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(Hypertension. 2002;39:744.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Prevalence of Left Ventricular Hypertrophy in Hypertensive Patients Without and With Blood Pressure Control

Data From the PAMELA Population

Giuseppe Mancia; Stefano Carugo; Guido Grassi; Arturo Lanzarotti; Riccardo Schiavina; Giancarlo Cesana; Roberto Sega

From the Clinica Medica e Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie, Università Milano-Bicocca, Ospedale San Gerardo (G.M., S.C., G.G., A.L., R. Schiavina, G.C., R. Sega), Monza Milano, Italy; Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università Milano-Bicocca (G.M., G.G.), Milano, Italy; and Istituto Auxologico Italiano (G.M., G.G.), Milano, Italy.

Correspondence to Prof Giuseppe Mancia, Clinica Medica, Università di Milano-Bicocca, Ospedale San Gerardo, Via Donizetti 106, 20052 Monza, Milan, Italy.

	Abstract

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Previous studies have shown that in the population, only a minority of treated hypertensive patients achieve blood pressure (BP) control. Whether and to what extent this inadequate control has reflection on hypertension-related organ damage has never been systematically examined. In 2051 subjects belonging to the PAMELA (Pressioni Arteriose Monitorate E Loro Associazioni) Study population, we measured office, home, and 24-hour ambulatory BP values, together with echocardiographic left ventricular mass and wall thickness. Based on the fraction on antihypertensive treatment and on measurements of increased or normal office, home, or 24-hour ambulatory BP values, subjects were classified as normotensives, untreated hypertensives, treated hypertensives with inadequate BP control, and treated hypertensives with effective BP control. Compared with values in the normotensive group, left ventricular mass index, left ventricular wall thickness, and prevalence of left ventricular hypertrophy were markedly increased not only in untreated hypertensive patients but also in treated hypertensives with inadequate BP control. Echocardiographic abnormalities were less in treated hypertensives with BP control than in patients with inadequate BP control, but values were still clearly greater than in normotensive subjects. This was the case regardless whether BP control was assessed by office, home, and/or ambulatory values. Our data provide evidence that in the hypertensive fraction of the population, cardiac structural alterations can be frequently found in both the presence and absence of antihypertensive treatment. They also imply that even effective treatment of hypertension does not allow complete reversal of the cardiac organ damage characterizing high BP states.

Key Words: drug therapy • hypertrophy, cardiac • blood pressure

	Introduction

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A large number of studies performed in various countries has shown that in the hypertensive (HT) fraction of the population, blood pressure (BP) control is rare.¹ Namely, a relatively high percentage of HT individuals remains untreated. And among patients under antihypertensive treatment, only a minority achieves an office BP that can be regarded as adequate, ie, <140 mm Hg systolic and 90 mm Hg diastolic.

What reflection this has on hypertension-related organ damage has never been systematically investigated. In the PAMELA Study (Pressioni Arteriose Monitorate E Loro Associazioni), we had a chance to address this issue, because the subjects recruited consisted of a large sample representative of a population within the age range in which hypertension is common and treatment is protective.^1–6 Furthermore, in all subjects, BP was measured not only in the doctor’s office but also at home and by ambulatory monitoring, thereby providing multiple independent information on its real value. Finally, measurements included an echocardiogram, which allowed organ damage to be assessed as an increase in left ventricular mass (LVM), ie, by a sensitive marker of cardiac structural alterations with proven prognostic significance.⁷

	Methods

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The PAMELA Study was performed cross-sectionally on 2051 subjects, part of a sample of 3200 subjects selected as being representative of the population of Monza (a town near Milan, Italy) for age (25 to 74 years), gender, socioeconomic status, and other criteria.⁸ Participation rate was 62%, and the demographic characteristics and medical history (phone interview) of the nonparticipants in the study were similar to those of the overall population.^2,9,10

BP Measurements
The methods have been described in detail previously.^2,9,10 After being informed of their selection, the subjects were invited to undergo a visit at an outpatient clinic in the St Gerardo University Hospital of Monza in the morning of a working day to obtain a full medical history, a physical examination, and 3 sphygmomanometric BP measurements (in the sitting position). Subjects were then fitted with an ambulatory BP oscillometric device (Spacelabs 90207), which was removed 24 hours later.^2,9,10 They were also instructed to take self-measurements of sitting BP at home using a semiautomatic oscillometric device (model HP 5331, Philips) at 7:00 PM and 7:00 AM.

Echocardiographic Measurements
An echocardiogram was obtained using an Accuson 128 C/F (Computer Sonography) to calculate left ventricular volume,¹¹ LVM¹² indexed to the body surface area,¹³ interventricular septal wall thickness (IVWT), and left ventricular posterior wall thickness sum (LVWT). The assessment of left ventricular hypertrophy (LVH), eccentric and concentric LVH, and left ventricular remodeling was based on the criteria proposed by Ganau et al.¹⁴ Echocardiographic tracings were obtained by 2 skilled operators and read by a third independent observer (intraobserver coefficients of variation 0.6% for left ventricular end-diastolic diameter, 3.1% for IVWT, and 3.2% for left ventricular posterior wall thickness).

Data Analysis
In each subject, averages were obtained for clinic, home, and ambulatory BP values, which were first edited from artifacts.^9,10 Valid ambulatory systolic and diastolic BP readings were 95.1% and 94.9%, respectively, of the planned 72 readings. Individual data were separately averaged for normotensive subjects, untreated HT subjects, treated HT subjects with inadequate BP control, and treated HT subjects with BP control. Normotension (or BP control) was defined by (1) office BP criteria, ie, systolic <140 mm Hg and diastolic <90 mm Hg; (2) home BP criteria, ie, systolic <132 mm Hg and diastolic <83 mm Hg; or (3) ambulatory BP criteria, ie, 24-hour average systolic <125 mm Hg and 24-hour average diastolic <79 mm Hg. Untreated hypertension was defined as values exceeding the above-mentioned ones, combined with no treatment for at least 15 days before study. Treated HT subjects (defined by a history of current antihypertensive treatment) were further subdivided into a group in whom BP was inadequately controlled and a group in whom BP was controlled, again based on office, home, or ambulatory BP criteria. In treated HT subjects, averages were also obtained for the small subgroup in whom all 3 pressures were controlled, and data were compared with those of the group in which all BPs were normal. Home and 24-hour average BP values separating normotension (or BP control) from hypertension (or lack of BP control) were those previously identified as the upper limits of home and 24-hour BP normality in the PAMELA population.^2,9,10

The statistical significance of the between-group differences was assessed by 2-way ANOVA, using Bonferroni correction for multiple comparisons. The between-group comparisons of echocardiographic variables were made also after adjustment for the effect of age, gender, and body mass index, using ANCOVA. A P<0.05 was taken as the level of statistical significance. Values are mean±SD.

An expanded Methods section can be found in an online data supplement available at http://www.hypertensionaha.org.

	Results

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Table 1 shows that compared with subjects with office normotension, office BP, LVM index, LVWT, and prevalence of LVH were markedly increased both in subjects with an untreated office hypertension and in treated HT subjects in whom office BP was inadequately controlled. In treated HT subjects in whom office BP was controlled, office BP was only moderately (systolic) or slightly (diastolic) increased compared with the values of subjects with office normotension. This was not the case, however, for LVM index, LVWT, and prevalence of LVH, which although less than those in the treated HT subjects in whom office BP was not controlled, were still all clearly greater than those in the group with office normotension. In each group, LVH of the eccentric type was much more frequent than that of the concentric type. Compared with normotensive subjects, untreated HT subjects and treated HT subjects with either uncontrolled or controlled office BP also showed a greater prevalence of concentric left ventricle remodeling.

View this table: [in this window] [in a new window]   Table 1. Office BP and Echocardiographic Data in Subjects With Normotension, Untreated HT Subjects, and Treated HT Subjects With Uncontrolled or Controlled BP

Similar findings were obtained when the subdivision in normotensive subjects, untreated HT subjects, treated HT subjects with inadequate BP control, and treated HT subjects with BP control was based on home (Table 2) and ambulatory (Table 3) BP criteria. In the treated HT group, treatment was reported to consist of a diuretic (23%), a ß-blocker (8%), a calcium antagonist (9%), an ACE inhibitor (18%), or a combination of 2 drugs or other treatments (42%). The corresponding percentages in treated patients with BP control were 18%, 19%, 7%, and 46%. Compared with subjects in whom office, home, and 24-hour average BP were all normal, LVM index, LVWT, and prevalence of LVH were also greater in the small number of treated HT subjects in whom all 3 pressures were controlled (Figure 1).

View this table: [in this window] [in a new window]   Table 2. Home BP and Echocardiographic Data in Subjects With Normotension, Untreated HT Subjects, and Treated HT Subjects With Uncontrolled or Controlled BP

View this table: [in this window] [in a new window]   Table 3. 24-Hour Mean BP and Echocardiographic Data in Subjects With Normotension, Untreated HT Subjects and Treated HT Subjects With Uncontrolled or Controlled BP

View larger version (33K): [in this window] [in a new window]   Figure 1. LVM index (LVMI), LVWT, and prevalence of LVH in treated HT subjects in whom office (open bars), home (dashed bars,) and 24-hour (solid bars) BPs were all controlled (CH). Data are compared with the normotensive fraction of the population (N), in whom all 3 pressures were normal. *P<0.05 between groups.

The normotensive group of the PAMELA population had an age that was less than that of the untreated HT group and more so than that of the treated HT group in which BP was uncontrolled or controlled. To determine whether this age imbalance was responsible for the differences in echocardiographic values, the normotensive group was divided in age tertiles, the oldest of which had an age similar or greater than that of the other 3 groups. As shown in Table 4 the between-group differences in LVM index remained in most instances statistically significant, with a greater value in the treated HT group in which BP was controlled regardless whether office, home, or 24-hour BP was considered. Similarly, the between-group differences in LVM index remained statistically significant in most instances when data were submitted to ANCOVA, considering the effect of age, gender, and body mass index (Figure 2 and specific symbols in Tables 1, 2, and 3).

View this table: [in this window] [in a new window]   Table 4. LVM Index Values in Patients With Untreated HT, Treated HT With BP Uncontrolled, and Treated HT With BP Controlled versus Those of the Eldest Age Tertile of the Normotensive Group

View larger version (55K): [in this window] [in a new window]   Figure 2. LVM index (LVMI) and LVWT in normotensive subjects (N, open bars), HT subjects with untreated hypertension (dashed bars), treated HT subjects with but no BP control (checkered bars), and treated HT subjects with controlled BP (solid bars). Small numbers at bottom refer to number of subjects in each group. Normotension, hypertension, and BP control are defined based on office, home, or 24-hour BP normality or elevation. Data resulting from ANCOVA (which considered age, gender, and body mass index) are shown. *P<0.05 vs N, P<0.05 vs untreated HT, and +P<0.05 vs treated HT with uncontrolled BP.

	Discussion

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In the PAMELA population, LVM index, LVWT, and prevalence of LVH were all significantly and markedly greater in subjects with untreated hypertension than in normotensive subjects. The new findings of the present study, however, are that (1) LVM index, LVWT, and prevalence of LVH were similarly or even more markedly increased in the treated fraction of the HT population that had BP values above the upper limit of normality and was thus defined as having inadequate BP control; (2) although less marked than in treated HT subjects with inadequate BP control, similar echocardiographic abnormalities also characterized treated HT subjects in whom systolic and diastolic BP values were reduced below the upper limit of normality and lead to BP control; and (3) the greater LVM index values seen in treated HT subjects were not owing to differences in gender or their older age, because the differences also remained significant when LVM index was adjusted for age and when comparisons were made with the eldest tertile of the normotensive population. This allows 3 conclusions to be made: (1) in the HT population, alterations of cardiac structure can be frequently found both in the presence and in the absence of antihypertensive treatment. (2) These alterations are made less common and pronounced by effective treatment, which, however, is not able to reverse them completely and make the cardiac structure of well-treated HT subjects similar to that of the normotensive population. (3) Because an increase in LVM and LVWT is accompanied by an increase in the incidence of cardiovascular disease,^7,15,16 the HT fraction of the population may remain at a higher cardiovascular risk even when treatment is apparently implemented and effective.

A unique feature of the PAMELA Study was that office BP was measured together with home and ambulatory BP, which allowed us to investigate whether in hypertension normalization of BPs other than those measured in the clinical environment might more accurately reflect the ability of treatment to cause regression of the echocardiographic abnormalities. This is a plausible hypothesis because home and ambulatory BP are (1) more reproducible than office BP,^17,18 (2) devoid of confounding factors such as the "white coat" effect and its variable attenuation by treatment,^19,20 and (3) more closely related to LVM than office BP.^18,21 The results, however, do not support it because in treated HT subjects, an increase in LVM index, LVWT, and prevalence of LVH was similarly manifest when (1) BP control by treatment was based on office, home, and ambulatory values; (2) treatment made 24-hour BP virtually superimposable to that of the normotensive fraction of the population; and (3) all 3 BPs had been reduced by treatment to the normal range, with home and office values superimposable to those of normotensive individuals. Thus, in treated HT subjects, echocardiographic abnormalities persist regardless whether BP control refers to office or daily life values. Furthermore, these observations do not disappear when the most important daily life BP values for LVM, ie, the ambulatory ones, are entirely normalized.

Two other results of our study deserve to be mentioned. First, in our population, eccentric LVH was much more frequent than concentric LVH, regardless of whether BP was normal or elevated and whether treatment did or did not achieve BP control. This is in line with the results of other studies,^22,23 to which we can add, however, that the relative prevalence of these 2 cardiac structural abnormalities is not substantially affected by the lesser or greater effectiveness of treatment. Second, a number of subjects showed a normal LVM to be accompanied by concentric left ventricular remodeling, the prevalence being greater in the HT fractions than in the normotensive fraction of the population. When home and ambulatory BP values were considered, these differences persisted after adjustment for body mass index. Thus, regardless the presence or absence of treatment and BP control, hypertension is responsible also for causing cardiac structural alterations that precede a LVM increase.

Our population study had a cross-sectional nature that makes clarification of the mechanisms responsible for the persistence of echocardiographic alterations in the treated fraction of the HT population (in whom office, home, or ambulatory BP were reduced, controlled, and even entirely normalized) difficult. Three (not mutually exclusive) possibilities can be discussed, however. First, because of its cross-sectional nature, in our study we could not obtain reliable information on the duration of treatment and on BP control. It is therefore possible that persistence of cardiac structural abnormalities depended on a time factor, ie, that BP treatment and control was not maintained for the time necessary for complete regression of echocardiographic abnormalities to occur.^24,25 Second, insufficient use was made of drugs that have been shown to more effectively allow regression of LVH to take place.^24,25 Indeed, several patients in whom BP control was achieved reported to be under treatment with diuretics and/or ß-blockers, which have been shown to be less effective in reducing an elevated LVM than other antihypertensive drugs.^24,25 Third, hypertension-related cardiac structural abnormalities can never completely regress because their appearance and progression are caused by not only the BP elevation but also the interaction of an increased cardiac workload with factors (genes, renin-angiotensin system, sympathetic nervous system, insulin, etc.)²⁶ that directly favor an increase in cardiac cell volume.

Our results, however, should not be interpreted as to imply that BP-lowering interventions have a limited beneficial effect on hypertension-induced structural alterations of the heart. It should be emphasized that in treated HT subjects with BP control, these alterations were much less evident than in HT subjects with inadequate BP control. Furthermore, because of the cross-sectional nature of our population study, we cannot exclude that in treated HT subjects with inadequate BP control, BP, LVM index, and LVWT values were much greater originally than at the time our study was made. Our observations, however, clearly document that cardiac structural alterations are (or remain) frequent in the HT population in which treatment is implemented and that this is the case also when an effective BP control is achieved. This implies that this population remains by and large at a high cardiovascular risk.

Received June 5, 2001; first decision June 20, 2001; accepted December 17, 2001.

	References

Top Abstract Introduction Methods Results Discussion References

 
1. 1999 World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension: Guidelines Subcommittee. J Hypertens. 1997; 17: 151–183.

2. Mancia G, Sega R, Milesi C, Cesana G, Zanchetti A. Blood pressure control in the hypertensive population. Lancet. 1997; 349: 454–457.[CrossRef][Medline] [Order article via Infotrieve]

3. Collins R, Peto R, MacMahon S, Hebert P, Fiebach NH, Eberlein KA, Godwin J, Qizilbash N, Taylor JO. Blood pressure, stroke, and coronary heart disease, 2: short-term reductions in blood pressure: overview of randomised drugs trials in their epidemiological context. Lancet. 1990; 335: 827–839.[CrossRef][Medline] [Order article via Infotrieve]

4. Dahlof B, Lindholm LH, Hansson L, Schersten B, Ekbom T, Wester PO. Morbidity and mortality in Swedish trial in old patients with hypertension (STOP-hypertension). Lancet. 1991; 338: 1281–1285.[CrossRef][Medline] [Order article via Infotrieve]

5. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension: final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA. 1991; 265: 3255–3264.[Abstract/Free Full Text]

6. Staessen JA, Fagard R, Thijs L, Celis H, Arabidze GG, Birkenhager WH, Bulpitt C, De Leeuw P, Dollery C, Fletcher A, Forette F, Leonetti G, Nacheu C, O’Brien E, Rosenfield J, Rodicio J, Tuomilheto J, Zanchetti A. Randomized double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. Lancet. 1997; 350: 757–764.[CrossRef][Medline] [Order article via Infotrieve]

7. 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; 332: 1561–1566.

8. Kuulasmaa K, Tunstall-Pedoe H, Dobson A, Fortmann S, Sans S, Tolonen H, Evans A, Ferrario M, Tuomilheto J. Estimation of contribution of changes in classic risk factors to trends in coronary-event rates across the WHO MONICA Project populations. Lancet. 2000; 355: 675–687.[CrossRef][Medline] [Order article via Infotrieve]

9. Mancia G, Sega R, Bravi C, De Vito G, Valagussa F, Cesana G, Zanchetti A. Ambulatory blood pressure normality: results from the PAMELA Study. J Hypertens. 1995; 13: 1377–1390.[Medline] [Order article via Infotrieve]

10. Sega R, Cesana G, Milesi C, Grassi G, Zanchetti A, Mancia G. Ambulatory blood pressure normality in the elderly. Hypertension. 1997; 30: 1–6.[Abstract/Free Full Text]

11. Sahn DY, De Maria A, Kinlo J, Weyman A, for the Committee on M-mode standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978; 58: 1072–1083.[Abstract/Free Full Text]

12. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Circulation. 1977; 55: 613–618.[Abstract/Free Full Text]

13. Dubois D, Dubois EF. A formula to estimate the approximative surface area if height and weight are known. Arch Intern Med. 1916; 17: 863–871.

14. Ganau A, Devereux RB, Roman MJ, De Simone G, Pickering T, Saba P, Vargiu P, Simongini I, Laragh J. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992; 19: 1550–1558.[Abstract]

15. De Simone G, Devereux RB, Koren M, Mensah GA, Casale PN, Laragh JH. Midwall left ventricular mechanics" an independent predictor of cardiovascular risk in arterial hypertension. Circulation. 1996; 93: 259–265.[Abstract/Free Full Text]

16. Schillaci G, Verdecchia P, Porcellati C, Cuccurullo O, Cosco C, Perticone F. Continuous relation between left ventricular mass and cardiovascular risk in essential hypertension. Hypertension. 2000; 35: 580–586.[Abstract/Free Full Text]

17. Trazzi S, Mutti E, Frattola A, Imholz B, Parati G, Mancia G. Reproducibility of non-invasive and intra-arterial blood pressure monitoring: implications for studies on antihypertensive treatment. J Hypertens. 1991; 9: 115–119.[CrossRef][Medline] [Order article via Infotrieve]

18. Fagard RH, Staessen JA, Thijs L. Prediction of cardiac structure and function by repeated clinic and ambulatory blood pressure. Hypertension. 1997; 29: 22–29.[Abstract/Free Full Text]

19. Mancia G, Bertinieri G, Grassi G, Parati G, Pomidossi G, Ferrari A, Gregorini L, Zanchetti A. Effects of blood pressure measurement by the doctor on patient’s blood pressure and heart rate. Lancet. 1983; 2: 690–695.[Medline] [Order article via Infotrieve]

20. Parati G, Ulian L, Sampieri L, Palatini P, Villani A, Vanasia A, Mancia G. Attenuation of the "white-coat effect" by antihypertensive treatment and regression of target organ damage. Hypertension. 2000; 35: 614–620.[Abstract/Free Full Text]

21. Mancia G, Zanchetti A, Agabiti-Rosei E, Benemio G, De Cesaris R, Fogari R, Pessina A, Porcellati C, Rappelli A, Salvetti A, Trimarco B. Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy: SAMPLE Study Group (Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation). Circulation. 1997; 95: 1464–1470.[Abstract/Free Full Text]

22. Hammond IW, Devereux RB, Alderman MH, Lutas EM, Spitzer MC, Crowley JS, Laragh JH. The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension. J Am Coll Cardiol. 1986; 7: 639–650.[Abstract]

23. Savage DD, Garrison RJ, Kannel WB, Levy D, Anderson SJ, Stokes J, Feinleib M, Castelli WP. The spectrum of left ventricular hypertrophy in a general population sample: the Framingham study. Circulation. 1987; 75 (suppl I): I-26–I-33.[Medline] [Order article via Infotrieve]

24. Jennings G, Wong J. Regression of left ventricular hypertrophy in hypertension: changing patterns with successive meta-analyses. J Hypertens. 1998; 16 (suppl 6): S29–S34.

25. Schmieder RE, Martus P, Klingbeil A. Reversal of left ventricular hypertrophy in essential hypertension: a meta-analysis of randomized double-blind studies. JAMA. 1996; 275: 1507–1513.[Abstract/Free Full Text]

26. Devereux RB, Roman MJ. Cardiac structure and function. In: Zanchetti A, Mancia G, eds. Handbook of Hypertension: Pathophysiology of Hypertension. Vol. 17. Amsterdam: Elsevier Science; 1997: 58–116.

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This Article Abstract Full Text (PDF) Data Supplement Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mancia, G. Articles by Sega, R. Search for Related Content PubMed PubMed Citation Articles by Mancia, G. Articles by Sega, R. Related Collections Hypertrophy Clinical Studies Echocardiography