Left ventricular mass and systolic dysfunction in essential hypertension

Schillaci, Giuseppe; Vaudo, Gaetano; Pasqualini, Leonella; Reboldi, Gianpaolo; Porcellati, Carlo; Verdecchia, Paolo

doi:10.1038/sj.jhh.1001302

Cited by 20 publications

(25 citation statements)

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“…The results of the present study are consistent with those of prior studies that identified hypertension, diabetes mellitus, and obesity as independent predictors of impaired LV structure and function [23][24][25][26][27][28][29] . Increased LV mass, RWT, and deceleration time have been reported in hypertensive subjects with metabolic syndrome compared with a hypertensive cohort without metabolic syndrome [22] .…”

Section: Discussionsupporting

confidence: 83%

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Global left ventricular performance in non-diabetic non-hypertensive metabolic syndrome adults

Sliem

Nasr²,

Ibrahiem³

2011

WJC

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AIM:To evaluate the left ventricular structure and function in isolated metabolic syndrome. METHODS:One hundred and fifty six consecutive adults with metabolic syndrome were enrolled in the study. Fifty nine had isolated metabolic syndrome (group A) and 97 had metabolic syndrome with hypertension and/or diabetes (group B). There was a control group of 34 healthy adults. In addition to classic echocardiographic assessment of myocardial structural and functional changes, the Tei index was used to evaluate global left ventricular performance. RESULTS:There were no statistically significant differences between group A and controls in all parameters of left ventricular structural, systolic, and diastolic function except global myocardial performance (Tei index). On the other hand, significant differences were observed between group B and the control group in most of the parameters of left ventricular structural and global performance. CONCLUSION:The early identification of isolated metabolic syndrome in non-diabetic, non-hypertensive adults may be an indication that aggressive preventive measures should not be postponed until overt obesity, hypertension or diabetes mellitus has developed.

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Section: Discussionsupporting

confidence: 83%

“…It is simple, noninvasive, easy to use and reproducible. Moreover, the calculation of the Tei index is independent of age, arterial pressure, heart rate, ventricular geometry, atrioventricular valve regurgitation, afterload, and preload in patients who are in a supine position [5,17,28,31,32] .…”

Section: Discussionmentioning

confidence: 99%

Global left ventricular performance in non-diabetic non-hypertensive metabolic syndrome adults

Sliem

Nasr²,

Ibrahiem³

2011

WJC

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“…Relative wall thickness was calculated as (2ϫposterior 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 withinobserver test-retest 90% interval of agreement for LV mass measurement is Ϫ16 to ϩ14 g. 26 The between-observer test-retest 90% interval of agreement is Ϫ20 to ϩ18 g.…”

Section: Echocardiographymentioning

confidence: 99%

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

et al. 2006

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Abstract-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 (PϽ0.003 for the multiplicative interaction term). Compared with women without the MS, those with the syndrome had a 24% greater LV mass (49.5Ϯ12 versus 40.0Ϯ10 gϫm Ϫ2.7 ; PϽ0.001), whereas the difference was only 9% in men (50.3Ϯ12 versus 46.1Ϯ10 gϫm Ϫ2.7 ; Pϭ0.003). A greater prevalence of LV hypertrophy was found in women (37% versus 14%; PϽ0.001) but not in men (39% versus 29%; Pϭ0.09) 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; PϽ0.001) but not in men. Women with the MS also had a greater LV relative wall thickness (0.42Ϯ0.07 versus 0.39Ϯ0.07; Pϭ0.004) and a depressed afterload-corrected midwall fractional shortening (94.0Ϯ12% versus 101.0Ϯ13%; PϽ0.001) 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 Ⅲ remodeling Ⅲ metabolism Ⅲ gender Ⅲ risk factors T he 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][3][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 al 11 have observed in a healthy population that the effect of MS on carotid intimamedia 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 b...

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“…4,[8][9][10] A recent study has shown that LVH is a determinant of LV dysfunction (assessed by midwall fractional shortening) independent of the concomitant changes in chamber geometry in a large population of subjects with uncomplicated, nevertreated essential hypertension. 11 Nonetheless, there is increasing evidence that the variability of LVM is only partially related to the levels of arterial pressure, suggesting that its magnitude can also be influenced by stimuli other than arterial pressure (Figure 1), such as activation of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system and metabolic risk factors including obesity, insulin resistance, and dyslipidaemia. 12,13 However, insulin resistance commonly occurs as part of a cluster of cardiovascular-metabolic abnormalities referred to as the 'insulin resistance syndrome' or 'metabolic syndrome'.…”

mentioning

confidence: 99%

Insulin resistance and vascular remodelling, in relation to left ventricular mass, geometry and function: an answer to LIFE?

Lee

Lip

2003

J Hum Hypertens

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Many pathophysiological processes have been intimately linked to hypertension and its complications, including insulin resistance, left ventricular mass (LVM) and geometry, central vascular hypertrophy and peripheral vascular remodelling, LV systolic and diastolic function, etc. What appears to be much less certain are the (complex) interrelations between all these diverse processes.In elderly patients with essential hypertension and LV hypertrophy (LVH), Olsen et al 1 recently reported that peripheral vascular remodelling (assessed as minimal forearm vascular resistance, MFVR), hypertrophy and low distensibility of the common carotid arteries are associated with increased systolic blood pressure (BP) but not with insulin resistance (as assessed by euglycaemic hyperinsulinaemic clamp) or hyperinsulinaemia. Their findings suggest that long-standing systolic BP load may be a far more important determinant of structural vascular changes than insulin resistance in hypertension. However, in never-treated hypertensives, insulin resistance and hyperinsulinaemia were associated with low distensibility of the common carotid arteries, independent of BP and lumen diameter; perhaps because of a direct effect of insulin on the carotid arteries, resulting in changes in collagen metabolism. 1 Indeed, the subsequent publication from Olsen et al 2 suggests that insulin sensitivity was unrelated not only to parameters of peripheral vascular remodelling, but also to endothelial function or microvascular rarefaction.In this issue of the Journal of Human Hypertension, Olsen et al 3 examine the association between insulin resistance, carotid hypertrophy and peripheral vascular remodelling on the one hand and LVH, diastolic LV filling and systolic function on the other. So, what more information can the present analysis add to their previous two publications? 1,2 We shall (hopefully) delineate these in a systematic manner.LVH by echocardiography has proved to be a strong independent predictor of cardiovascular (CV) morbidity and mortality in hypertensive patients. Patients with a concentric hypertrophy geometry (increased LVM and relative wall thickness) appear to carry the highest risk, while an eccentric hypertrophy geometry (increased LVM but normal relative wall thickness) carries an intermediate risk for target organ damage. 4,5 In addition, the former is associated with especially high arterial pressure while the latter is associated with obesity and elevated volume load. On the other hand, central vascular hypertrophy, in particular carotid intimamedia thickness (IMT) is generally regarded as 'marker' of atherosclerotic burden as well as a 'predictor' of future CV events in prospective epidemiological studies. 6 Indeed, arterial remodelling, hypertrophy, and stiffness are common alterations in hypertensive patients, as well as LV diastolic dysfunction, and all have been linked to LVH. 7 However, diastolic dysfunction is also well recognised in patients with hypertension, even in the absence of LVH, but whether its assessment ...

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Left ventricular mass and systolic dysfunction in essential hypertension

Cited by 20 publications

References 36 publications

Global left ventricular performance in non-diabetic non-hypertensive metabolic syndrome adults

Global left ventricular performance in non-diabetic non-hypertensive metabolic syndrome adults

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

Insulin resistance and vascular remodelling, in relation to left ventricular mass, geometry and function: an answer to LIFE?

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