Decrease of glutathione peroxidase in arrhythmic cardiac pathology in young individuals and its therapeutic implications.

Glutathione peroxidase (GPx), as an antioxidant enzyme, is involved in the regulation of processes that cause cellular oxidative stress, with implications in various pathologies. The aim of the present study was to evaluate GPx variations in patients with arrhythmic, non-structural cardiac disorders. The research was performed on 120 patients, with a mean age of 33 years old, divided into 3 equal groups, of which 2 groups included patients with cardiac arrhythmias, the first group, associated with dyslipidemia and the second one, without dyslipidemia, and a control group consisting of healthy individuals. The method for determining GPx was based on the GPx enzyme catalysis reaction of the reduced glutathione (GSH) oxidation reaction by cumene hydroperoxide. The results revealed that GPx variation was decreased in patients with cardiac arrhythmias, with or without dyslipidemia, up to 66 and 74% of mean control values, respectively, the differences being statistically significant, showing the existence of an oxidative stress imbalance, that may be involved in triggering arrhythmogenic electrochemical mechanisms. The GPx deficiency determined in relation to cardiac arrhythmias was in dyslipidemic and non-lipidemic patients as follows: 29-35% in sinus bradycardia, 31-35% in associated cardiac arrhythmias, 30-33% in sinus tachycardia, 27-33% in atrial fibrillation, 32-33% in atrial flutter, 27-32% in atrial extrasystolic arrhythmia, 28-30% in ventricular extrasystolic arrhythmia and 18-26% in paroxysmal supraventricular tachycardia. Collectively, the results revealed that GPx, an antioxidant enzyme, is a specific biomarker, whose decrease indicated the existence of oxidative stress in young individuals with cardiac arrhythmias and its involvement in arrhythmogenic electrochemical processes. In addition, GPx deficiencies were between 18-35% in all types of cardiac arrhythmias, the highest being recorded in sinus bradycardia and the lowest in paroxysmal supraventircular tachycardia. Furthermore, the oxidative stress favored by the decrease of GPx induced lipid oxidation, regardless of the presence or absence of dyslipidemia, which triggered the formation of anti-lipid antibodies and a subclinical endothelial aggression, with early atherosclerotic potential. GPx evaluation may argue for the existence of oxidative stress in non-structural cardiac arrhythmias, and by its proper correction (antioxidants), prophylaxis of atherogenic dysfunction.

Variation of Total Antioxidant Activity in Young People with Non-Lesional Cardiac Arrhythmias.

Total antioxidant activity status (TAS) represents the body's response to oxidative stress, important in the pathogenic assessment of oxidations. AIM: To determine TAS variations in young subjects, with non-lesional cardiac arrhythmias, with/without dyslipidemia and to assess the risk of lipid oxidation. PATIENTS AND METHODS: The research was performed on 120 young subjects (mean age 33 years), with various types of cardiac arrhythmias, on normal heart, without co-existing lesions. Subjects were divided into 3 groups (40 persons). The first 2 groups included subjects with cardiac arrhythmias. Group I also associated dyslipidemia; group II, without dyslipidemia and group III: control. Determination of TAS values was performed using ABTS (2-azino-di-3-ethylbenzthiazoline sulfonate) colorimetic method. Results were statistically processed. RESULTS: TAS values were decreased in all patients with cardiac arrhythmias, representing 52-54% of the values of healthy controls, the data being highly statistically significant. The variation of TAS decrease by types of arrhythmias was thus found in patients with arrhythmias and associated dyslipidemia and, respectively, without dyslipidemia, compared to controls. The deficit of antioxidant activity, between 48%-46% triggers electrochemical processes with implications in arrhythmogenesis and lipid oxidation. Coffee and vegetables-rich diet have antioxidant effect, reducing TAS deficiency. CONCLUSIONS: 1. TAS was decreased in all subjects with non-lesional arrhythmias. The study showed decreasing TAS level at 52-54% in patients with arrhythmias, with/without dyslipidemia, compared to controls. 2. TAS deficiency was associated with various types of dysrhythmias, ranging from 62% to 33%. 3. Decreased TAS also triggers lipid oxidation, as risk factor for early atherosclerotic lesions.

Calcium fructoborate coating of titanium-hydroxyapatite implants by chemisorption deposition improves implant osseointegration in the femur of New Zealand White rabbit experimental model.

BACKGROUND: The identification of biocomposites that improve cell adhesion and reduce bone integration time is a great challenge for implantology and bone reconstruction. AIM: Our aim was to evaluate a new method of chemisorption deposition (CD) for improving the biointegration of hydroxyapatite-coated titanium (HApTi) implants. CD method was used to prepare a calcium fructoborate (CaFb) coating on a HApTi (HApTiCaFb) implant followed by evaluation of histological features related to bone healing at the interface of a bioceramic material in an animal model. METHODS: The coating composition was investigated by high-performance thin-layer chromatography/mass spectrometry. The surface morphology of the coating was studied by scanning electron microscopy (SEM), before and after the in vitro study. We implanted two types of bioceramic cylinders, HApTi and HApTiCaFb, in the femur of 10 New Zealand White (NZW) rabbits. RESULTS: The release of CaFb from HApTiCaFb occurred rapidly within the first three days after phosphate-buffered saline immersion; there was then a linear release for up to 14 days. SEM analysis showed similar morphology and particle size diameter for both implants. Around the porous HApTiCaFb implant, fibrosis and inflammation were not highlighted. CONCLUSIONS: Easily applied using CD method, CaFb coatings promote HApTi implant osseointegration in the femur of NZW rabbits.

Visceral and tissular reactivity in acute heart failure due to supraventricular tachyarrhythmia in a young patient.

Observation of major pathological alterations in a young person involves etiological and clinical justifications, in order to properly assess, treat and control these conditions. The aim of this paper is to present severe, acute pathological lesions, installed in a young person, secondary to hypodiastolic heart failure, due to persistent supraventricular tachyarrhythmia, triggered by a post-traumatic external stimulus, with complete remission post-electrical conversion. Pathological and clinical modification are revealed, in a young person, shortly after a minor thoracic trauma, in the absence of traumatic injury but with high-frequency palpitations onset and progressive installation of vascular, visceral and interstitial stasis modifications, as well as of vascular and tissular hypoperfusion with reactive vasoconstriction. These clinical and paraclinical aspects were: stasis hepatomegaly with hepatojugular reflux, pulmonary congestion with stasis rales, peripheral edema, transudative polyserositis - pericarditis, hydrothorax, ascites, dilatation of inferior vena cava and suprahepatic veins, decrease of arterial blood pressure, tissue and cutaneous vasoconstriction. Anatomical and clinical aspects, with major alterations (Vth degree hepatomegaly, polyserositis, peripheral edema, tachyarrhythmic heart contractions, hypotension, pallor accentuated by vasoconstriction) acutely installed in a previously healthy young person, require a rapid lesions diagnosis and emergency treatment due to vital risk, control of acute heart failure manifestations remission and proper monitoring. Differential diagnosis was focused on determining possible aspects like: acute heart failure (of various etiology), internal post-traumatic lesions or hemorrhages, tuberculosis polyserositis, collagenosis, nephrotic syndrome, protein deficiencies, neoplasia with hepatic determinations, hematological diseases (lymphomas, leukemias), considered in young patients. Severe visceral, vascular and tissular pathological alterations were reactively induced in a young person, by stasis and hypoperfusion due to hypodiastolic heart failure caused by persistent supraventricular tachyarrhythmia triggered post-traumatic, on a proarrhythmic structural heart.