Myocardial mechanics in metabolic syndrome and aging populations

Cardiovascular disease (CVD) is the number one cause of death worldwide. The clustering of metabolic risk factors, defined as metabolic syndrome (MetS), and aging are two separate factors that significantly increase the risk of CVD. Both aging and MetS influence CVD by impairing heart tissue (myocardial) function. However, the exact understanding of mechanisms and evolution of these impairments are incomplete in MetS and aging populations. One of the most accessible and utilised techniques for assessing myocardial function is conventional transthoracic echocardiography, and more recently speckle tracking echocardiography (STE); a robust and sensitive modality of echocardiography, capable of assessing myocardial function in both the longitudinal and circumferential axes

Increased myocardial dysfunction, dyssynchrony, and epicardial fat across the lifespan in healthy males

International audienceBackground: Evaluation of sensitive myocardial mechanics with speckle tracking echocardiography (STE) across the lifespan may reveal early indicators of cardiovascular disease (CVD) risk. Epicardial adipose tissue (EAT) and left ventricular (LV) myocardial dyssynchrony; subclinical risk-factors of CVD, are of particular clinical interest. However, the evolution of EAT and LV-dyssynchrony across the lifespan, and their influence on myocardial dysfunction remains unclear. We aimed to establish a profile of the healthy aging-heart using conventional, tissue-Doppler imaging (TDI) and speckle-tracking echocardiography (STE), while also exploring underlying contributions from EAT and LV-dyssynchrony towards LV myocardial mechanics, independent of blood biology. Methods: Healthy males aged 19–94 years were recruited through University-wide advertisements in Victoria and New-South Wales, Australia. Following strict exclusion criteria, basic clinical and comprehensive echocardiographic profiles (conventional, TDI and STE) were established. LV-dyssynchrony was calculated from the maximum-delay of time-to-peak velocity/strain in the four LV-annulus sites (TDI), and six LV-segments (STE longitudinal and circumferential axes). Epicardial fat diameter was obtained from two-dimensional grey-scale images in the parasternal long-axis. Blood biological measures included glycemia, hsCRP, triglycerides, total cholesterol, high-density and low-density lipoprotein levels. Results: Three groups of 15 were assigned to young (<40 years), middle (40–65 years), and older (>65) aged categories. Five participants were excluded from STE analyses due to inadequate image quality. Decreased longitudinal strain, increased circumferential apical strain and LV twist were age-related. Moreover, independent of blood biology, significant increases were observed across age categories for EAT (young: 2.5 ± 0.9 mm, middle: 3.9 ± 1.0 mm, older 5.7 ± 2.4 mm; p < 0.01), longitudinal STE-dyssynchrony (young: 42 ± 7.7 ms, middle: 58.8 ± 18.9 ms, older 88.6 ± 18.2 ms; p < 0.05), and circumferential-basal STE-dyssynchrony (young: 50.2 ± 20.5 ms, middle: 75.9 ± 20.6 ms, older 97.9 ± 20.2 ms; p < 0.05). These variables collectively explained 37% and 31% (p < 0.01) of longitudinal strain and LV twist, respectively. Conclusions: This study enabled comprehensive profiling of LV mechanics at different stages of aging using sensitive echocardiographic technology. Novel findings included increased epicardial fat, and both longitudinal and circumferential LV-dyssynchrony across the healthy age groups. These factors may be key underlying contributors to myocardial dysfunction during aging, and their recognition may promote an advanced understanding of early signs of cardiovascular disease

Cardiovascular risk of adipokines: A review

Over the last two decades, the understanding of adipose tissue has undergone radical change. The perception has evolved from an inert energy storage tissue to that of an active endocrine organ. Adipose tissue releases a cluster of active molecules named adipokines. The severity of obesity-related diseases does not necessarily correlate with the extent of body fat accumulation but is closely related to body fat distribution, particularly to visceral localization. There is a distinction between the metabolic function of central obesity (visceral abdominal) and peripheral obesity (subcutaneous) in the production of adipokines. Visceral fat accumulation, linked with levels of some adipokines, induces chronic inflammation and metabolic disorders, including glucose intolerance, hyperlipidaemia, and arterial hypertension. Together, these conditions contribute to a diagnosis of metabolic syndrome, directly associated with the onset of cardiovascular disease. If it is well known that adipokines contribute to the inflammatory profile and appetite regulation, this review is novel in synthesising the current state of knowledge of the role of visceral adipose tissue and its secretion of adipokines in cardiovascular risk

Left ventricular myocardial dyssynchrony is already present in nondiabetic patients with metabolic syndrome

The presence of left ventricular (LV) dyssynchrony in individuals with metabolic syndrome (MetS), a predictor of type 2 diabetes (T2D), lacks clarity. We compared LV dyssynchrony in MetS individuals with and without T2D, and healthy control subjects using speckle-tracking imaging echocardiography. Ninety-two MetS participants (64 without, 28 with T2D) and 40 control subjects underwent echocardiographic and clinical/biological analyses. LV-dyssynchrony in the longitudinal axis only was present in all MetS individuals, but was not further exacerbated by T2D. Strong associations were found with systemic inflammation, abdominal obesity, and LV mass. Investigations of myocardial dyssynchrony in the nondiabetic MetS stage might facilitate timely and more effective prevention

Effects of lifestyle intervention on left ventricular regional myocardial function in metabolic syndrome patients from the RESOLVE randomized trial

Aims: The purpose of our study was to determine the effect of lifestyle intervention on left ventricular (LV) regional myocardial function in patients with metabolic syndrome (MetS) and investigate the relationships of the changes in myocardial function to changes in epicardial adipose tissue (EAT), inflammatory profile and MetS components. Methods: Eighty-seven MetS patients were enrolled in a 6 month lifestyle intervention program based on dietary management and increased physical activity, and compared with 44 aged and sex-matched healthy controls. MetS individuals were allocated to different groups randomized (computer-generated randomization) on exercise modalities (high-intensity dominant resistance or aerobic training, and moderate-intensity of both modes). EAT was measured by transthoracic echocardiography and LV longitudinal strains and strain rates were obtained using vector velocity imaging. Blood chemistry allowed assessments of adipocytokines (TNF-α: tumor necrosis factor α, PAI active: active plasminogen activator inhibitor-1 and adiponectin) and glucose tolerance markers. Results: Regardless of exercise training modalities, lifestyle intervention improved significantly LV strains and strain rates (p < 0.001) as well as metabolic and inflammatory profiles. Stepwise multiple regression analyses revealed EAT (β = 0.73, p < 0.01), log adiponectin (β = − 0.13, p < 0.05) and log TNF-α (β = 0.15, p < 0.05) as independent predictors of LV longitudinal strain (R2 = 0.74, p < 0.001) while myocardial function improvement consecutive to lifestyle intervention was explained by EAT changes only (R2 = 0.54, p < 0.001). Conclusion: The mechanisms through which regional myocardial function is impaired in MetS and improved consecutive to intervention involved EAT, possibly via paracrine effects of adipocytokines. EAT should be considered as a future therapeutic target of interest in the treatment of metabolic-related cardiac diseases

Right ventricle free wall mechanics in metabolic syndrome without type-2 diabetes: effects of a 3-month lifestyle intervention program

International audienceBackground: Growing evidence demonstrates subtle left ventricular myocardial dysfunction in patients with metabolic syndrome (MetS), with central obesity, glucose intolerance and inflammation emerging as important contributors. Whether these results can be translated to the right ventricle (RV) is not yet fully elucidated. Furthermore, although lifestyle intervention favorably impacts MetS components and inflammatory biomarkers, its effect on RV myocardial function remains unknown today. Methods: Thirty-nine MetS adults free of diabetes were enrolled in a three month lifestyle intervention program including diet and physical exercise, and compared with forty healthy controls. Blood biochemistry, echocardiography including tissue Doppler imaging (TDI), and vector velocity imaging of the RV free wall to assess global longitudinal strain (GLS) and strain rates (SR) were obtained at baseline and after the intervention. Results: Compared with controls, MetS patients presented similar right atrial and RV morphology but reduced systolic (P = 0.04) and early diastolic (P = 0.02) velocities of the tricuspid annulus. They showed attenuated RV GLS (−21.4 ± 4.5vs-25.7 ± 4.9%, P < 0.001) as well as early diastolic (P = 0.003) and systolic (P < 0.001) SR. Multiple regression analyses revealed log PAI-1 active, (P < 0.001), log adiponectin, (P = 0.01), LV mass indexed (P = 0.004) and central fat (P = 0.03) as independent predictors of RV GLS (R 2 = 0.46, P < 0.001). Biological markers of MetS and inflammation as well as RV GLS (−21.8 ± 3.8vs-24.3 ± 3.0%, P = 0.009) and systolic (P = 0.003) and early diastolic (P = 0.01) SR, but not TDI indexes, significantly improved after diet and exercise training, and vector velocity imaging data in MetS following the lifestyle intervention no longer differed from controls. Conclusions: MetS is associated with subtle impairments in both RV free wall diastolic and systolic myocardial function which could be partly related to central-obesity induced changes in pro-and anti-inflammatory cytokines and left ventricular remodeling. The favorable impact of healthy dieting and physical activity on RV free wall mechanics indicates that cellular and sub-cellular alterations responsible for the RV myocardial abnormalities are probably not permanent and modifiable throughout adequate interventional strategies. Trial registration: American National Institutes of Health database NCT00917917

Cardiovascular risk of adipokines: a review

Over the last two decades, the understanding of adipose tissue has undergone radical change. The perception has evolved from an inert energy storage tissue to that of an active endocrine organ. Adipose tissue releases a cluster of active molecules named adipokines. The severity of obesity-related diseases does not necessarily correlate with the extent of body fat accumulation but is closely related to body fat distribution, particularly to visceral localization. There is a distinction between the metabolic function of central obesity (visceral abdominal) and peripheral obesity (subcutaneous) in the production of adipokines. Visceral fat accumulation, linked with levels of some adipokines, induces chronic inflammation and metabolic disorders, including glucose intolerance, hyperlipidaemia, and arterial hypertension. Together, these conditions contribute to a diagnosis of metabolic syndrome, directly associated with the onset of cardiovascular disease. If it is well known that adipokines contribute to the inflammatory profile and appetite regulation, this review is novel in synthesising the current state of knowledge of the role of visceral adipose tissue and its secretion of adipokines in cardiovascular risk