Decrease in QRS amplitude in juvenile female competitive athletes during the initial twenty-one months of intensive training

Background: The aim of this project was to study changes in QRS amplitude in junior female athletes during the initial twenty-one months of competitive training programme in aerobic gymnastics. Methods: Somatometric parameters, heart rate (HR), blood pressure (BP) and 12-lead ECGs were recorded in 12 female athletes, aged 13-17 years (average 13.8) at 3-month intervals over a period of 21 months. The Sokolow-Lyon index (SLI) and the maximum QRS spatial vector magnitude (QRSmax), approximated from RV5, RaVF and SV2 voltages, were analyzed. Results: The mean values of QRSmax and SLI decreased gradually during the study period. The difference between the mean QRSmax values at the beginning and at the end of the study period was -0.8 mV (30.8%), p < 0.001, and between the initial and final values of SLI was -0.6 mV (24%), p < 0.001. The somatometric parameters changed only slightly, HR and systolic BP values did not change significantly. Conclusions: This study showed that 21 months of competitive aerobic gymnastics training led to a decrease in the QRSmax magnitude. This finding is in contrast with the classical hypothesis on the ECG diagnostics of LVH and is in agreement with an alternative hypothesis on the relative voltage deficit during the early stage of LVH development. (Cardiol J 2007; 14: 260-265

Zmniejszenie amplitudy zespołu QRS u młodych kobiet uprawiających sport podczas początkowego okresu intensywnego treningu fizycznego trwającego 21 miesięcy

Wstęp: Celem niniejszego badania była ocena zmian wartości amplitudy napięcia zespołu QRS u młodych kobiet uprawiających sport podczas 21-miesięcznego okresu intensywnego treningu rywalizacyjnego w zakresie aerobiku gimnastycznego. Metody: Przez okres 21 miesięcy w grupie uprawiających sport 12 młodych kobiet w wieku 13-17 lat (średnio 13,8 roku) w co 3-miesięcznych odstępach analizowano parametry antropometryczne, częstość akcji serca, ciśnienie tętnicze oraz wybrane wskaźniki 12-odprowadzeniowego badania elektrokardiograficznego. Analizie poddano wyliczone wcześniej: wskaźnik Sokołowa- Lyona (SLI) oraz wartość tak zwanego maksymalnego wektora przestrzennego zespołu QRS (QRSmax), ocenionego na podstawie wartości amplitudy załamków: R w odprowadzeniu V5 (RV5), R w odprowadzeniu aVF (RaVF) oraz S w odprowadzeniu V2 (SV2). Wyniki: Średnia wartość QRSmax oraz SLI stopniowo zmniejszyła się podczas trwania okresu treningu. Różnica między średnią wartością QRSmax na początku oraz na końcu badania wynosiła: -0,8 mV (30,8%, p < 0,001), zaś pomiędzy początkową i końcową wartością SLI: -0,6 mV (24%, p < 0,001). Parametry antropometryczne uległy jedynie niewielkiej zmianie, częstość akcji serca oraz skurczowe ciśnienie tętnicze nie zmieniły się w istotny sposób. Wnioski: W badaniu wykazano, że wdrożenie trwającego 21 miesięcy rywalizacyjnego treningu w zakresie aerobiku gimnastycznego spowodowało zmniejszenie wartości maksymalnego wektora przestrzennego zespołu QRS. Wyniki te są odmienne niż klasyczna hipoteza, na której opiera się elektrokardiograficzna diagnostyka przerostu lewej komory oraz zgodne z założeniami hipotezy alternatywnej, mówiącej o relatywnym obniżeniu wartości woltażu podczas wstępnej fazy rozwoju przerostu lewej komory. (Folia Cardiologica Excerpta 2007; 2: 477&#8211;484

Endurance training provokes Arrhythmogenic Right Ventricular Cardiomyopathy phenotype in heterozygous Desmoglein 2 mutants:Alleviation by preload reduction

Desmoglein-2 mutations are detected in 5–10% of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Endurance training accelerates the development of the ARVC phenotype, leading to earlier arrhythmic events. Homozygous Dsg2 mutant mice develop a severe ARVC-like phenotype. The phenotype of heterozygous mutant (Dsg2mt/wt) or haploinsufficient (Dsg20/wt) mice is still not well understood. To assess the effects of age and endurance swim training, we studied cardiac morphology and function in sedentary one-year-old Dsg2mt/wt and Dsg20/wt mice and in young Dsg2mt/wt mice exposed to endurance swim training. Cardiac structure was only occasionally affected in aged Dsg20/wt and Dsg2mt/wt mice manifesting as small fibrotic foci and displacement of Connexin 43. Endurance swim training increased the right ventricular (RV) diameter and decreased RV function in Dsg2mt/wt mice but not in wild types. Dsg2mt/wt hearts showed increased ventricular activation times and pacing-induced ventricular arrhythmia without obvious fibrosis or inflammation. Preload-reducing therapy during training prevented RV enlargement and alleviated the electrophysiological phenotype. Taken together, endurance swim training induced features of ARVC in young adult Dsg2mt/wt mice. Prolonged ventricular activation times in the hearts of trained Dsg2mt/wt mice are therefore a potential mechanism for increased arrhythmia risk. Preload-reducing therapy prevented training-induced ARVC phenotype pointing to beneficial treatment options in human patients

Isoproterenol-induced heart failure in the rat is associated with nitric oxide-dependent functional alterations of cardiac function

The role of nitric oxide (NO) in heart failure (HF) is complex and remains controversial. We tested the hypothesis that the role of NO in isolated atria and cardiomyocytes is altered in isoproterenol-induced HF. Rats received isoproterenol (ISO, 5 mg/kg/day, intraperitoneally) or vehicle for 1 week. Haemodynamic parameters were obtained by left ventricular catheterization. Effects of NOS inhibition on isolated atria and on electrically paced left ventricular myocytes were determined. Additionally, expressions of nitric oxide synthases and their allosteric modulators hsp90, caveolin-1, and caveolin-3 proteins in the left ventricles were measured. ISO increased left ventricular mass by 33% and decreased indices of left ventricular systolic and diastolic function dp/dtmin and dp/dtmax (both P <0.05). Isolated atria from HF rats had a lower spontaneous beating rate (P <0.05). NOS inhibition by L-NAME increased basal frequency and attenuated the positive chronotropic effect of beta-adrenergic stimulation in the HF group (P <0.05). Ventricular myocytes from failing hearts had impaired cell shortening. L-NAME decreased contractility of control, but not failing myocytes. Left ventricular expressions of eNOS, hsp90, iNOS, but not nNOS or caveolins, were increased. Despite the increased capacity for NO synthesis in isoproterenol-induced HF, NO does not sustain contractility of failing myocytes. NO may contribute to the decreased basal heart rate and it may accelerate beta-adrenergic stimulation of chronotrop

In vitro investigating of anticancer activity of new 7-MEOTA-tacrine heterodimers

A combination of biochemical, biophysical and biological techniques was used to study calf thymus DNA interaction with newly synthesized 7-MEOTA-tacrine thiourea 12–17 and urea heterodimers 18–22, and to measure interference with type I and II topoisomerases. Their biological profile was also inspected in vitro on the HL-60 cell line using different flow cytometric techniques (cell cycle distribution, detection of mitochondrial membrane potential dissipation, and analysis of metabolic activity/viability). The compounds exhibited a profound inhibitory effect on topoisomerase activity (e.g. compound 22 inhibited type I topoisomerase at 1 µM concentration). The treatment of HL-60 cells with the studied compounds showed inhibition of cell growth especially with hybrids containing thiourea (14–17) and urea moieties (21 and 22). Moreover, treatment of human dermal fibroblasts with the studied compounds did not indicate significant cytotoxicity. The observed results suggest beneficial selectivity of the heterodimers as potential drugs to target cancer cells

NR1H3 p.Arg415Gln Is Not Associated to Multiple Sclerosis Risk

Aarno Palotie ja Janna Saarela ovat työryhmän Int Multiple Sclerosis Genetics Co jäseniä.A recent study by Wang et al. (2016a) claims that the low-frequency variant NR1H3 p.Arg415Gln is sufficient to cause multiple sclerosis in certain individuals and determines a patient's likelihood of primary progressive disease. We sought to replicate this finding in the International MS Genetics Consortium(IMSGC) patient collection, which is 13-fold larger than the collection of Wang et al. (2016a), but we find no evidence that this variant is associated with either MS or disease subtype. Wang et al. (2016a) also report a common variant association in the region, which we show captures the association the IMSGC reported in 2013. Therefore, we conclude that the reported low-frequency association is a false positive, likely generated by insufficient sample size. The claim of NR1H3 mutations describing a Mendelian form of MS-of which no examples exist-can therefore not be substantiated by data. This Matters Arising paper is in response to Wang et al. (2016a), published in Neuron. See also the related Matters Arising paper by Minikel and MacArthur (2016) and the response by Wang et al. (2016b), published in this issue.Non peer reviewe