Abstract
The oxidative stress state is characterized by an increase in oxygen reactive species that overwhelms the antioxidant defense; we do not know if these pathological changes are correlated with alterations in left ventricular mechanics. The aim was correlating the oxidative stress state with the left ventricular global longitudinal strain (GLS) and the left ventricular end diastolic pressure (LVEDP). Twenty-five patients with essential hypertension and 25 controls paired by age and gender were studied. All of the participants were subjected to echocardiography and biochemical determination of oxidative stress markers. The hypertensive patients, compared with control subjects, had significantly (p < 0.05) higher levels of oxidized proteins (5.03 ± 1.05 versus 4.06 ± 0.63 nmol/mg), lower levels of extracellular superoxide dismutase (EC-SOD) activity (0.045 ± 0.02 versus 0.082 ± 0.02 U/mg), higher LVEDP (16.2 ± 4.5 versus 11.3 ± 1.6 mm Hg), and lower GLS (−12% versus −16%). Both groups had preserved ejection fraction and the results showed a positive correlation of oxidized proteins with GLS (r = 0.386, p = 0.006) and LVEDP (r = 0.389, p = 0.005); we also found a negative correlation of EC-SOD activity with GLS (r = −0.404, p = 0.004) and LVEDP (r = −0.347, p = 0.014).
Highlights
An increasing body of evidence suggests that oxidative stress is involved in endothelial dysfunction, a factor that is present in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia, atherosclerosis, hypertension, diabetes, and heart failure [1,2,3,4]; endothelial dysfunction is what all of these diseases have in common [5]
ROS generates various stimuli, including angiotensin II, endothelin-1, cytokine, and growth factorinduced redox-sensitive signals, and oxidative stress state produces the decrease of extracellular superoxide dismutase (EC-SOD) activity and increased oxidized proteins leading to the accumulation of extracellular matrix proteins, interstitial and perivascular fibrosis, and myocyte hypertrophy, which cause left ventricular (LV) remodeling as in the case of diabetic cardiomyopathy [27,28,29]
The echocardiographic determination of atrial and LV dimensions in hypertensive patients clearly indicated that this group of patients had concentric LV hypertrophy, as the patients reported by Qu and collaborators [39], and that it was associated with the highest degree of diastolic dysfunction
Summary
An increasing body of evidence suggests that oxidative stress is involved in endothelial dysfunction, a factor that is present in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia, atherosclerosis, hypertension, diabetes, and heart failure [1,2,3,4]; endothelial dysfunction is what all of these diseases have in common [5].In healthy individuals, the endothelium plays a key role in vascular homeostasis through the release of a variety of antiatherogenic substances that exert an effect by way of platelet aggregation and adhesion inhibition, smooth muscle cell proliferation, and leukocyte adhesion [6,7,8,9,10,11,12,13,14,15,16,17].The evidence that oxidative stress state occurs in hypertensive patients is based on increased levels of biomarkers such as oxidized protein and lipid oxidation and on the decreased activity of antioxidants such as superoxide dismutase, glutathione peroxidase, and catalase [18,19,20] as well as on the shorter telomere length found in these patients [21, 22]. It is clear that oxidative stress has an important role in the impairment of cellular signal pathways and the modulation of Oxidative Medicine and Cellular Longevity growth, apoptosis, hypertrophy, inflammation, and remodeling of cardiac muscle [24] through the activation of various signaling cascades and redox state-sensitive transcription factors [25, 26]. ROS generates various stimuli, including angiotensin II, endothelin-1, cytokine, and growth factorinduced redox-sensitive signals, and oxidative stress state produces the decrease of extracellular superoxide dismutase (EC-SOD) activity and increased oxidized proteins leading to the accumulation of extracellular matrix proteins, interstitial and perivascular fibrosis, and myocyte hypertrophy, which cause left ventricular (LV) remodeling as in the case of diabetic cardiomyopathy [27,28,29]
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