Oxidative Stress and Left Ventricular Performance in Patients with Different Glycometabolic Phenotypes

Abstract

The aim of the present study was to evaluate the possible correlation between oxidative stress and subclinical myocardial damage, assessed with speckle tracking echocardiography (STE), in normal glucose tolerance (NGT) patients with one-hour plasma glucose values ≥ 155 mg/dL (NGT ≥ 155), comparing them to NGT < 155 subjects, impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) newly diagnosed patients. We enrolled 100 Caucasian patients. All subjects underwent OGTT. The serum values of oxidative stress markers (8-isoprostane and Nox-2) were assessed with an ELISA test. Echocardiographic recordings were performed using an E-95 Pro ultrasound system. We observed significant differences, among the four groups, for fasting plasma glucose (p < 0.0001), one-hour postload (p < 0.0001), and two-hour postload plasma glucose (p < 0.0001). As compared with NGT < 155, NGT ≥ 155 exhibited significantly worse insulin sensitivity and higher values of hs-CRP. No significant differences were observed between NGT ≥ 155 and IGT patients. There was a significant increase in 8-isoprostane (p < 0.0001) and Nox-2 (p < 0.0001), from the first to fourth group, indicating an increase in oxidative stress with the worsening of the metabolic status. Serum levels of 8-isoprostane and Nox-2 were significantly increased in NGT ≥ 155 compared to the NGT < 155 group, but similar to IGT. The global longitudinal strain (GLS) appeared progressively lower proceeding from the NGT < 155 to T2DM group (p < 0.0001). For similar values of left ventricular ejection fraction (LVEF), NGT ≥ 155 exhibited reduced GLS compared to NGT < 155 (p = 0.001), but similar to IGT patients. Our study demonstrated that NGT ≥ 155 subjects exhibit early functional impairment of myocardial contractile fibres, these alterations are correlated with increased oxidative stress.

Short-term effect of sacubitril/valsartan on endothelial dysfunction and arterial stiffness in patients with chronic heart failure

“…Notably, RHI and PWV follow-up values were comparable to those of newly diagnosed hypertensive patients without diabetes or CV complications ( Sciacqua et al, 2012 ; Cassano et al, 2021 ). Similarly, the indicators of inflammation, in particular hs-CRP, and of oxidative stress significantly improved with Sacubitril/Valsartan to such an extent that they were comparable to those of normotolerant hypertensive patients ( Cassano et al, 2022 ) ( Figure 4 ).…”

“…In addition, our results demonstrated a significant improvement in metabolically in-dices such as FPG, FPI, HbA1c and HOMA, and these data are in agreement with our previous evidence ( Armentaro et al, 2022 ). Many studies demonstrated that hyperglycemia triggers vascular damage by creating imbalance between NO availability and ROS accumulation ( Kaur et al, 2018 ; Cassano et al, 2022 ). Moreover, chronic hyperglycaemia injures vascular wall by many cellular mechanisms, including an increased production of intracellular advanced glycation end products (AGEs), raised expression of AGE receptors (RAGE) and ligands, activation of protein kinase C (PKC), augmented polyol and hexosamine flux and over activation of the hexosamine pathway.…”

“…It is known that inflammation and oxidative stress, characterized by increased 8,12-isoprostane F (2α) concentration, low endothelium-bound extracellular superoxide dismutase activity and increased endothelium-bound xanthine oxidase (XO) activity and cytokines production, play a central role in pathogenesis of both endothelial dysfunction and HF ( Bulua et al, 2011 ; Odegaard et al, 2016 ; Alem, 2019 ; Cassano et al, 2022 ). Moreover, endothelial dysfunction attracts circulating inflammatory cells through Intercellular adhesion molecules (ICAMs) and inflamed endothelium interacts with cardiomyocytes and platelets ( El-Battrawy et al, 2016b ).…”

One‐hour post‐load glucose and subclinical left atrial myocardial dysfunction in hypertensive patients

“…4 Notably, we recently demonstrated that NGT≥155 exhibit premature functional impairment of myocardial contractile fibre assessed by speckle tracking echocardiography (STE) and increased oxidative stress biomarkers in comparison with NGT < 155, with values similar to IGT patients. 5 All these observations emphasise the correlation between precocious variation of glucose tolerance and subclinical myocardial damage.…”

Endothelial Dysfunction Is Associated with Decreased Nitric Oxide Bioavailability in Dysglycaemic Subjects and First-Degree Relatives of Type 2 Diabetic Patients

“…Furthermore, our previous studies have shown that coronary flow reserve (CFR), a marker of coronary microcirculation, as well as LV myocardial strain, is impaired in first-degree relatives (FDR) of diabetic patients and dysglycaemic subjects compared with normoglycaemic subjects [ 10 , 11 ]. A recent study revealed that subjects with normal glucose tolerance with one-hour glucose levels ≥ 155 mg/dL during an oral glucose tolerance test (OGTT) had subclinical impairment in LV myocardial performance, and this finding was correlated with increased oxidative stress [ 12 ]. However, little is known about the association of endothelial glycocalyx, coronary microcirculation and LV myocardial function with the kinetics of oxidative stress markers and nitrite/nitrate levels during postprandial hyperglycaemia.…”