Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Hypertension. 2006;47:881-886
Published online before print April 3, 2006, doi: 10.1161/01.HYP.0000216778.83626.39
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
47/5/881    most recent
01.HYP.0000216778.83626.39v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schillaci, G.
Right arrow Articles by Mannarino, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schillaci, G.
Right arrow Articles by Mannarino, E.
Related Collections
Right arrow Risk Factors
Right arrow Hypertrophy
Right arrow Glucose intolerance
Right arrow Clinical Studies

(Hypertension. 2006;47:881.)
© 2006 American Heart Association, Inc.

Original Articles

Different Impact of the Metabolic Syndrome on Left Ventricular Structure and Function in Hypertensive Men and Women

Giuseppe Schillaci; Matteo Pirro; Giacomo Pucci; Massimo R. Mannarino; Fabio Gemelli; Donatella Siepi; Gaetano Vaudo; Elmo Mannarino

From the Unit of Internal Medicine, Angiology and Arteriosclerosis, University of Perugia, Perugia, Italy.

Correspondence to Giuseppe Schillaci, Unit of Internal Medicine, Angiology and Arteriosclerosis, University of Perugia Medical School, Hospital "S. Maria della Misericordia", piazzale Menghini, 1, 06132 Perugia, Italy. E-mail skill{at}unipg.it


*    Abstract
up arrowTop
 *Abstract
down arrowIntroduction
 down arrowMethods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Metabolic syndrome (MS) is increasingly recognized as an important cardiovascular risk factor in hypertension, but its influence on left ventricular (LV) mass and function in the 2 genders has not been specifically addressed. Among 618 nondiabetic, untreated hypertensive subjects, echocardiographically detected LV mass was significantly greater in subjects with MS. A significant interaction was observed between sex and the MS (P<0.003 for the multiplicative interaction term). Compared with women without the MS, those with the syndrome had a 24% greater LV mass (49.5±12 versus 40.0±10 gxm–2.7; P<0.001), whereas the difference was only 9% in men (50.3±12 versus 46.1±10 gxm–2.7; P=0.003). A greater prevalence of LV hypertrophy was found in women (37% versus 14%; P<0.001) but not in men (39% versus 29%; P=0.09) with the MS. After adjustment for the effect of age, body mass index, 24-hour systolic blood pressure, and several confounders, the MS was independently associated with a greater LV mass index in women (regression coefficient, 4.80; P<0.001) but not in men. Women with the MS also had a greater LV relative wall thickness (0.42±0.07 versus 0.39±0.07; P=0.004) and a depressed afterload-corrected midwall fractional shortening (94.0±12% versus 101.0±13%; P<0.001) than women without the syndrome, whereas no differences emerged in men. We conclude that, in untreated hypertension, MS has a different impact on LV hypertrophy and function in men and women. The effect of MS is more pronounced in women and is partly independent from the effect of several hemodynamic and nonhemodynamic determinants of LV mass.


Key Words: hypertrophy • remodeling • metabolism • gender • risk factors


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowMethods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
The metabolic syndrome (MS), a clustering of lipid and nonlipid cardiovascular risk factors, is increasingly recognized as an independent predictor of cardiovascular disease in hypertension.1 The notion that the MS may have different relative importance for atherogenesis and cardiovascular disease in the 2 genders arises from observations indicating that elevated triglycerides and decreased high-density lipoprotein cholesterol, 2 basic components of the syndrome, are better predictors of the risk of adverse outcomes in women than in men.2–4 Moreover, in those studies in which the prognostic impact of the MS has been examined separately in men and women, the coronary or cardiovascular morbidity/mortality hazard ratios associated with the syndrome were almost invariably found to be higher in the female sex.1,5–10 Similarly, Iglseder et al11 have observed in a healthy population that the effect of MS on carotid intima-media thickness is more pronounced in women than in men.

Left ventricular (LV) hypertrophy, a major manifestation of hypertensive heart disease, is a strong and independent herald for cardiovascular morbidity and mortality,12,13 and its treatment-induced regression has been unequivocally associated with an improved cardiovascular prognosis, even after accounting for the confounding effect of treatment-induced blood pressure (BP) reduction.14,15 Echocardiographic studies conducted in hypertensive subjects or in the general population have generally concluded that participants with metabolic risk factors16,17 or with the MS18–21 have elevated LV mass or increased prevalence of LV hypertrophy. We hypothesized that a sex-specific effect of MS on LV hypertrophy might be one basic mechanism underlying the stronger adverse prognostic significance of the MS in women. Therefore, the aim of the present study was to investigate the impact of the MS on LV hypertrophy and function in hypertensive men and women taken separately. This question was addressed in a sample of white adult patients with essential hypertension, free from diabetes and cardiovascular disease, who had never received antihypertensive drug treatment.


*    Methods
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 *Methods
down arrowResults
 down arrowDiscussion
 down arrowReferences
 
We analyzed data of 748 consecutive subjects with never-treated essential hypertension, who were referred to our hypertension outpatient clinic by their general practitioners for baseline, off-treatment evaluation. All of the subjects fulfilled the following inclusion criteria: (1) recent (<3 years) diagnosis of hypertension (office BP ≥140/90 mm Hg on ≥3 visits at a 1-week interval); and (2) no clinical or laboratory evidence of heart failure, coronary heart disease, previous stroke, valvular defects, or secondary causes of hypertension, diabetes, or important concomitant disease. The duration of hypertension was established after cross-checking the patients’ history and the records of the general practitioners. The self-reported duration of hypertension was cross-checked with the records of the general practitioners. A total of 119 patients (16%) were excluded from the study for poor-quality echocardiograms, and 11 (1%) were excluded for poor-quality 24-hour BP monitoring, thus leaving 618 patients for analysis. Subjects with suboptimal echocardiographic tracings were older (54.0±12 versus 47.8±11 years; P<0.01) and had higher body mass index (28.3±4 versus 27.3±4 kgxm–2; P<0.01), but not BP (155±20/95±11 versus 153±18/95±10 mm Hg, P value was not significant), than subjects with technically adequate tracings. The MS was defined, according to the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults,22 by the presence, in addition to hypertension, of ≥2 of the following criteria: (1) serum triglyceride levels ≥1.69 mmol/L (150 mg/dL), (2) serum HDL cholesterol <1.04 mmol/L (40 mg/dL) in men and <1.30 mmol/L (50 mg/dL) in women, (3) fasting plasma glucose ≥6.11 mmol/L (110 mg/dL), and (4) waist circumference >102 cm in men or >88 cm in women. All of the subjects gave informed consent to the study, which was approved by the institutional ethics committee.

Waist circumference was measured with a soft tape on standing subjects at the iliac crest, at the end of a normal expiration. Office BP was measured by a physician in the hospital outpatient clinic with a mercury sphygmomanometer, with the subject sitting for ≥10 minutes. The average of 6 measurements on ≥2 sessions was considered for the analysis. Ambulatory BP was recorded using an oscillometric device (models 90202 and 90207, SpaceLabs), set to take a reading every 15 minutes throughout the 24 hours.23 Fasting plasma glucose, serum total cholesterol, and triglycerides were determined by enzymatic colorimetric method. Serum high-density lipoprotein cholesterol was measured by enzymatic colorimetric method after precipitation with polyethilenglycole. Low-density lipoprotein cholesterol was calculated by means of the Friedewald formula. Plasma insulin levels, determined by ELISA (Mercodia AB), were available in 418 subjects. The intraassay and interassay coefficients of variation for insulin were 3.5% and 3.2%, respectively. Insulin sensitivity was estimated from the homeostasis model assessment [(glucose in mmol/Lxinsulin in µU/mL)/22.5].

Echocardiography
The M-mode echocardiographic study of the left ventricle was performed under 2D control, as reported previously,12 by 2 investigators (G.S. and F.G.) who were unaware of patients’ clinical data. LV mass was indexed by height2.7 24 to correct for the effect of overweight. LV hypertrophy was defined as a LV mass index ≥51 gxm–2.7 in both sexes. Relative wall thickness was calculated as (2xposterior wall thickness/LV internal diameter). LV end-diastolic and end-systolic volumes and stroke volume were calculated using the formula of Teichholz et al.25 In our laboratory, the within-observer test-retest 90% interval of agreement for LV mass measurement is –16 to +14 g.26 The between-observer test-retest 90% interval of agreement is –20 to +18 g.

The excess of LV mass evaluated in relation to the needs to sustain cardiac load, a well-known physiological concept referred to as inappropriately high LV mass,27 was estimated on the basis of the following equation that we developed in a reference population of 121 normotensive, normal-weight adults, aged 18 to 84 years (R2=0.53; SE of the estimate, 27.3 g; P<0.001): predicted LV mass (g)=–11.4+(0.44xstroke work)+(17.9xheight2.7)+(18.2xsex), where sex=2 for men and 1 for women. Stroke work was estimated as systolic BP times stroke volume and converted to gxm by multiplying by 0.0144.

LV mechanics were assessed at both the chamber level, as endocardial fractional shortening (FS), and the midwall level, according to a geometric model that takes into account the nonuniform systolic thickening of LV wall.28,29 FS was considered both in absolute terms and, after correction for afterload, as a percentage of the value predicted from end-systolic circumferential wall stress with regression equations from previously studied normal subjects.30 An observed/predicted LV midwall FS of 133% identified the 95th percentile of its distribution in the reference population. Among hypertensive patients, those subjects with observed/predicted LV midwall FS >133% were classified as having inappropriately high LV mass.

The pulsed Doppler interrogation of the LV inflow was performed from the apical transducer position on subjects in partial left lateral decubitus during expiratory apnea, as described previously.31 The peak velocity of early rapid filling (E velocity) and the peak velocity of atrial filling (A velocity) were recorded, and the E/A ratio was calculated and adjusted for age and heart rate.31 The isovolumic relaxation time was measured from the closure spike of the aortic valve to the onset of mitral inflow.

Statistical Analysis
SPSS statistical package (SPSS Inc) was used for all of the statistical analyses. The effects of sex and the MS on LV mass index and other cardiac parameters were assessed by general linear model analysis, first without any adjustments and then with adjustment for potential confounders. Interaction between sex and the MS was formally tested by assessing the significance of the multiplicative 2-way interaction term "sexxMS" along with the main effects of sex and the MS. The influence on LV mass index of several potentially relevant variables was identified using linear stepwise regression. Together with a dummy variable indicating the MS, age, body mass index, office and average 24-hour systolic and diastolic BP, office heart rate, duration of hypertension, smoking, alcohol intake, serum creatinine, and serum cholesterol were considered as explanatory variables in the adjusted models.


*    Results
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 *Results
down arrowDiscussion
 down arrowReferences
 
The MS was present in 67 (26.5%) of 253 women and in 101 (27.8%) of 365 men. Some demographic and clinical characteristics of the study participants are reported in Table 1. Subjects with the MS did not differ from controls in terms of age, smoking habits, duration of hypertension, and total and low-density lipoprotein cholesterol concentration. Men with the MS had higher heart rate and 24-hour systolic BP values, whereas no significant differences in BP values were found in women. By selection, significant differences were found for the remaining components of the MS and for body mass index, as well as for fasting insulin and homeostasis model assessment-insulin resistance values.


View this table:
[in this window]
[in a new window]
  		TABLE 1. Clinical Characteristics of 618 Hypertensive Women and Men by Metabolic Pattern

In the whole population, a 2-factor ANOVA model revealed a significant effect of sex (F=12.831; P<0.001) and the MS (F=50.484; P<0.001) on height-adjusted LV mass (Table 2). The analysis of the interaction term "sexxMS" revealed a highly significant effect of sex on the association between the MS and LV mass index, both before (F=7.433; P=0.007) and after adjustment for the effect of age (F=8.283; P=0.004). As shown in Table 2, women with the MS had a significant 24% increase in LV mass index than women without the syndrome (49.5 versus 40.0 gxmn2.7; P<0.001), whereas this difference was only 9% in men (50.3 versus 46.1 gxm–2.7; P=0.002). Women, but not men, with the MS had a higher prevalence of LV hypertrophy and a more concentric geometric pattern (Table 2). In women, an inappropriately high LV mass for cardiac workload and body size was found more often in the presence than in the absence of the MS (28% versus 5%; P<0.001), whereas no significant difference was observed in men.


View this table:
[in this window]
[in a new window]
  		TABLE 2. Echocardiographic Characteristics of Hypertensive Women and Men by Metabolic Pattern

In a multiple regression model (Table 3), after adjustment for the effect of age, 24-hour systolic BP, body mass index, and smoking (all P<0.05), the MS was independently associated with a greater LV mass index in women (regression coefficient, 4.80; P<0.001) but not in men. Among women, LV mass was higher in individuals with the MS both before (48.4±10 versus 37.3±8 gxm–2.7; P<0.001) and after the menopause (50.8±10 versus 42.9±10 gxm–2.7; P=0.001). In either group, these differences held in fully adjusted regression models, which included all of the above variables (adjusted LV mass 44.1 versus 38.7 gxm–2.7, P=0.006, and 49.6 versus 43.7 gxm–2.7, P=0.022, respectively).


View this table:
[in this window]
[in a new window]
  		TABLE 3. Independent Predictors of LV Mass Index (gxm–2.7) in Hypertensive Women and Men in a Stepwise Linear Regression Model

The analysis of the relationship between the single components of the MS and LV structure (Table 4) showed that, in women, low high-density cholesterol concentration and high triglyceride concentration were independently associated with a higher LV mass index after taking into account the effects of age, body mass index, average 24-hour systolic BP, smoking, and alcohol intake. Additional adjustment for the confounding effect of waist circumference weakened the relation of LV mass to high triglycerides (P=0.087), whereas the relation with HDL cholesterol remained significant (P=0.021). In contrast, none of these associations were significant in men.


View this table:
[in this window]
[in a new window]
  		TABLE 4. Multivariate-Adjusted Values of LV Mass Index (in gxm–2.7) in Hypertensive Men and Women Subdivided by Presence or Absence of the Single Components of the MS

LV chamber systolic function, assessed through endocardial FS, was slightly and nonsignificantly reduced in women with the MS (Table 2). However, significant differences appeared when midwall FS, a more physiological measure of myocardial function, was considered. Women with the MS had depressed afterload-corrected midwall FS compared with women without the syndrome (94.0±12% versus 101.0±13%; P<0.001), whereas no difference emerged in men (92.3±16% versus 93.5±16%; P=0.52). In the whole population, sex significantly modified the relation between the MS and midwall FS (women=4.317; P<0.04 for the interaction term). Age- and heart rate-adjusted E/A velocity ratio at transmitral Doppler examination was lower in women in the presence of the MS (P=0.064), whereas no difference was found among men. However, no significant interaction between sex and the MS was observed.


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
down arrowReferences
 
Previous studies have shown that the MS is associated with elevated LV mass.18–21 This study confirms those findings in a large sample of subjects with essential hypertension. However, the main new finding of the present study is that a remarkable sex difference exists in the association between the MS and LV hypertrophy. Indeed, in the present study, Adult Treatment Panel III–defined MS was a strong determinant of LV mass in women beyond the influence of body size and hemodynamic variables, whereas the relation was weaker and fully explained by the effect of confounding factors in men.

We have observed previously that the association with LV mass of 2 of the components of the MS, that is, low high-density lipoprotein cholesterol and elevated triglycerides, was somewhat stronger in women than in men.32 In the Hoorn study, impaired glucose metabolism and type 2 diabetes mellitus have been associated with increased LV mass in women, but not in men,33 although in that work, LV mass was normalized for body surface area, a measure that includes body fat, and this might not be the most appropriate indexation, because it tends to exclude the effects of obesity on LV mass. Sex-specific relations between LV mass and insulin resistance, estimated by the homeostasis model assessment, have been examined in the Framingham Heart Study.34 In that article, a relation between insulin resistance and LV mass was found only among women, but the difference was no longer significant after adjustment for body mass index.34 In a large black cohort of the Atherosclerosis Risk in Communities Study,17 components of the MS were associated with increased LV mass. Of note, hypertension had the strongest influence on LV mass, and an additional contribution of dyslipidemia and glucose intolerance (including diabetes) was described only in women but not in men. This is generally in line with our results. In that study, however, as many as 23% of the population had frank diabetes, a well-known determinant of LV hypertrophy,35 and it cannot be excluded that diabetes played a leading role in the observed association between metabolic factors and LV mass. Moreover, black people have a greater prevalence of metabolic disorders36 and cardiac hypertrophy,37 and findings obtained in blacks may not be extended to a white population. To the best of our knowledge, the present study is the first to explore directly the influence of sex on the association between the MS and cardiac structure and function in white subjects.

The possible mechanisms underlying the interaction of sex on the association between the MS and LV mass remain hypothetical. Increased large-artery stiffness, a correlate of the MS in hypertension,38 might contribute to increase LV mass by elevating cardiac afterload. However, the increase in LV mass in women was found to be independent of increased arterial stiffness in the Hoorn Study.33 Moreover, insulin resistance might counterbalance the favorable cardiovascular effects of estrogen in women,39 thus canceling some of their effects on LV mass.40 Our finding of a strong effect of the MS on cardiac structure both before and after menopause seems to support this hypothesis. Further studies are needed to elucidate the potential explanations of the present findings.

In the present study, we have demonstrated a link between the MS and a cluster of LV geometric and functional abnormalities, which might provide prognostic information beyond the contribution of LV mass in subjects with essential hypertension.29,31,40,41 Indeed, in our study, women with the MS had a concentric LV geometric pattern,41 a prolonged LV relaxation,31 a reduced midwall systolic function,29 and a higher proportion of inappropriately high LV mass, that is, values of LV mass exceeding levels needed to compensate hemodynamic load.42

Study Strengths and Limitations
In this study, exclusion of subjects with overt cardiovascular disease, diabetes, and previous or current antihypertensive treatment allowed us to eliminate the influence of several major confounding factors. Moreover, the well-established influence of BP values on the association between MS and LV mass was excluded by adjustment for the effect of average 24-hour BP (Tables 3 and 4Up), a stronger predictor of cardiovascular risk than office BP in hypertension.43 Our cross-sectional investigation does not permit any causal inferences. This study was carried out in a population of white adult hypertensive patients, and results may not be directly applicable to the general population and to other ethnicities. However, high BP is by far the most frequent component of the MS and, in the general population, >90% of the subjects with MS have increased BP.44 Although prevalence of the MS was slightly underestimated by focusing on participants with valid echocardiograms in the present study, recent evidence suggests that cardiovascular risk does not differ for those with adequate and inadequate echocardiograms.45

Perspectives
Our findings that LV hypertrophy and several patterns of subclinical hypertensive heart disease are present in hypertensive women with the MS over and above the confounding effect of 24-hour BP, as well as several hemodynamic and nonhemodynamic factors, have important clinical and public-health implications. Indeed, echocardiographically determined LV hypertrophy has been implicated as a major contributor to cardiovascular disease outcomes in essential hypertension.12,13 These results are in line with several previous studies showing that women with diabetes lose their advantage over men in terms of cardiovascular disease46 and extend those findings to nondiabetic hypertensive subjects with the MS.


*    Acknowledgments
 
This work was supported in part by the grant 2004060902 from the Italian Ministry for University and Scientific Research. We are grateful to Dr Gianpaolo Reboldi for his helpful comments and suggestions.

Received February 6, 2006; first decision February 23, 2006; accepted February 24, 2006.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 up arrowDiscussion
 *References
 

  1. Schillaci G, Pirro M, Vaudo G, Gemelli F, Marchesi S, Porcellati C, Mannarino E. Prognostic value of the metabolic syndrome in essential hypertension. J Am Coll Cardiol. 2004; 43: 1817–1822.[Abstract/Free Full Text]
  2. Williams CM. Lipid metabolism in women. Proc Nutr Soc. 2004; 63: 153–160.[CrossRef][Medline] [Order article via Infotrieve]
  3. Howard BV, Cowan LD, Go O, Welty TK, Robbins DC, Lee ET. Adverse effects of diabetes on multiple cardiovascular disease risk factors in women: the Strong Heart Study. Diabetes Care. 1998; 21: 1258–1265.[Abstract]
  4. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996; 3: 213–219.[Medline] [Order article via Infotrieve]
  5. Onat A, Ceyhan K, Basar O, Erer B, Toprak S, Sansoy V. Metabolic syndrome: major impact on coronary risk in a population with low cholesterol levels: a prospective and cross-sectional evaluation. Atherosclerosis. 2002; 165: 285–292.[CrossRef][Medline] [Order article via Infotrieve]
  6. Malik S, Wong ND, Franklin SS, Kamath TV, L’Italien GJ, Pio JR, Williams GR. Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults. Circulation. 2004; 110: 1245–1250.[Abstract/Free Full Text]
  7. McNeill AM, Rosamond WD, Girman CJ, Golden SH, Schmidt MI, East HE, Ballantyne CM, Heiss G. The metabolic syndrome and 11-year risk of incident cardiovascular disease in the Atherosclerosis Risk In Communities study. Diabetes Care. 2005; 28: 385–390.[Abstract/Free Full Text]
  8. Levantesi G, Macchia A, Marfisi RM, Franzosi MG, Maggioni AP, Nicolosi GL, Schweiger C, Tavazzi L, Tognoni G, Valagussa F, Marchioli R, on behalf of the GISSI-Prevenzione Investigators. Metabolic syndrome and risk of cardiovascular events after myocardial infarction. J Am Coll Cardiol. 2005; 46: 277–283.[Abstract/Free Full Text]
  9. Koren-Morag N, Goldbourt U, Tanne D. Relation between the metabolic syndrome and ischemic stroke or transient ischemic attack: a prospective cohort study in patients with atherosclerotic cardiovascular disease. Stroke. 2005; 36: 1366–1371.[Abstract/Free Full Text]
  10. Hunt KJ, Resendez RG, Williams K, Haffner SM, Stern MP. National Cholesterol Education Program versus World Health Organization metabolic syndrome in relation to all-cause and cardiovascular mortality in the San Antonio Heart Study. Circulation. 2004; 110: 1251–1257.[Abstract/Free Full Text]
  11. Iglseder B, Cip P, Malaimare L, Ladurner G, Paulweber B. The metabolic syndrome is a stronger risk factor for early carotid atherosclerosis in women than in men. Stroke. 2005; 36: 1212–1217.[Abstract/Free Full Text]
  12. 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]
  13. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991; 114: 345–352.[Medline] [Order article via Infotrieve]
  14. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Reboldi G, Porcellati C. Prognostic significance of serial changes in left ventricular mass in essential hypertension. Circulation. 1998; 97: 48–54.[Abstract/Free Full Text]
  15. Verdecchia P, Angeli F, Borgioni C, Gattobigio R, de Simone G, Devereux RB, Porcellati C. Changes in cardiovascular risk by reduction of left ventricular mass in hypertension: a meta-analysis. Am J Hypertens. 2003; 16: 895–899.[CrossRef][Medline] [Order article via Infotrieve]
  16. de Simone G, Palmieri V, Bella JN, Celentano A, Hong Y, Oberman A, Kitzman DW, Hopkins PN, Arnett DK, Devereux RB. Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN study. J Hypertens. 2002; 20: 323–331.[CrossRef][Medline] [Order article via Infotrieve]
  17. Burchfiel CM, Skelton TN, Andrew MJ, Garrison RJ, Arnett DK, Jones DW, Taylor HA, Jr. Metabolic syndrome and echocardiographic left ventricular mass in blacks: the Atherosclerosis Risk in Communities (ARIC) Study. Circulation. 2005; 112: 819–827.[Abstract/Free Full Text]
  18. Cuspidi C, Meani S, Fusi V, Severgnini B, Valerio C, Catini E, Leonetti G, Magrini F, Zanchetti A. Metabolic syndrome and target organ damage in untreated essential hypertensives. J Hypertens. 2004; 22: 1991–1998.[CrossRef][Medline] [Order article via Infotrieve]
  19. Leoncini G, Ratto E, Viazzi F, Vaccaro V, Parodi D, Parodi A, Falqui V, Tomolillo C, Deferrari G, Pontremoli R. Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients. J Intern Med. 2005; 257: 454–460.[CrossRef][Medline] [Order article via Infotrieve]
  20. Chinali M, Devereux RB, Howard BV, Roman MJ, Bella JN, Liu JE, Resnick HE, Lee ET, Best LG, de Simone G. Comparison of cardiac structure and function in American Indians with and without the metabolic syndrome (the Strong Heart Study). Am J Cardiol. 2004; 93: 40–44.[Medline] [Order article via Infotrieve]
  21. Mulè G, Nardi E, Cottone S, Cusimano P, Volpe V, Piazza G, Mongiovi R, Mezzatesta G, Andronico G, Cerasola G. Influence of metabolic syndrome on hypertension-related target organ damage. J Intern Med. 2005; 257: 503–513.[CrossRef][Medline] [Order article via Infotrieve]
  22. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001; 285: 2486–2497.[Free Full Text]
  23. Schillaci G, Verdecchia P, Borgioni C, Ciucci A, Gattobigio R, Sacchi N, Benemio G, Porcellati C. Predictors of diurnal blood pressure changes in 2042 subjects with essential hypertension. J Hypertens. 1996; 14: 1167–1173.[Medline] [Order article via Infotrieve]
  24. de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, De Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and the impact of overweight. J Am Coll Cardiol. 1992; 20: 1251–1260.[Abstract]
  25. Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy. Am J Cardiol. 1976; 37: 7–11.[CrossRef][Medline] [Order article via Infotrieve]
  26. Schillaci G, Vaudo G, Pasqualini L, Reboldi G, Porcellati C, Verdecchia P. Left ventricular mass and systolic dysfunction in essential hypertension. J Hum Hypertens. 2002; 16: 117–122.[Medline] [Order article via Infotrieve]
  27. de Simone G, Devereux RB, Kimball TR, Mureddu GF, Roman MJ, Contaldo F, Daniels SR. Interaction between body size and cardiac workload: influence on left ventricular mass during body growth and adulthood. Hypertension. 1998; 31: 1077–1082.[Abstract/Free Full Text]
  28. Shimizu G, Hirota Y, Kita Y, Kawamura K, Saito T, Gaasch WH. Left ventricular midwall mechanics in systemic arterial hypertension: myocardial function is depressed in pressure-overload hypertrophy. Circulation. 1991; 83: 1676–1684.[Abstract/Free Full Text]
  29. de Simone G, Devereux RB, Koren MJ, 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]
  30. Schillaci G, Verdecchia P, Reboldi G, Pede S, Porcellati C. Subclinical left ventricular dysfunction in systemic hypertension and the role of 24-hour blood pressure. Am J Cardiol. 2000; 86: 509–513.[CrossRef][Medline] [Order article via Infotrieve]
  31. Schillaci G, Pasqualini L, Verdecchia P, Vaudo G, Marchesi S, Porcellati C, de Simone G, Mannarino E. Prognostic significance of left ventricular diastolic dysfunction in essential hypertension. J Am Coll Cardiol. 2002; 39: 2005–2011.[Abstract/Free Full Text]
  32. Schillaci G, Vaudo G, Reboldi G, Verdecchia P, Lupattelli G, Pasqualini L, Porcellati C, Mannarino E. High-density-lipoprotein cholesterol and left ventricular hypertrophy in essential hypertension. J Hypertens. 2001; 19: 2265–2270.[CrossRef][Medline] [Order article via Infotrieve]
  33. Henry RMA, Kamp O, Kostense PJ, Spijkerman AMW, Dekker JM, van Eijck R, Nijpels N, Heine RJ, Bouter LM, Stehouwer CDA. Left ventricular mass increases with deteriorating glucose tolerance, especially in women: independence of increased arterial stiffness or decreased flow-mediated dilation: the Hoorn Study. Diabetes Care. 2004; 27: 522–529.[Abstract/Free Full Text]
  34. Rutter MK, Parise H, Benjamin EJ, Levy D, Larson MG, Meigs JB, Nesto RW, Wilson PW, Vasan RS. Impact of glucose intolerance and insulin resistance on cardiac structure and function: sex-related differences in the Framingham Heart Study. Circulation. 2003; 107: 448–454.[Abstract/Free Full Text]
  35. Palmieri V, Bella JN, Arnett DK, Liu JE, Oberman A, Schuck MY, Kitzman DW, Hopkins PN, Morgan D, Rao DC, Devereux RB. Effect of type 2 diabetes mellitus on left ventricular geometry and systolic function in hypertensive subjects: Hypertension Genetic Epidemiology Network (HyperGEN) study. Circulation. 2001; 103: 102–107.[Abstract/Free Full Text]
  36. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, Wiedmeyer HM, Byrd-Holt DD. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults: the Third National Health and Nutrition Examination Survey, 1988–1994. Diabetes Care. 1998; 21: 518–524.[Abstract]
  37. Chapman JN, Mayet J, Chang CL, Foale RA, Thom SA, Poulter NR. Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient. Am J Hypertens. 1999; 12: 437–442.[CrossRef][Medline] [Order article via Infotrieve]
  38. Schillaci G, Pirro M, Vaudo G, Mannarino MR, Savarese G, Pucci G, Franklin SS, Mannarino E. Metabolic syndrome is associated with aortic stiffness in untreated essential hypertension. Hypertension. 2005; 45: 1078–1082.[Abstract/Free Full Text]
  39. Peiris AN, Aiman EJ, Drucker WD, Kissebah AH. The relative contributions of hepatic and peripheral tissue to insulin resistance in hyperandrogenic women. J Clin Endocrin Metab. 1989; 68: 715–720.[Abstract]
  40. van Eickels M, Grohe C, Cleutjens JP, Janssen BJ, Wellens HJ, Doevendans PA. 17ß-estradiol attenuates the development of pressure-overload hypertrophy. Circulation. 2001; 104: 1419–1423.[Abstract/Free Full Text]
  41. Muiesan ML, Salvetti M, Monteduro C, Bonzi B, Paini A, Viola S, Poisa P, Rizzoni D, Castellano M, Agabiti-Rosei E. Left ventricular concentric geometry during treatment adversely affects cardiovascular prognosis in hypertensive patients. Hypertension. 2004; 43: 731–738.[Abstract/Free Full Text]
  42. de Simone G, Palmieri V, Koren MJ, Mensah GA, Roman MJ, Devereux RB. Prognostic implications of the compensatory nature of left ventricular mass in arterial hypertension. J Hypertens. 2001; 19: 119–125.[CrossRef][Medline] [Order article via Infotrieve]
  43. Verdecchia P. Prognostic value of ambulatory blood pressure: current evidence and clinical implications. Hypertension. 2000; 35: 844–851.[Abstract/Free Full Text]
  44. Wilson PWF, D’Agostino RB, Parise H, Sullivan L, Meigs JB. Metabolic syndrome as a precursor of cardiovascular disease and type 2 diabetes mellitus. Circulation. 2005; 112: 3066–3072.[Abstract/Free Full Text]
  45. Devereux RB, Roman JM, Liu JE, Lee ET, Wang W, Fabsitz RR, Welty TK, Howard BV. An appraisal of echocardiography as an epidemiological tool: the Strong Heart Study. Ann Epidemiol. 2003; 13: 238–244.[CrossRef][Medline] [Order article via Infotrieve]
  46. Natarajan S, Liao Y, Cao G, Lipsitz SR, McGee DL. Sex differences in risk for coronary heart disease mortality associated with diabetes and established coronary heart disease. Arch Intern Med. 2003; 163: 1735–1740.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 HeartHome page
J Sundstrom, J Arnlov, K Stolare, and L Lind
Blood pressure-independent relations of left ventricular geometry to the metabolic syndrome and insulin resistance: a population-based study
Heart, July 1, 2008; 94(7): 874 - 878.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart JHome page
Authors/Task Force Members:, G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, G. Grassi, A. M. Heagerty, S. E. Kjeldsen, et al.
2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)
Eur. Heart J., June 11, 2007; (2007) ehm236v1.
[Full Text] [PDF]

Home page
 HypertensionHome page
G. Mancia, M. Bombelli, G. Corrao, R. Facchetti, F. Madotto, C. Giannattasio, F. Q. Trevano, G. Grassi, A. Zanchetti, and R. Sega
Metabolic Syndrome in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) Study: Daily Life Blood Pressure, Cardiac Damage, and Prognosis
Hypertension, January 1, 2007; 49(1): 40 - 47.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
47/5/881    most recent
01.HYP.0000216778.83626.39v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schillaci, G.
Right arrow Articles by Mannarino, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schillaci, G.
Right arrow Articles by Mannarino, E.
Related Collections
Right arrow Risk Factors
Right arrow Hypertrophy
Right arrow Glucose intolerance
Right arrow Clinical Studies

Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.