Obesity and Myocardial Infarction-The Place of Obesity Among Cardiovascular Risk Factors-Retrospective Study.

Since the 21st century, the leading cause of death is cardiovascular disease, with myocardial infarction being the most common. The incidence and prevalence of obesity has risen sharply in recent years, and it is commonly recognised as a cardiovascular risk factor among tobacco smoking, dyslipidemia (high LDL-C, high triglycerides, low HDL-C), hypertension, diabetes, age, gender, hereditary predisposition. MATERIALS AND METHODS: This study is a retrospective study conducted at the Craiova Emergency Clinical Hospital between October 2020 and January 2023. Enrolled patients are 60, 36 patients with ST-segment elevation myocardial infarction and 24 patients with non-ST-segment elevation acute myocardial infarction. The data was collected from the hospital's official database and then analyzed using Microsoft Excel and the Toolbar Data Analysis. RESULTS: The mean age of the patients in the study was 62 years with a minimum of 34 years and a maximum of 84 years. 23(38.3%) of patients were smokers, 7(11.6%) were ex-smokers and 30(50%) were non-smokers. 49(81.6%) patients were hypertensive. 44(73%) had cholesterol greater than 200mg/dl. 54(90%) had LDL>100mg/dl, 18(30%) had HDL>45mg/gl, 24(40%) patients had serum TG>150mg/dl, 17(28%) were overweight and 13(22%) were obese, 30(50%) were normal weight. 18(30%) patients had type 2 diabetes. CONCLUSIONS: Among the cardiovascular risk factors in the patients studied, hypertension was the most common, followed by dyslipidemia, obesity, smoking, diabetes mellitus, and very rarely the use of drugs and anabolic substances.

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.

Motor unit changes in normal aging: a brief review.

Aging is explored by multiple lines of research, in a pursuit of understanding this natural process. The motor response is usually the main dependent variable in studies regarding physical or cognitive decline in aging. It is therefore critical to understand how the motor function changes with age. The present review, aims at presenting briefly some of the most recently published works in the field, focusing on the three key components of the motor unit. The changes that the skeletal muscle undergoes aging sarcopenia, alteration of fiber type distribution and also intimate metabolic transformations. The neuromuscular junction suffers at cellular and molecular level, with possible implications of various cell components, mediators and oxidative stress. Motoneuron loss and change in their physiological properties accompany remodeling in the motor units. The applicability of knowledge in this field lies in possible interventions intended to counteract these age-related losses.

Corpuscular Haemolytic Anaemias - Lepore Haemoglobinopathy.

Haemoglobinopathies are hereditary conditions in which the fundamental lesion affects the synthesis rate or the structure of the globin in normal hemoglobin. The synthesis of the polypeptide chains in globin is genetically coded. Clinically, haemoglobinopathies manifest most commonly in the form of hemolytic anemia and, more rarely, cyanosis and polyglobulia. They differ from "acquired haemoglobinopathies", such as methemoglobinemia, in which hemoglobin is usually compromised due to the action of toxic substances. The clinical aspects are in close relationship to the nature and level of the structural anomaly of the Hb molecule. The heterozygous form of the Lepore syndrome is hematologically characterized by a similar pattern to minor ß-thalassemia and electrophoretically by abnormal Hb D fractions at a rate of 5-10% and a decreased percentage of HbA. In homozygous forms, Lepore Hb represents 10-20% on electrophoresis, the rest consisting of HbF; HbA and HbA2 are completely absent. From a clinical point of view, Hb Lepore heterozygotes are similar to those with minor ß - thalassemia.