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Background: Left ventricular hypertrophy (LVH) is risk, and 5% very high risk subjects. The detection of LVH
an important predictor of cardiovascular risk, and its de- by ECHO provoked a significant change in the risk strata
tection contributes to risk stratification. The aims of the distribution, particularly in those patients initially classi-
present study were to estimate the prevalence of echocar- fied as being at medium risk. In this group, 40% of
diographic LVH and to evaluate the influence of echocar- subjects were reclassified as high risk subjects according
diography (ECHO) on cardiovascular risk stratification in to ECHO information. The new classification was as fol-
hypertensive patients presenting in primary care. lows: 23% low risk, 30% medium risk, 42% high risk, and
Methods: In this cross-sectional study, 250 patients 5% very high risk subjects.
recently diagnosed with mild hypertension underwent Conclusions: A substantial proportion of mildly hy-
clinical evaluation including electrocardiography (ECG), pertensive patients presenting in primary care have LVH
microalbuminuria measurement, 24-h blood pressure mon- determined by ECHO. Our results suggest that this proce-
itoring and ECHO. Level of cardiovascular risk was strat- dure could significantly improve cardiovascular risk strat-
ified, initially using routine procedures including ECG to ification in those patients with multiple risk factors, but no
assess target organ damage and then again after detection evidence of target organ damage by routine investigations.
of LVH by ECHO. Am J Hypertens 2003;16:556 –563 © 2003 American
Results: The frequency of echocardiographic LVH was Journal of Hypertension, Ltd.
32%, substantially higher than that detected by ECG (9%).
Initial cardiovascular risk stratification yielded the follow- Key Words: Mild hypertension, primary care, left ven-
ing results: 30% low risk, 49% medium risk, 16% high tricular hypertrophy, echocardiography.
L
eft ventricular hypertrophy (LVH) is a well known essential hypertension average 40% (range 12% to
independent predictor of cardiovascular morbidity 70%),3–9 depending to a large degree on the measurement
and mortality in hypertensive patients.1 Epidemio- technique used. Standard electrocardiography (ECG), for
logic studies have shown that LVH is the most powerful example, has only a limited ability to detect the presence
risk factor for sudden death, ventricular arrhythmias, myo- of increased LVM,10 even if new, improved criteria are
cardial ischemia, coronary heart disease, and congestive applied.11 Original estimates of the prevalence of LVH
heart failure.2 have therefore increased considerably with the advent of
Estimates of the prevalence of LVH in patients with the more sensitive echocardiography (ECHO).
Received November 8, 2002. First decision December 20, 2002. Ac- (Project FIS 97/56:0 –12) and AstraZeneca Pharmaceuticals, Madrid.
cepted February 27, 2003. Authors’ affiliations are included in the Appendix.
From the Primary Care and Hospital Research Unit, Hospital La Paz, Address correspondence and reprint requests to Dr. Maria Angeles
Universidad Autónoma de Madrid, Madrid, Spain. Martı́nez, Avda del Llano Castellano 3. 5°B, Madrid 28034, Spain;
This work was supported by research grants from Ministry of Health e-mail: jrvillagrasa@terra.es
To date, most studies on the prevalence of LVH deter- of urea nitrogen, creatinine, glucose, uric acid, cholesterol,
mined by ECHO and its influence on cardiovascular risk sodium, potassium, and calcium. Biochemical serum de-
stratification in hypertensive subjects have been performed in terminations were performed using a Hitachi 747 autoana-
hypertension clinics or academic settings where participating lyzer (Boehringer Mannheim, Mannheim, Germany).
patients had been referred for clinical evaluation.3–5,9,12,13 To detect cardiac organ damage, an ECG was per-
The population studied in these reports may not be represen- formed on all patients. We used the sex-specific Cornell
tative of that seen in a primary care setting while patients are criteria15 to define LVH: sum of amplitudes of the S wave
receiving their usual medical care. in V3 and the R wave in a VL ⬎28 mm in men and ⬎20
The aims of the present study were to estimate the mm in women.
prevalence and determinants of echocardiographic LVH in
a population of mildly hypertensive subjects, and to eval- Echocardiography
uate the impact of ECHO on a more precise stratification
with those previously published by the Joint National Table 1. Demographic and clinic characteristics of
Committee (JNC).20 The remaining hypertensive subjects the study population
were considered to have sustained hypertension. Daytime
systolic BP and nighttime systolic BP loads were defined Men Women
Variable (n ⴝ 117) (n ⴝ 133)
as the percentage of daytime and night-time readings,
respectively, that exceeded 135 mm Hg. Similarly, day- Age (y) 47.4 ⫾ 12.1 50.8 ⫾ 11.3
time diastolic BP and nighttime diastolic BP loads were Systolic clinic BP
(mm Hg) 144.7 ⫾ 13.4 143.2 ⫾ 11.5
defined as the percentage of daytime and nighttime read- Diastolic clinic BP
ings, respectively, that exceeded 85 mm Hg. (mm Hg) 95.6 ⫾ 7.4 91.7 ⫾ 5.3
Body mass index
Urinary Albumin Excretion (kg/m2) 24.3 ⫾ 11.5 22.5 ⫾ 12.1
Serum glucose
BP ⫽ blood pressure.
Stratification of Patients by Absolute Data are expressed as mean ⫾ SD.
* Values refer to 117 patients and are expressed as median and
Level of Cardiovascular Risk range.
Statistical Analysis
Results
Study Population
Data were stored and analyzed using the SPSS for Win-
dows, version 10, statistical package (SPSS Inc., Chicago, Out of 320 eligible patients, 290 agreed to participate in
IL). For the study, it was calculated that it would be the study. Of these 290 cases, 40 (13.8%) were excluded
necessary to recruit 246 patients to have a power of 95% from analysis because of insufficient visualization of the
at the 5% significance level to estimate a prevalence of cardiac structure on ECHO. Data from 250 patients (all of
LVH of 20%. This prevalence feature is similar to that white European ethnicity) were therefore evaluated in this
obtained in a Spanish series of untreated patients with mild study. Table 1 shows the clinical and demographic char-
hypertension.21 acteristics of the study population. The main demographic
Urinary albumin excretion data were analyzed as a characteristics (age, sex, and level of absolute cardiovas-
continuous variable with logarithmic transformation. Pear- cular risk) of the 40 excluded patients were similar to
son’s correlations were used to study the linear relation- those of the patients included in the analysis.
ship between LVMI and other continuous variables. A Ambulatory BP recordings were excluded in seven
stepwise multivariate regression analysis was used to iden- patients because of an insufficient number of BP readings.
tify the clinical factors determining LVMI. Similarly, a Urinary albumin excretion measurement was not possible
stepwise logistic analysis was used to identify the predic- in five patients because of deficiencies in urine sample
tive factors for LVH. In both types of analysis, the inde- collection.
AJH–July 2003–VOL. 16, NO. 7 LEFT VENTRICULAR HYPERTROPHY IN MILD HYPERTENSION 559
Men Women
Variable All (n ⴝ 117) (n ⴝ 133) P
LV mass index (g/m2) 119.4 ⫾ 22.4 126.1 ⫾ 26.4 103.3 ⫾ 19.5 .02
LV internal diameter (mm) 45.8 ⫾ 4.2 47.1 ⫾ 4.9 44.2 ⫾ 3.9 .07
PW thickness (mm) 9.9 ⫾ 1.5 10.9 ⫾ 1.9 9.3 ⫾ 1.4 .02
IV septal thickness (mm) 11.2 ⫾ 1.7 12.3 ⫾ 1.9 10.8 ⫾ 1.7 .4
Relative wall thickness 0.43 ⫾ 0.09 0.47 ⫾ 0.1 0.42 ⫾ 0.08 .08
Factors Associated
With Increased LVM Table 3. Pearson correlation coefficients between
clinical parameters and left ventricular mass index
Table 3 shows the correlation between LVMI and several
clinical variables. The strongest correlation was found for Variable r P
age (P ⫽ .27, P ⬍ .01). Other factors with significant Age (y) 0.27 ⬍.01
positive correlation were UAE (0.25, P ⬍ .01), and several Body mass index
ambulatory BP variables. In a multiple linear regression (g/m2) 0.04 NS
Log urinary albumin
model age, sex, and night time systolic BP load were
excretion (g/min) 0.25 ⬍.01
predictors of LVMI. This regression model could only Clinic systolic BP
explain 26.2% of LVMI variability. However, in a logistic (mm Hg) 0.17 ⬍.05
model, only age and daytime systolic BP load were inde- Clinic diastolic BP
pendently associated with LVH. (mm Hg) 0.11 NS
Daytime ambulatory
systolic BP (mm Hg) 0.15 ⬍.05
Influence of ECG and Daytime ambulatory
ECHO Evaluation on diastolic BP (mm Hg) 0.12 NS
Cardiovascular Risk Stratification 24-h Ambulatory systolic
BP (mm Hg) 0.17 ⬍.05
Initial evaluation of cardiovascular risk (which included 24-h Ambulatory diastolic
ECG assessment as part of the routine procedure) indi- BP (mm Hg) 0.23 ⬍.01
cated that only 74/250 (30%) patients had no cardiovas- Nighttime ambulatory systolic
cular risk factors (other than hypertension) or any target BP (mm Hg) 0.17 ⬍.05
Nighttime ambulatory diastolic
organ damage, and were therefore classified in the low risk BP (mm Hg) 0.22 ⬍.01
group, according to the 1999 WHO/ISH guidelines14 (Fig. Daytime systolic load (%) 0.14 ⬍.05
1). A further 123/250 subjects (49%) had concomitant risk Daytime diastolic load (%) 0.12 NS
factors, without evidence of target organ damage, and Nighttime systolic load (%) 0.10 NS
were classified in the medium risk group and the remain- Nighttime diastolic load (%) 0.17 ⬍.01
ing 53/250 patients (21%) were considered to be high risk NS ⫽ not significant; other abbreviation as in Table 1.
(n ⫽ 40) or very high risk (n ⫽ 13) patients. Correlation was analyzed by the Pearson test.
560 LEFT VENTRICULAR HYPERTROPHY IN MILD HYPERTENSION AJH–July 2003–VOL. 16, NO. 7
than was clinic BP.24,31 Nighttime ambulatory BP showed medical care and which therefore is the context in which
a higher correlation with LVMI than daytime BP. This the first therapeutic decision is usually made.
finding, also observed for microalbuminuria in previous The present study has two potential limitations. First,
studies,32 could be related to the fact that nighttime am- our routine procedures to detect target organ damage did
bulatory BP values are usually more reproducible than not include funduscopic examination, a procedure recom-
daytime values33 because of the limited physical activity mended by international guidelines (WHO/ISH and JNC).
during that period. Interestingly, previous studies on hypertensive patients
In a stepwise multiple linear regression model, with showed significant correlations between retinal vascular
LVMI as the dependent variable, age, sex, and nighttime changes and LVM38,39 and a low incidence of retinopathy
diastolic BP load were predictors of LVMI. The associa- in subjects with no LVH.38 According to this evidence, we
tion with urinary albumin excretion that was found in the could hypothesize that funduscopic findings would not
univariate analysis did not remain after taking these fac-
5. Liebson PR, Grandits GA, Dianzumba S, Prineas RJ, Grimm RH, tensive subjects: Hospitalet study in mild hypertension. Am J Hy-
Neaton JD, Stamler J: Comparison of five antihypertensive mono- pertens 1999;12:1084 –1090.
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receiving nutritional-hygienic therapy in the Treatment of Mild A, on behalf of the RACE study group: ACE inhibitor ramipril is
Hypertension Study (TOMHS). Circulation 1995;91:698 –706. more effective than beta-blocker atenolol in reducing left ventricular
6. Coca A, Gabriel R, De la Figuera M, López-Sendón JL, Fernández mass in hypertension. Results of the RACE (ramipril cardioprotec-
R, Sagastagoitia JD, Garcı́a JJ, Barajas R: The impact of different tive evaluation) study. J Hypertens 1995;13:1325–1334.
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tricular hypertrophy in essential hypertension: the VITAE study. Roman MJ, Papademetria V, Ibsen H, Rokkedal J, Bevereux RB:
J Hypertens 1999;17:1471–1480. Impact of different partition values on prevalence of left ventricular
7. Hammond IW, Devereux RB, Alderman MH, Lutas EM, Spitzer hypertrophy and concentric geometry in a large hypertensive study
MC, Crowley JS, Laragh JH: The prevalence and correlates of echo in the Life Study. Hypertension 2000;35:6 –12.
left ventricular hypertrophy among employed patients with uncom- 24. Martı́nez MA, Garcı́a-Puig J, Martin JC, Guallar-Castillón P, Agu-
plicated hypertension. J Am Coll Cardiol 1986;7:639 –650. irre de Cárcer A, Torre A, Armada A, Nevado A, Madero R:
38. Dahlof B, Stenkula S, Hansson L: Hypertensive retinal vascular Nevado, Roberto Cabrera, Alberto Galgo; CS Chopera: Al-
changes: relationship to left ventricular hypertrophy and arteriolar varo Aguirre, Paloma Seguido, Luisa Pascual, Antonio
changes before and after treatment. Blood Press 1992;1:35–44.
39. De Leonardis V, Becucci A, De Scalzi M, Cinelli P: Low incidence
González, Jaime Gallo, Juan J González, Luis Zorita-Viota,
of cardiac hypertrophy in essential hypertensive with no retinal Mariano Ferrer, Concepción Miranda, Carmen Villar,
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Ana B Garcia; CS Paracuellos: José M Rubio, Monserrat
Appendix: Blas, Carmen Conles, Sonia Puerta, Matilde del Castillo,
The members of the Monitorización Ambulatoria de la Pre- Rosario Paramio, Elena Aymerich, Carlos del Valle, Javier
sión Arterial (MAPA)–Madrid Working Group that partici- Salas, Ignacio Valverde; CS Dr Tamames (Coslada): José L
pated in this study were: Hospital La Paz, Unidad de Antón, Gema Herranz, Luis F Gimbel, José Sanz, Marı́a J
Investigación: Rosario Madero; Servicio de Medicina In- Gomera, Sol Blesa, Eva Cruz, Raquel Martı́nez, Teresa