Metabolic Syndrome and Morphofunctional Characteristics of the Left Ventricle in Clinically Hypertensive Nondiabetic Subjects

Grandi, Anna Maria; Maresca, Andrea Maria; Giudici, E; Laurita, Emanuela; Marchesi, Chiara; Solbiati, Francesco; Nicolini, E.; Guasti, Luigina; Venco, Achille

doi:10.1016/j.amjhyper.2005.07.024

Cited by 49 publications

(52 citation statements)

References 29 publications

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“…Recently, population-based studies report that MS patients also present mild but significant left ventricular (LV) diastolic dysfunction (2,3). Cardiac fibrosis, a major cause of diastolic dysfunction, is prevalent in these MS patients.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Interleukin-18 Aggravates Cardiac Fibrosis and Diastolic Dysfunction in Fructose-Fed Rats

Shen

Tan

et al. 2010

Mol Med

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Inflammation plays an important role in the pathophysiology of the metabolic syndrome (MS). We determined whether the overexpression of interleukin (IL)-18 could aggravate left ventricular (LV) remodeling and diastolic dysfunction in fructose-fed rats (FFRs). To create an animal model for MS, male Wistar rats received 10% fructose in water for 8 months. We used an adenovirus encoding rat IL-18 to overexpress IL-18 in FFRs by intravenous administration. IL-18 overexpression led to increases in collagen volume fraction and collagen deposition. LV systolic function was unaltered. But the LV end-diastolic pressure and the time constant of isovolumic relaxation (tau) were increased. Peak negative value of time derivative of LV pressure (-dp/dt) was decreased. Isovolumic relaxation time and myocardial index, as assessed by echocardiography, were increased. Overexpression of IL-18 leads to aggravated LV remodeling and dysfunction in FFRs. Attenuation of the inflammatory process may provide a novel therapeutic strategy in treating metabolic cardiomyopathy.

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Section: Introductionmentioning

confidence: 99%

Overexpression of Interleukin-18 Aggravates Cardiac Fibrosis and Diastolic Dysfunction in Fructose-Fed Rats

Shen

Tan

et al. 2010

Mol Med

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“…Activation of the RAAS and associated oxidative stress can result in mitochondrial abnormalities, altered bioenergetics and the accumulation of lipids in the heart, and thereby increase susceptibility to metabolic cardiomyopathy. 4 Although left ventricular (LV) remodeling and dysfunction have been observed in individuals with MetS, 5,6 the extent of cardiac injury in such individuals has remained unclear. A diet with a moderate fat content was found to induce metabolic abnormalities but did not result in LV diastolic dysfunction in obesity-prone Sprague-Dawley rats.…”

Section: Introductionmentioning

confidence: 99%

Cardiac remodeling and diastolic dysfunction in DahlS.Z-Leprfa/Leprfa rats: a new animal model of metabolic syndrome

et al. 2011

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We recently characterized male DahlS.Z-Lepr fa /Lepr fa (Dahl salt-sensitive (DS)/obese) rats, which were established from a cross between Dahl salt-sensitive and Zucker rats, as a new animal model of metabolic syndrome (MetS). We have now investigated cardiac pathophysiology and metabolic changes in female DS/obese rats in comparison with homozygous lean female littermates (DahlS.Z-Lepr + /Lepr + , or DS/lean, rats). Animals were maintained on a normal diet and were subjected to echocardiography followed by various pathological analyses at 15 weeks of age. Systolic blood pressure was significantly higher in female DS/obese rats than in DS/lean females at 12 weeks of age and thereafter. The survival rate of DS/obese rats was significantly lower than that of DS/lean rats at 15 weeks. Body weight, as well as visceral and subcutaneous fat mass were significantly increased in DS/obese rats, which also manifested left ventricular (LV) diastolic dysfunction and marked LV hypertrophy and fibrosis. In addition, myocardial oxidative stress and inflammation were increased in DS/obese rats compared with DS/lean rats. Serum insulin and triglyceride levels as well as the ratio of low-density lipoprotein-to high-density lipoprotein-cholesterol levels were markedly elevated in DS/obese rats, whereas fasting serum glucose concentrations were similar in the two rat strains. The phenotype of female DS/obese rats is similar to that of MetS in humans. These animals also develop salt-sensitive hypertension and LV diastolic dysfunction as well as LV hypertrophy and fibrosis, and these changes are associated with increased cardiac oxidative stress and inflammation. Keywords: cardiac hypertrophy; diastolic dysfunction; metabolic syndrome; myocardial fibrosis; salt-sensitive hypertension INTRODUCTION Metabolic syndrome (MetS), a complex of highly debilitating disorders including hypertension, diabetes mellitus and dyslipidemia, is associated with the development of visceral obesity. 1 Adipocytes in visceral fat of obese humans secrete a variety of biological agents that are known as adipocytokines and include proinflammatory cytokines such as tumor necrosis factor (TNF)-a and interleukin (IL)-6 as well as angiotensinogen and leptin. 2 Recent studies have revealed intricate interactions among adipocytes, the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) that contribute to the disturbed metabolic state associated with obesity. 3 Indeed, adipose tissue is thought to have an important role in the development of both hypertension and other complications related to insulin resistance. Activation of the RAAS and associated oxidative stress can result in mitochondrial abnormalities, altered bioenergetics and the accumulation of lipids in the heart, and thereby increase susceptibility to metabolic cardiomyopathy. 4

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“…Previous reports have shown that MetS is associated with elevated LVM, 6,7,12,[16][17][18][19][20][21][22][23][24][25] but the potential influence of gender on MetS-related LVH is controversial. 6,17,24,25 In a study conducted on 618 hypertensive patients a remarkable sex difference in the association between MetS and LVH was found; indeed, in that study, MetS was a strong determinant of LVM in women beyond the influence of body size and haemodynamic variables, whereas the relation was weaker and fully explained by the effect of confounding factors in men.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 Subjects with left ventricular mass (LVM) in the upper normal range already have increased risk for CV events. 15 MetS has been associated with an increased LVM in recent reports conducted in hypertensive patients and in general population, 6,7,12,[16][17][18][19][20][21][22][23][24][25] independently of various confounding factors, such as BP values and age. However, only in a few of these studies the impact of MetS on LVM was separately analysed by gender, with conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Relationships between metabolic syndrome and left ventricular mass in hypertensive patients: does sex matter?

et al. 2008

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Several studies documented an association between metabolic syndrome (MetS) and left ventricular (LV) hypertrophy. However, only in a few of these studies the impact of MetS on left ventricular mass (LVM) was separately analysed by gender, with conflicting results. The aim of our study was to verify, in a wide sample of essential hypertensive patients, the influence of gender, if any, on the relationship between MetS and LVM. We enrolled 475 non-diabetic subjects (mean age: 46 ± 11 years), with mild-to-moderate essential hypertension, of whom 40% had MetS, defined on the basis of Adult Treatment Panel III (ATPIII) criteria. All the patients underwent a 24-h ambulatory blood pressure monitoring and an echocardiogram. LVM indexed for height 2.7 (LVMH 2.7 ) was significantly (Po0.001) higher in women with MetS (n ¼ 83) than in those without it (n ¼ 97; 54 ± 17 vs 42±11 g m À2.7). An equally significant difference in LVMH 2.7 was documented also in male gender between the two groups with (n ¼ 105) and without MetS (n ¼ 190; 51 ± 14 vs 43±11 g m À2.7 ; Po0.001). The relationship between MetS and LVMH 2.7 remained statistically significant (Po0.001) in both sexes, in multiple regression analyses, even after adjustment for potential confounding factors. Our results seem to suggest that the relationship between MetS and LVM is not significantly affected by gender, being LVM increased in both hypertensive women and men with MetS.

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Metabolic Syndrome and Morphofunctional Characteristics of the Left Ventricle in Clinically Hypertensive Nondiabetic Subjects

Cited by 49 publications

References 29 publications

Overexpression of Interleukin-18 Aggravates Cardiac Fibrosis and Diastolic Dysfunction in Fructose-Fed Rats

Overexpression of Interleukin-18 Aggravates Cardiac Fibrosis and Diastolic Dysfunction in Fructose-Fed Rats

Cardiac remodeling and diastolic dysfunction in DahlS.Z-Leprfa/Leprfa rats: a new animal model of metabolic syndrome

Relationships between metabolic syndrome and left ventricular mass in hypertensive patients: does sex matter?

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