Background: The Valsalva Maneuver (VM) is the first-line treatment for paroxysmal supra-ventricular tachycardia, but a recent, novel, and efficient tool to restore sinus rhythm has been described, i.e., the Reverse Valsalva (RV). This study aims to compare changes in cardiovascular hemodynamics and autonomic system activity (ANS) based on heart rate variability (HRV) analysis during both maneuvers.
Methods: Fifteen healthy participants performed the VM and RV maneuvers three times in a sitting position for durations of 15 s and 10 s, respectively. Blood pressure (BP) and heart rate (HR) were continuously monitored before, during and after the tests. Autonomic system activity was evaluated using frequency-domain analysis of HRV.
Results: The decrease in HR from baseline to the lowest values, expressed as a ratio, was similar during both maneuvers (0.81 during the RV vs. 0.79 during the VM, p = 0.27). However, the final lowest HR in response to the RV was higher than that in response to the VM, 70/min vs. 59/min (p <0.001). The activation of the autonomic nervous system during the most bradycardic phase of the RV (phase II) and VM (phase IV) showed that the total power of HRV was less prominent during the RV than during the VM (p <0.012), with similar levels of parasympathetic activation. Conclusions: Our results showed less HR slowdown during the RV than during the VM. The changes in HRV parameters during both procedures in particular phases of the RV and VM suggest that the auto-nomic nervous system is activated alternately, so these tests can be used complementarily in a clinical setting with different results.

Platelet aggregation contributes to the pathogenesis of cardiovascular diseases. After activation it leads to dense granule secretion and 5-HT release. The question arises; how platelet aggregation is endogenously controlled during blood circulation. In preliminary studies, we observed that human plate-lets aggregate more rapidly when suspended in buffer as compared to those suspended in plasma (PRP). These observations point to the presence of an endogenous substance that may inhibit arachidonic acid– induced platelet aggregation. An analysis of plasma Cohn fractions demonstrated that most of the plasma inhibitory activity was associated with albumin–rich and α-globulin rich protein fractions. The identity of plasma endogenous inhibitors of platelet aggregation (EIPA) was established by affinity chromatography on Cibacron Blue F3G-A for specific removal of albumin. The association of α-globulins to EIPA activity was recognized as due to haptoglobin by affinity chromatography on a column of hemoglobin-sepharose. In addition, we also found that the distribution of EIPA activity varies according to sex and physiological state. These findings reveal that EIPA may act by modulation of arachidonic acid metabolism or seques-tering the fatty acid substrate.

Microvascular angina (MVA) is a condition characterized by the presence of angina-like chest pain, a positive response to exercise stress tests, and no significant stenosis of coronary arteries in coronary angiography, with absence of any other specific cardiac diseases. The etiology of this syndrome is still not known and it is probably multifactorial. Coronary microvascular dysfunction is proposed as the main pathophysiological mechanism in the development of MVA. Altered somatic and visceral pain perception and autonomic imbalance, in addition to myocardial ischemia, has been observed in subjects with MVA, involving dynamic variations in the vasomotor tone of coronary microcirculation with consequent tran-sient ischemic episodes. Other theories suggest that MVA may be a result of a chronic inflammatory state in the body that can negatively influence the endothelium or a local imbalance of factors regulating its function. This article presents the latest information about the epidemiology, diagnostics, etiopathogen-esis, prognosis, and treatment of patients with MVA.

Anorexia nervosa (AN) is an eating disorder characterized by distinct etiopathogenetic concepts that are gradually being linked together to unravel the dominant pathophysiological pathways underlying the disease. Excessive food restrictions, often accompanied by over-exercise and undertaken to lose weight, lead to the development of numerous complications. The biological concept of neurohormonal dysfunc-tion in AN seems incomplete without demonstrating or excluding the role of the enteric nervous system (ENS). Using an animal model of activity-based anorexia (ABA), we conducted the preliminary assess-ment of the ENS structure. Here we show, in preparations stained by immunohistochemistry with anti- ChAT, anti-NOS, anti-PGP 9.5, anti-c-fos, and anti-TH antibodies, a lower density of cholinergic and nitrergic nerve fibers as well as reduced neuronal activity in myenteric plexus. Such structural and functional damage to the ENS may be responsible for a number of gastrointestinal symptoms that worsen the course of the disease. In addition, we expanded the study to address the unresolved issue of mechanical and thermal pain sensitivity in AN. The Von Frey and hot plate tests revealed, that in ABA animals, the pain threshold for mechanical stimulus decreases while for thermal increases. In this way, we have sig-nificantly supplemented the background of AN with potentially observable nervous system changes which may influence the evolution of the therapeutic approach in the future.