⬍ 0.01) and
serum creatinine (p ⫽ 0.03), LV hypertrophy was associated with an increased risk of events
(RR [relative risk] 2.08; 95% CI [confidence interval]: 1.22 to 3.57). For each 39 g/m2 (1 SD)
increase in LV mass there was an independent 40% rise in the risk of major cardiovascular
events (95% CI: 14 to 72; p ⫽ 0.0013).
CONCLUSIONS Our findings show a strong, continuous and independent relationship of LV mass to
subsequent cardiovascular morbidity. This is the first study to extend such demonstration to
a large nationwide multicenter sample of uncomplicated subjects with essential hypertension.
(J Am Coll Cardiol 2001;38:1829 –35) © 2001 by the American College of Cardiology
OBJECTIVES
It is generally established that left ventricular (LV) mass
determined at echocardiography is a powerful predictor of
cardiovascular disease in apparently uncomplicated subjects
with essential hypertension (1,2). However, only two singlecenter studies explored the prognostic value of LV mass
(3,4) in the specific setting of initially uncomplicated subjects with essential hypertension. Evidence that serial
changes in LV mass over time predict prognosis is also
limited (5–7). The other outcome-based studies on the
prognostic value of LV mass have been conducted in
subjects with suspected coronary artery disease (8), previous
myocardial infarction (MI) (9), renal failure (10,11), or in
the general population (12,13). Hence, although a large
body of evidence indicates the prognostic value of LV mass
in different clinical settings, the specific applicability of
these results to the clinical management of the vast majority
of uncomplicated subjects with essential hypertension remains poorly supported.
To explore the prognostic value of LV mass at echocardiography in the specific setting of uncomplicated subjects
From the ANMCO Research Center, Via La Marmora, 36 Firenze, Italy. Please
see appendix for MAVI Study Group participants. This study was supported in part
by Pfizer Italia, S.p.A.
Manuscript received December 30, 2000; revised manuscript received August 14,
2001, accepted August 29, 2001.
with essential hypertension, we planned the MAssa Ventricolare sinistra nell’Ipertensione arteriosa (MAVI) study, a
prospective, observational, multicenter investigation.
METHODS
Design. The MAVI study was a multicenter, prospective,
observational study carried out in 58 hospital centers in Italy
and endorsed by the Italian Association of Hospital Cardiologists (ANMCO, Associazione Nazionale Medici Cardiologi Ospedalieri). The protocol of MAVI had been published before the start of the study (14). The prespecified
aim (14) was the assessment of the independent prognostic
value of LV mass at echocardiography in subjects with
essential hypertension. In brief, admission criteria to the
MAVI study included clinic blood pressure (BP) in sitting
position ⱖ140 mm Hg systolic or 90 mm Hg diastolic or
current treatment for hypertension, no previous cardiovascular morbid events, age ⱖ50, and absence of valvular heart
disease. Both genders have been included. Patients with
cancer, other important diseases or serum creatinine ⱖ2.0
mg/dl were excluded. Patients under antihypertensive treatment were not required to withdraw their medications when
they entered the study.
Clinical data were stored on a computer using an ad hoc
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Verdecchia et al.
Left Ventricular Mass in Hypertension
Abbreviations and Acronyms
ANMCO ⫽ Associazione Nazionale Medici Cardiologi
Ospedalieri
BP
⫽ blood pressure
BSA
⫽ body surface area
ECG
⫽ electrocardiography
LV
⫽ left ventricular
MAVI
⫽ Massa Ventricolare Sinistra nell’Ipertensione
MI
⫽ myocardial infarction
software for hypertension laboratories provided by ANMCO and sent to the study headquarters in Florence.
Prespecified primary outcome events included fatal and
nonfatal MI, sudden cardiac death, fatal and nonfatal
stroke, other cardiovascular deaths, all-cause death, severe
heart failure requiring hospitalization and severe renal failure requiring dialysis. Secondary events included new-onset
angina (typical chest pain symptoms plus objective evidence
of ischemic changes at electrocardiography [ECG]), transient ischemic attack, and peripheral arteries occlusive disease verified at angiography.
Original source documents of patients who suffered an
end-point event were collected by centers and sent to the
study headquarters. Standard international criteria were
used for definition of outcome events. Myocardial infarction
was diagnosed on the basis of at least two of three standard
criteria (typical chest pain, QRS changes at ECG, transient
elevation of myocardial enzymes by more than twofold the
upper normal laboratory limits). New-onset angina was
defined by chest pain accompanied by typical ischemic
changes on the ECG. Sudden death was defined as a
witnessed death that occurred within an hour after the onset
of acute symptoms, with no history that violence or accident
played any role in the fatal outcome. Stroke was diagnosed on
the basis of rapid onset of localizing and persistent neurological
deficit in the absence of any other disease process explaining
the symptoms. Transient ischemic attack was defined by the
diagnosis, made by a physician, of any sudden focal neurological deficit that cleared completely in less than 24 h.
Electrocardiography. The original ECG tracings were
sent to a central laboratory for reading. The ECG reading
was manual and was performed by one expert reader.
Readers for echocardiographic and ECG tracings were
different, did not work together and were not aware of the
clinical characteristics of patients. The ECGs were recorded
at 25 mm/s and 1 mV/cm calibration. Subjects with
complete bundle branch block, previous MI, WolffParkinson-White syndrome and atrial fibrillation were excluded from analysis. The LV hypertrophy at ECG was
diagnosed using the Perugia score (15,16), which requires
positivity of at least one of the following three criteria:
SV3 ⫹ RaVL ⬎2.4 mV in men or ⬎2.0 mV in women, a
typical strain pattern, or a Romhilt-Estes point score ⱖ5.
Echocardiography. A two-dimensional-targeted M-mode
echocardiographic study was carried out at the beginning of
JACC Vol. 38, No. 7, 2001
December 2001:1829–35
the study in the context of a complete diagnostic workup
including laboratory examinations, ECG and clinical examination. Working meetings among involved investigators
were held periodically. Echocardiograms were recorded on
tape and sent to a central laboratory for reading. Three
expert readers examined the tracings, and the allocation of
tapes to readers was randomized. All measurements were
made on the screen using calipers. A long-axis parasternal
approach was first examined to check perpendicularity of the
ultrasonic beam with respect to the septum. Then, the
short-axis approach was used to take LV diastolic and
systolic measurements (the average of three consecutive
cycles on the best single reading set was considered). The
M-mode study was performed under 2D control using
commercially available instruments. End-diastolic and endsystolic measurements were taken with the patient in partial
left lateral decubitus according to the American Society of
Echocardiography recommendations (17,18). Frames with optimal visualization of interfaces and showing simultaneous
visualization of septum, LV internal diameter and posterior
wall were used for reading. The LV mass was calculated using
the following formula introduced by Devereux et al. (19) on
the basis of necropsy validation studies:
LV mass (g) ⫽ 0.80 ⫻ {1.04 ⫻ [(septal thickness ⫹
LV internal diameter ⫹ posterior wall thickness)3 ⫺
(LV internal diameter)3]} ⫹ 0.6 g
For definition of LV hypertrophy we considered an LV
mass ⱖ125 g/body surface area (BSA) [m2], a partition
point supported by ample prognostic evidence (3–7,17), and
an LV mass ⬎51.0 g/height [m2.7], in order to provide a
more stringent allowance for obesity (20).
Statistical analysis. On the basis of previous data (3,4), we
predicted a prevalence of echocardiographic LV hypertrophy of 30% and a rate of events of 2 per 100 person-years in
the absence versus 4 per 100 person-years in the presence of
LV hypertrophy (14). On this basis, a sample size of 1,811
subjects with an average follow-up time of two years per
patient was estimated to detect a significant difference
between the groups (two-tailed test) with a type I error of
5% and a type II error of 10%. Survival curves were
determined using the Kaplan-Meier product-limit method
(21) and compared by the Mantel (log-rank) test (22). The
effect of prognostic factors on survival was evaluated by the
stepwise Cox model (23). The tested variables were age
(years), gender (men, women), systolic and diastolic BP at
entry and after a median of three years of follow-up,
evidence of coronary heart disease in the father at age ⬍55
or in the mother at age ⬍65 (yes, no), body mass index
(weight[kg]/height[m2]), current cigarette smoking (yes,
no), diabetes (yes, no), serum cholesterol (mg/dl), serum
creatinine (mg/dl), LV mass (g/BSA[m2]) and antihypertensive treatment (no drugs; diuretics and beta-blockers
alone or combined; different antihypertensive regimens).
For the subjects who experienced multiple events, survival
Verdecchia et al.
Left Ventricular Mass in Hypertension
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Table 1. Characteristics of the Study Population
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RESULTS
percent of the subjects did not show any concomitant
traditional risk factors (1,2) in addition to hypertension, and
the remaining 62% showed at least one risk factor. Diabetes
was present in 7.3% of subjects, family history of premature
coronary artery disease in 8.3%, cigarette smoking in 13.5%,
body mass index ⬎30 kg/height [m2] in 21.1%, a serum
cholesterol ⬎250 mg/dl or a total cholesterol/high density
lipoprotein cholesterol ratio ⱖ6.0 in 28.1% of subjects.
Prevalence of LV hypertrophy at echocardiography was
28.5% using the cutoff of 125 g/BSA [m2], and 47.5% using
51.0 g/height [m2.7]. Prevalence of LV hypertrophy at ECG
was 19.7%.
Follow-up. After a median of three years of follow-up,
average BP was 146/86 mm Hg (SD 15/8). Only 32.5% of
subjects achieved adequate BP control (BP ⬍140 mm Hg
systolic and ⬍90 mm Hg diastolic). The distribution of
antihypertensive regimens at entry and on follow-up is
reported in Figure 1.
Cardiovascular events. The subjects who developed a first
cardiovascular event during follow-up numbered 83. Fiftyfive of these were in the group (n ⫽ 1,033) who had
good-quality echocardiographic tracings (Table 2). Thirty
of the 55 cardiovascular events were primary events. Total
event rate (per 100 person-years) did not differ between the
subjects with suboptimal tracings and the other group (1.6
vs 1.8, respectively; p ⫽ 0.54 [log-rank test]). In the subset
with good-quality echocardiographic tracings, event rate
was 1.8 in the total population, 1.3 in the subset with
normal LV mass (⬍125 g/BSA [m2]) and 3.2 in that with
increased LV mass (log-rank test: p ⫽ 0.0005). Incidence of
total cardiovascular events in the two groups is shown in
Figure 2.
Overall, there were 4 subjects with sudden cardiac death,
9 with MI, 13 with stroke, 9 with transient ischemic attack,
3 with heart failure, 11 with new-onset unstable angina, 5
with arterial occlusive disease and 1 with severe progressive
renal failure requiring dialysis.
Organization. The MAVI study began in October 1995 in
58 hospital centers within Italy. Overall, 1,857 subjects were
enrolled up to December 1998 and follow-up was concluded
on December 31, 1999. Incomplete follow-up, predefined
by follow-up information available in ⬍50% of subjects, was
reason for exclusion from the study for 13 centers and 197
subjects. The remaining 45 centers enrolled 1,660 subjects.
Of these, 627 (38%) were rejected because of echocardiographic tracings of suboptimal technical quality on judgment of the reading center, thus leaving 1,033 subjects for
the final analysis.
Baseline findings. Table 1 shows some baseline characteristics of these subjects. Distribution of antihypertensive
regimens at entry and on follow-up is shown in Figure 1.
Distribution of the six stages of the Joint National Committee VI classification (optimal BP, normal BP, highnormal BP, stage I, stage II, stage III) (1) was 0.3%, 2.1%,
8.9%, 45.2%, 33.0% and 10.4%, respectively. Thirty-eight
MULTIVARIATE ANALYSIS. As shown in Table 3, after adjustment for the significant influence of age, cigarette
smoking and diabetes, there was an independent 37%
increase in the risk of primary events for any 39 g (1 SD)
increase in LV mass (95% CI: 5 to 80; p ⫽ 0.020).
Furthermore, after adjustment for age, cigarette smoking,
serum creatinine concentration and diabetes, for any 39 g
(1 SD) increase in LV mass there was a 40% rise in the risk
of total cardiovascular events (95% CI: 14 to 73; p ⫽
0.0013). None of the other variables yielded statistical
significance, including LV hypertrophy at ECG. When LV
mass entered the Cox analysis as a binary variable (below vs.
above 125 g/m2), the risk associated with LV hypertrophy
remained significant for total cardiovascular events (RR ⫽
2.08; 95% CI: 1.22 to 3.57; p ⫽ 0.007) and primary events
(RR ⫽ 1.51; 95% CI: 1.19 to 1.92; p ⫽ 0.008). Systolic and
diastolic BP at entry and on follow-up did not achieve
significance.
Characteristic
Value
Number
Age (yrs)
Gender distribution (men/women)
Weight (kg)
Height (cm)
Body mass index (kg/m2)
Diabetes mellitus (%)
Cigarette smoking
Current smokers (%)
Ex-smokers (%)
Never smokers (%)
Antihypertensive treatment
Untreated (%)
Current treatment (%)
Clinic systolic/diastolic BP (mm Hg)
LV hypertrophy at ECG (%)
Interventricular septum (cm)
LV end-diastolic diameter (cm)
LV posterior wall (cm)
Shortening fraction (%)
LV mass
g
g/body surface area [m2]
g/height2.7 [g/m2.7]
Glucose (mg/dl)
Creatinine (mg/dl)
Uric acid (mg/dl)
Total cholesterol (mg/dl)
HDL cholesterol (mg/dl)
LDL cholesterol (mg/dl)
Triglycerides (mg/dl)
Sodium (mmol/l)
Potassium (mmol/l)
1,033
60 (7)
396/637
72 (12)
163 (9)
27.1 (3.7)
7.3
14
13.5
72.5
15
85
154 (18)/92 (9)
19.7
1.09 (0.22)
4.98 (0.63)
0.99 (0.17)
38 (7)
197 (72)
111 (39)
53.0 (19)
103 (29)
0.95 (0.18)
5.10 (1.3)
225 (40)
53 (14)
144 (38)
139 (67)
141 (3)
4.3 (0.4)
Data expressed as mean (⫾SD).
ECG ⫽ electrocardiogram; BP ⫽ blood pressure; LDL ⫽ low density lipoprotein;
LV ⫽ left ventricular; HDL ⫽ high density lipoprotein.
analysis was restricted to the first event. In two-sided tests,
p values ⬍0.05 were considered significant.
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Left Ventricular Mass in Hypertension
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December 2001:1829–35
Figure 1. Distribution of antihypertensive regimens at entry and on follow-up. ACE ⫽ angiotension-converting enzyme.
There were only 13 fatal events and their rate (⫻100
person-years) was 0.23 in the subset with normal LV mass
(⬍125 g/BSA [m2]) and 0.99 in that with increased LV
mass (log-rank test: p ⫽ 0.007). The low number of fatal
events precluded their multivariate assessment.
Left ventricular mass was also corrected by height2.7 to
improve allowance for obesity. Event rate (⫻100 personyears) was 1.36 in the subset with LV mass ⱕ51.0
g/height2.7 (20), and 2.41 in that with greater LV mass (p ⫽
0.034; log-rank test). When gender-adjusted cutoff values
were used for definition of LV hypertrophy (104 g/m2 in
women and 116 g/m2 in men) (24,25), prevalence of LV
hypertrophy was 47.1% and event rate (⫻100 person-years)
was 1.46 in the subset with normal LV mass and 2.45 in
that with LV hypertrophy (log-rank test: p ⫽ 0.025). The
list of independent predictors of outcome in the Cox
analysis remained unchanged.
DISCUSSION
The present study is the first to extend demonstration of the
prognostic value of LV mass to a nationwide multicenter
sample, the largest available so far, of uncomplicated subjects with essential hypertension. Qualifying features of the
present study were its prospective design, with prespecified
definition of primary and total outcome events, and the
central blind reading of ECG and echocardiographic tracings. These characteristics may have reduced the possibility
of technical biases potentially inherent to single-center
studies.
Table 2. Baseline Clinical Characteristics of the Subjects With and Without Subsequent
Cardiovascular End Points
Characteristic
Age (yrs)
Women (%)
Body mass index (kg/m2)
Cigarette smoking (%)
Diabetes (%)
TC (mg/dl)
HDL-C (mg/dl)
LDL-C (mg/dl)
TC/HDL-C
Triglycerides (mg/dl)
Creatinine (mg/dl)
Glucose (mg/dl)
Clinic BP (mm Hg)
Systolic/diastolic
LV mass (g/body surface area[m2])
LV mass (g/height [m2.7])
No Cardiovascular
End Points
(n ⴝ 978)
Cardiovascular
End Points
(n ⴝ 55)
p Value
61 (7)
62
27.1 (4)
12.8
6.5
225 (39)
53 (14)
144 (37)
4.58 (1.2)
140 (67)
0.94 (0.18)
102 (27)
64 (7)
53
26.6 (4)
25.5
20.0
223 (58)
51 (12)
145 (51)
4.62 (1.7)
136 (61)
1.00 (0.22)
116 (51)
0.0001
0.19
0.54
0.001
0.0001
0.75
0.40
0.74
0.71
0.66
0.009
0.001
154 (17)/92 (9)
109 (36)
52.4 (18)
160 (19)/92 (11)
134 (39)
63.8 (31)
0.011/0.85
0.0001
0.0001
Data expressed as mean (⫾SD).
BP ⫽ blood pressure; HDL-C ⫽ high density lipoprotein cholesterol; LDL-C ⫽ low density lipoprotein cholesterol; LV ⫽
left ventricular; TC ⫽ total cholesterol.
Verdecchia et al.
Left Ventricular Mass in Hypertension
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December 2001:1829–35
1833
Figure 2. Cumulative incidence (left) and crude rate (right) of cardiovascular (CV) events in the subjects with and without left ventricular (LV) hypertrophy
at echocardiography. BSA ⫽ body surface area.
Previous studies. In several observational studies, conducted in a variety of clinical conditions (3–13), the predictive power of LV mass remained significant after adjustment
for the confounding effect of age, BP and other risk markers
including diabetes, smoking, serum lipids and coronary
lesions, whose number and prognostic impact differed across
these studies. However, one could question to what extent
the conclusions of these studies can be applied to the
majority of subjects with uncomplicated essential hypertension. In fact, only a few of these studies have been
specifically conducted in uncomplicated hypertensive subjects (3,4). Most studies have been done in quite different
settings including subjects undergoing cardiac catheterization for presumed coronary artery disease (8), survivors of
MI (9), subjects with renal failure (10,11) or in the general
population (12,13).
It is out of the question that this large body of evidence
strongly supports, in general, the prognostic value of LV
mass. This, however, might lead to a partially unsupported
feeling of scientific and clinical confidence in the use of LV
mass for cardiovascular risk stratification in the specific
setting of uncomplicated subjects with essential hypertension, which could become a target for excessive extrapolation of conclusions not specifically obtained in these subjects.
The LV mass and prognosis. In the present study, LV
hypertrophy at echocardiography doubled the risk of both
primary and total events, and for any increase in LV mass by
1 ⫾ SD (39 g/m2) there was an independent 40% rise in the
risk of events. The relation between LV mass and subsequent cardiovascular risk persisted after adjustment for the
influence of several traditional risk factors, while other
factors including baseline BP and antihypertensive treatment did not achieve significance. The overall event rate
(1.8 ⫻ 100 patient-years) was somewhat lower than expected in the year 1995 when the study was designed (2.5 ⫻
Table 3. Results of the Multivariate Analysis
Variable
Primary events
Age
Cigarette smoking
Diabetes
LV mass (g/BSA[m2])
Total events
Age
Cigarette smoking
Serum creatinine
Diabetes
LV mass (g/BSA[m2])
Comparison
Relative Risk (95%
Confidence Intervals)
p Value
5 years
Yes vs. No
Yes vs. No
39 g
1.15 (1.87–1.93)
4.00 (1.80–8.91)
3.41 (1.36–7.72)
1.37 (1.05–1.80)
0.0008
0.0007
0.0079
0.020
5 years
Yes vs. No
0.20 mg/dl
Yes vs. No
39 g
1.40 (1.16–1.68)
3.02 (1.61–5.63)
1.32 (1.03–1.70)
2.61 (1.31–5.17)
1.40 (1.14–1.73)
0.0004
0.0005
0.028
0.0059
0.0013
LV ⫽ left ventricular; BSA ⫽ body surface area.
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Verdecchia et al.
Left Ventricular Mass in Hypertension
100 patient-years), but the absolute excess risk associated
with LV hypertrophy remained virtually as expected (1.9
events vs. 2.0 events predicted). Also, the observed prevalence of LV hypertrophy (28.5%) was comparable to that
expected (30.0%).
The apparently high prevalence of LV hypertrophy at
ECG (19.7%) resulted from the use of the Perugia score
(15,16), a diagnostic score that is positive in the presence of
typical LV strain, a Romhilt-Estes score of 5 points or
more, or Cornell voltage exceeding 2.0 mV in women or 2.4
mV in men (15,16). In a previous study (15), the combination of three specific criteria (Romhilt-Estes, LV strain and
Cornell) in this score produced a rise in sensitivity to about
34% without excessive deterioration of specificity (93%),
with a prevalence of LV hypertrophy at ECG of about 18%.
A recent analysis of the Losartan Intervention For Endpoint (LIFE) study showed that accuracy of the Perugia
score for diagnosis of LV hypertrophy is independent of
overweight or obesity (26). In the present study, LV
hypertrophy at ECG did not achieve significance as a
predictor of cardiovascular risk after controlling for LV
mass.
In addition to the expected concomitant effect of age,
diabetes and cigarette smoking, our study showed an independent association between serum creatinine and subsequent risk of total cardiovascular events. Previous studies in
hypertensive subjects showed an association between elevated creatinine levels and subsequent cardiovascular events
(27–29). Also, high-normal levels of serum creatinine appear to be predictive of future cardiovascular events in
subjects with essential hypertension (30). Because renal
function was normal in all subjects at entry into the study,
our data suggest that serum creatinine levels within the
normal range may work as a marker of long-term exposure
to high BP values, and therefore predict outcome also in
nonrenal target organs.
Our epidemiological findings are unable to define the
basic mechanisms underlying the prognostic value of LV
mass in subjects with essential hypertension. The LV mass
is generally considered a biological assay, which reflects and
integrates the long-term cumulative level of activity of
several risk factors for cardiovascular disease (31). Increased
LV mass is a powerful predictor not only of ischemic cardiac
events, an association partially expected by the unfavorable
effects of LV hypertrophy on the balance between myocardial oxygen requirement and supply (32), but also of stroke
(33).
Study limitations. Because our study was conducted
among white subjects, results may not be extended to
different ethnic groups. Another limitation was the lack of
assessment of the prognostic value of serial changes in BP
and LV mass over time (5–7). The large percentage of
subjects with inadequate echocardiographic tracings reflects
the use of stringent criteria in the central reading process.
Central reading of echocardiographic tracings in clinical
trials frequently results in a large percentage of rejections
JACC Vol. 38, No. 7, 2001
December 2001:1829–35
due to suboptimal quality (34,35). In the Framingham
Heart Study, 20.7% of echocardiographic tracings from men
and 21.1% from women were rejected because of inadequate
technical quality (13).
Conclusions. Our study is the first to demonstrate a
powerful association between LV mass determined at echocardiography and subsequent occurrence of cardiovascular
disease in a nationwide representative multicenter sample of
uncomplicated subjects with essential hypertension. These
findings support the view that both prevention of LV
hypertrophy development and regression of hypertrophy
once established are key targets in the management of
asymptomatic patients with essential hypertension.
Reprint requests and correspondence: Dr. Paolo Verdecchia,
ANMCO Research Center, Via La Marmora, 39, 50121-Firenze,
Italy. E-mail: [email protected].
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APPENDIX
Steering Committee: E. Giovannini (chairman), G.C. Carini,
A. Circo, E.V. Dovellini, M. Lombardo, P. Solinas, P.
Verdecchia.
Scientific and Organizing Secretariat: S. Ghione, M.
Gorini, D. Lucci, A.P. Maggioni.
Echocardiogram and ECG Central Reading: C. Borgioni,
A. Ciucci, G. Gozzellino, A. Milletich.
Participating clinical centers: Avola (E. Mossuti, G. Canonico, G. Romano), Bari Policlinico (I. De Luca, N.
Ciriello), Bazzano (A. Baldini, G. Castelli), Belluno (G.
Catania, L. Tarantini), Bologna Osp. S. Orsola-M. Malpighi (E. Ambrosioni, F. Marchetta), Brindisi Osp. Di
Summa (G. Ignone, D. Zuffianò, A. Storelli), Cagliari Osp.
Binaghi (G. Isaia, E. Muscas), Camerino (R. Amici, B.
Coderoni), Capua (E. Mercaldo, R. Esposito), Casale
Monferrato (M. Ivaldi, G. Gozzelino, A. Capilli), Casarano
(G. Pettinati, M. Ieva, A. Marzo), Caserta (G. Corsini, S.
Romano, A. Martone), Catanzaro Policlinico (F. Perticone,
C. Cosco), Chieti Villa Pini D’Abruzzo (C. Ciglia, P. Di
Giovanni), Citta’ Della Pieve (G. Benemio, G. Schillaci, N.
Sacchi), Cosenza INRCA (E. Feraco, A. M. Nicoletti),
Desio (V. Baldini, M. Cristofari), Firenze Osp. Careggi
(P. F. Fazzini, D. Antoniucci, E. V. Dovellini, E. Taddeucci), Firenze Osp. Camerata (F. Marchi, A. Buzzigoli),
Foligno (M. Massi Benedetti, C. Pagnotta, R. Liberati),
Gallarate (R. Canziani, G. Cozzi, M. Alberio), Gioia Del
Colle (F. Barba), Gorizia (A. Fontanelli, R. Marini, L.
Scarpino), Grottaglie (V. Portulano, G. Sportelli), Matera
(L. Veglia, T. Scandiffio), Mesoraca (F. Schipani, C. Tangari), Messina Osp. Papardo (L. Cavallaro, G. Sergi, S.
Mangano), Messina Policlinico Universitario (S. Coglitore,
C. De Gregorio, D. Cento), Milano Osp. Niguarda (A.
Pezzano, M. Lombardo), Monfalcone (T. Morgera, G.
Zilio, D. Chersevani), Napoli Osp. Cardarelli (L.
D’Aniello, F. D’Isanto), Oliveto Citra (G. D’angelo, V.
Iuliano, P. Bottiglieri), Palermo Osp. Ingrassia (P. Di
Pasquale, F. Clemenza, S. Cannizzaro, G. Caramanno),
Perugia (C. Porcellati, P. Verdecchia, A. Ciucci, C. Borgioni), Pieve Di Cadore (J. Dalle Mule, M. Mazzella),
Polistena (R. M. Polimeni, F. Catananti, F. Terranova),
Pontedera (G. Squarcini, S. Giaconi), Pordenone (G. B.
Cignacco, G. Zanata, D. Pavan), Potenza (A. Lopizzo, M.
Chiaffitelli, M. Faruolo), Prato (A. Petrella, M. Paoletti),
Roma CTO (M. Uguccioni, D. Mocini), Roma Osp.
Forlanini (A. Majid Tamiz, A. Avallone), Roma Osp. San
Camillo II Divisione (E. Giovannini, A. Chiantera, F. De
Santis), Roma Osp. San Camillo Servizio (P. Tanzi, L.
Boccardi, D. Colecchia), Rovigo (P. Zonzin, A. Bortolazzi,
S. Aggio), San Giovanni Rotondo (R. Fanelli, A. Russo, A.
De Vita), San Pietro Vernotico (L. Vergallo, S. Pede, A.
Renna), Sarzana (G. Filorizzo, D. Bertoli, M. Corradeghini), Scorrano (E. De Lorenzi, A. Bergamo, A.
Colizzi), Sesto San Giovanni (R. Melloni, E. Choicca),
Sondalo (G. Occhi, G. Frisullo), Sondrio (S. Giustiniani,
1835ii
Verdecchia et al.
Left Ventricular Mass in Hypertension
M. Marieni, M. L. Ghirimoldi), Soveria Mannelli (G.
Bellieni, A. Marotta, A. Andricciola), Termoli (D. Staniscia, T. Alfieri), Udine (P. Fioretti, L. Pilotto), Vasto (G. Di
JACC VOl. 38, No. 7, 2001
December 2001:1829–35
Marco, G. Levantesi, L. Cavasinni), Viareggio (A. Pesola,
G. Marracci, M. Pardini), Viterbo (R. Guerra, A. Achilli, S.
De Spirito, R. Castellani).