Muscular exercise results in an increased production of free radicals and other forms of reactive oxygen species (ROS). Further, developing evidence implicates cytotoxins as an underlying etiology of exercise-induced stimuli in muscle redox status, which could result in muscle fatigue and/or injury. Two major classes of endogenous protective mechanisms (enzymatic and nonenzymatic antioxidants) work together to reduce the harmful effects of oxidants in the cell. This study examined the effects of acute physical exercise on the enzymatic antioxidant systems of different athletes and comparison was made to the mechanism of action of three main antioxidant enzymes in the blood. Handball players (n = 6), water-polo players (n = 20), hockey players (n = 22), basketball players (n = 24), and a sedentary control group (n = 10 female and n = 9 male) served as the subjects of this study. The athletes were divided into two groups according to the observed changes of activity of superoxide dismutase enzyme. The antioxidant enzyme systems were characterized by catalase (CAT), glutathione-peroxidase (GPX), and superoxide-dismutase (SOD) and measured by spectrophotometry. An important finding in the present investigation is that when the activities of SOD increased, the activities of GPX and CAT increased also and this finding related to the physical status of interval-trained athletes. Positive correlation between SOD and GPX activities was observed (r = 0.38 females, r = 0.56 males; p < 0.05). We have observed that the changes in the primary antioxidant enzyme systems of athletes are sport specific, and different from control subjects. Presumably, with interval-trained athletes, hydrogen-peroxide is significantly eliminated by glutathione-peroxidase. From these results it can be concluded that the blood redox status should be taken into consideration when establishing a fitness level for individual athletes.

The use of direct acting vasodilators (the combination of hydralazine and isosorbide dinitrate -Hy+ISDN-) in heart failure with reduced ejection fraction (HFrEF) is supported by evidence, but rarely used.However, treatment with Hy+ISDN is guideline-recommended for HFrEF patients who cannot receive either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers due to intolerance or contraindication, and in self-identified African-American HFrEF patients who are symptomatic despite optimal neurohumoral therapy.The Hy+ISDN combination has arterial and venous vasodilating properties. It can decrease preload and afterload, decrease left ventricular end-diastolic diameter and the volume of mitral regurgitation, reduce left atrial and left ventricular wall tension, decrease pulmonary artery pressure and pulmonary arterial wedge pressure, increase stroke volume, and improve left ventricular ejection fraction, as well as induce left ventricular reverse remodelling. Furthermore, Hy+ISDN combination has antioxidant property, it affects endothelial dysfunction beneficially and improves NO bioavailability. Because of these benefits, this combination can improve the signs and symptoms of heart failure, exercise capacity and quality of life, and, most importantly, reduce morbidity and mortality in well-defined subgroups of HFrEF patients.Accordingly, this therapeutic option can in many cases play an essential role in the treatment of HFrEF.

Background: Recently published studies suggested that digoxin may increase mortality in heart failure with reduced ejection fraction (HFrEF). However, in the vast majority of former trials serum digoxin concentration (SDC) was not measured and therapy was not SDC-guided. Aim: To assess the impact of SDC-guided digoxin therapy on mortality in HFrEF patients. Methods: Data of 580 HFrEF patients were retrospectively analyzed. In patients on digoxin, SDC was measured every 3 months and digoxin dosage was SDC-guided (target SDC: 0.5-0.9 ng/mL). All-cause mortality of digoxin users and nonusers was compared after propensity score matching (PSM). Results: After 7.1 ± 4.7 years follow-up period (FUP) all-cause mortality of digoxin users (n = 180) was significantly higher than nonusers (n = 297

The ACE I allele is a genetic marker for higher endurance efficiency in acute physical activity and higher adaptation of the cardiovascular system. The measurement of acute physical status needs to be completed with examination of genotype, which is related to the athletic excellence also, because the D allele could be associated with good performance by endurance athletes in future world championships. Further studies are needed to assess the view that the ACE D allele has a significant role in athletic efficiency.

A patient with dilated cardiomyopathy and DDD pacemaker experienced paroxysmal returns of her symptoms. IEGM revealed VA cross-talk resulting in functional undersensing of the following P wave that occurred during the PVARP and initiating a pacemaker syndrome with the pacemaker as a bystander.