The Metabolic Syndrome and ECG Detected Left Ventricular Hypertrophy – Influences from IGF-1 and IGF-Binding Protein-1

Objective: To assess the prevalence of left ventricular hypertrophy (LVH) and linked cardiovascular risk factors in civilian aircrew.Methods: Cardiovascular risk factors were assessed among flight and cabin crew undergoing routine clinical and biological evaluation for initial or renewal of aeromedical license. The evaluation also included a standard 12-lead ECG and echocardiography. Echo-based LVH was LVM ≥ 49 g/m2.7 (men) or ≥ 45 g/m2.7 (women). LVH was categorized as mild (men: 49-55 g/m2.7; women: 45-51 g/m2.7), moderate (men: 56-63 g/m2.7; women: 52-58 g/m2.7), or severe (men: ≥ 64 g/m2.7; women: ≥ 59g/m2.7) according to Lang’s report.Results: Among the 379 aircrew members (70.4% men; 23% Caucasians; 62.5% flight crew; mean age 40.6 ± 12.8 years), LVH was present in 36 individuals (9.5%) with mild, moderate and severe pattern observed respectively in 19.4%, 33.3% and 47.2% of the cases. The rate of LVH amounted to 16.7% in normotensive subjects, 25.0% in those with prehypertension, and 58.3% among hypertensive individuals. In addition to age of 40-59y (OR: 8.48; 95% CI: [2.23-12.23]; p = .002) or more (4.22 [1.57-11.35]; p = .004), hypertension (3.55 [1.50 - 8.41]; p = .004), overweight/obesity (5.33 [1.14 - 25.05]; p = .034) and hyperuricemia (5.05 [2.11 - 12.09]; p = .001), all well-known constituents of the metabolic syndrome, were the main factors significantly associated with LVH.Conclusion: The frequency and link of LVH to the components of the metabolic syndrome highlights the need for a comprehensive approach to the management of cardiovascular risk factors in civilian aircrew.

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The metabolic syndrome and left ventricular hypertrophy – the influence of gender and physical activity

Blood Pressure ◽

10.3109/08037051.2012.641267 ◽

2011 ◽

Vol 21 (3) ◽

pp. 153-160 ◽

Cited By ~ 11

Author(s):

Mats Halldin ◽

Per Fahlstadius ◽

Ulf de Faire ◽

Max Vikström ◽

Mai-Lis Hellénius

Keyword(s):

Physical Activity ◽

Metabolic Syndrome ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

The Metabolic Syndrome

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Electrocardiographic Left Ventricular Hypertrophy Regression Induced by an Angiotensin Receptor Blocker-Based Regimen in Hypertensive Patients With the Metabolic Syndrome: Data From the SARA Study

Journal of Clinical Hypertension ◽

10.1111/j.1751-7176.2008.07596.x ◽

2008 ◽

Vol 10 (3) ◽

pp. 208-214 ◽

Cited By ~ 6

Author(s):

Carlos Escobar ◽

Vivencio Barrios ◽

Alberto Calderón ◽

Sara Barrios ◽

Rocio Echarri ◽

...

Keyword(s):

Metabolic Syndrome ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Angiotensin Receptor Blocker ◽

Left Ventricular ◽

Receptor Blocker ◽

Angiotensin Receptor ◽

Hypertensive Patients ◽

The Metabolic Syndrome ◽

Left Ventricular Hypertrophy Regression

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PO21-660 PREVALENCE OF LEFT VENTRICULAR HYPERTROPHY AND ITS ASSOCIATION TO VARIABLES OF THE METABOLIC SYNDROME IN 60-YEAR OLD MEN AND WOMEN

Atherosclerosis Supplements ◽

10.1016/s1567-5688(07)71670-7 ◽

2007 ◽

Vol 8 (1) ◽

pp. 177

Author(s):

M. Halldin ◽

U. de Faire ◽

M-L. Hellénius

Keyword(s):

Metabolic Syndrome ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Men And Women ◽

The Metabolic Syndrome ◽

Old Men

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Abstract 2657: The Increased Local Insulin-like Growth Factor-1 To IGF Binding Protein-3 Ratio In The Pathogenesis Of The Left Ventricular Hypertrophy In Humans: Augmentation By Matrix Metalloproteinase-2 Activity

Circulation ◽

10.1161/circ.116.suppl_16.ii_589 ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Naoki Abe ◽

Toshiro Matsunaga ◽

Kunihiko Kameda ◽

Hirofumi Tomita ◽

Tomohiro Osanai ◽

...

Keyword(s):

Growth Factor ◽

Ventricular Hypertrophy ◽

Binding Protein ◽

Left Ventricular ◽

Valvular Disease ◽

Free Form ◽

Insulin Like Growth Factor ◽

Igf Binding ◽

Igf Binding Protein ◽

Igfbp 3

Insulin-like growth factor (IGF)-1 is a potent mitogen and is said to enhance ventricular hypertrophy. IGF-1 is present as an IGF-1-IGF binding protein-3 (IGFBP-3) complex, and its free form shows bioactivity. Recently, the matrix metalloproteinases (MMPs) were shown to facilitate IGF-1 bioactibity through the degradation of IGFBP-3. To clarify the relation of IGF-1 and IGFBP-3 to MMPs and their roles in human cardiac hypertrophy, we measured levels of total IGF-1, IGFBP-3, MMP-2, and MMP-9 in the pericardial fluid, which reflects the myocardial interstitial fluid, obtained from 51 patients with aortic valvular disease (AVD) (n=36) (aortic stenosis (n=24), aortic regurgitation (n=12)) and mitral valvular disease (MVD) (n=15) (mitral stenosis (n=6), mitral regurgitation (n=9)) who underwent open heart surgery. Levels of total IGF-1 and IGFBP-3 were measured by enzyme immunoassay, and the activities of MMP-2 and MMP-9 by gelatin zymography. Left ventricular mass index (LVMI) was estimated by echocardiography. Pericardial total IGF-1 level (ng/ml) in AVD (32±19) was higher than that in MVD (20±17) (p<0.05). Pericardial IGFBP-3 level (ng/ml) was not different between AVD (715±318) and MVD (857±441). When total IGF-1/IGFBP-3 ratio, indicative of potency of IGF-1 action, was estimated in each patient, it was significantly higher in AVD than in MVD (p<0.017). There was no difference in MMP-9 activity between AVD and MVD, while MMP-2 activity in AVD was higher than that in MVD (p<0.05). LVMI in AVD was significantly greater than in MVD (p<0.05). In the linear regression analysis for all patients, pericardial total IGF-1/IGFBP-3 ratio was positively correlated with LVMI (r=0.3, p<0.05). To further clarify the relationship among total IGF-1, IGFBP-3 and MMP-2, we examined the effect of IGF-1 on smooth muscle cell (SMC) proliferation. IGF-1 (250 ng/ml) induced SMC proliferation, and this was inhibited by IGFBP-3 (2500 ng/ml). This inhibiting effect of IGFBP-3 was reversed by co-treatment with MMP-2 (0.005 unit). These findings suggest that cardiac IGF-1/IGFBP-3 system, which is augmented by MMP-2, plays an important role in the pathogenesis of LV hypertrophy.

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