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We performed a prospective cohort study of 311 outpatients with non-severe COVID-19 (187 women, median age 39 years). Of the 214 (68.8%) who completed the 6-week follow-up questionnaire, 115 (53.7%) had recovered. Others mostly reported dyspnea (n = 86, 40.2%), weight loss (n = 83, 38.8%), sleep disorders (n = 68, 31.8%), and anxiety (n = 56, 26.2%). Of those who developed ageusia and anosmia, these symptoms were still present at week 6 in, respectively, 11/111 (9.9%) and 19/114 (16.7%). Chest CT scan and lung function tests found no explanation in the most disabled patients (n = 23). This study confirms the high prevalence of persistent symptoms after non-severe COVID-19., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The aim of this study is to evaluate the cost-effectiveness of ECG in combination with family and personal history and physical examination in order to detect cardiovascular diseases that might cause sudden death in athletes. The study was conducted on a cohort of 6,634, mainly young professional and recreational athletes, 1,071 from Algeria and 5,563 from Europe (France, Germany and Greece). Each athlete underwent medical history, physical examination, and resting 12-lead ECG. 293 athletes (4.4 %), 149 in Europe (2.7 %) and 144 in Algeria (13.4 %) required further tests, and 56 were diagnosed with cardiovascular disease and thus disqualified. The cost-effectiveness ratio (CER) was calculated as the ratio between the cost of screening and the number of statistical life-years saved by the intervention. The estimated reduced risk of death deriving from treatment or disqualification resulted in the saving of 79.1 statistical life-years in Europe and 136.3 in Algeria. CER of screening was 4,071 purchasing-power-parity-adjusted US dollars ($PPP) in Europe and 582 $PPP in Algeria. The results of this study strongly support the utilisation of 12-lead ECG in the pre-participation screening of young athletes, especially in countries where secondary preventive care is not highly developed.

This study examined the effects of a dual treatment combining insulin treatment and exercise training on basal cardiac function and signaling pathways involving β3-AR, NOS1, and RyR2 in type 1 diabetic rats. Male Wistar rats were assigned into a diabetic group receiving no treatment (D), an insulin-treated diabetic (Ins), a trained diabetic (TD), and a trained insulin-treated diabetic (TIns) group. Control group (C) was included in order to confirm the deleterious effects of diabetes. Insulin treatment and/or treadmill exercise training were conducted for 8 weeks. Basal cardiac function was evaluated by Langendorff technique. Cardiac protein expression of β3-AR, NOS1, and RyR2 was assessed using Western blots. Diabetes induced a decrease of both basal diastolic and systolic (±dP/dt) cardiac function (P < 0.05). Moreover, diabetes was associated with an increase of β3-AR and NOS1 and a decrease of RyR2 expression (P < 0.05). Although combined treatment was not able to normalize -dP/dt, it succeeded to normalize +dP/dt of diabetic rats. Combined treatment led to an overexpression of RyR2. Effects of this combined treatment on +dP/dt and RyR2 were greater than the effects of insulin and exercise training, applied solely. Treatments, applied solely or in combination, resulted in a complete normalization of β3-AR and in a down-regulation of NOS1 because this protein expression in all treated diabetic rats became lower than control values (P < 0.01). Our study shows that unlike single treatments, dual treatment combining insulin treatment and exercise training was able to normalize basal systolic function of diabetic rats by a specific regulation of β3-AR-NOS1-RyR2 signaling pathways.

Physical training induces cardiovascular autonomic nervous system regulation adaptations, which could result from beta adrenergic receptor (AR) modifications. Among them, beta(3 )AR alterations have been recently reported but their functional effect remained to discuss. To explain the beta(3) AR gene expression in relation to function, we simultaneously studied the left ventricle (LV) beta(3) AR mRNA and protein levels and the myocardial functional effects of a beta(3) AR agonist following physical training. Forty rats were assigned to either a control (C; N = 20) or a trained (T; N = 20) group. The treadmill running protocol was performed for 8 weeks. Histological measurements on LV slices were quantified. The beta(3) AR mRNA abundance was studied with RT-PCR and beta(3) AR protein density with Western-Blot analysis. Myocardial functional effects of a beta(3) AR agonist, BRL37344 (10(-8) M), were studied in Langendorff-perfused hearts. Histological data confirmed the adapted patterns of the physiological cardiac hypertrophy observed in T (P < 0.01), with a significant increase in arteries density (P < 0.01) and an unchanged collagen concentration. The beta(3) AR protein density was increased in T (154 +/- 38% in T vs. 100 +/- 24% in C; P < 0.05), but no change was noted concerning the beta(3) AR mRNA level. After BRL37344 perfusion LVDP, +dP/dT and -dP/dT, in C (P < 0.01), and only +dP/dT in T (P < 0.05) were decreased. Moreover, all LV hemodynamic parameters were more altered after BRL37344 in C than in T (P < 0.01).Thus, in this physiological model of cardiac hypertrophy, an increase of beta(3) AR density without beta(3) AR mRNA alteration was observed. Classical negative myocardial lusitropic and inotropic effects induced by a specific agonist of beta(3) AR were diminished in trained rats.

Background and Aims: In the older population, the reliability of heart rate variability (HRV) has only been evaluated in a few studies, in the supine position, and covering a broad sample of age and patients of both sexes. To document the relevance of using HRV analysis in healthy older women, the aim of this study was to evaluate the reliability of HRV indexes during three classical tests., Methods: 33 healthy women (66.9+/-0.7 years old) performed two test sessions. Each session consisted of an ECG recorded in the supine position, first with free breathing (Test 1), then with controlled breathing (Test 2), and in the upright position (Test 3). Time and frequency HRV indexes were obtained by processing the ECG signals. Reliability was assessed between sessions using Student's paired t-test, intraclass correlation coefficient (ICC) and coefficient of variation (CV)., Results: There were no differences between the sessions. ICC showed good reliability for all HRV indexes. CV was low for absolute HRV indexes, except in Test 3 for parasympathetic indexes with modest CV. The CV of HRV ratio indexes were modest to high in all three tests., Conclusions: Time and absolute frequency HRV indexes are reliable when testing healthy older women. Our results support the use of such indexes in gerontology research, to assess the effects of clinical or pharmacological interventions on the autonomic nervous system.

The aim of the present study was to test the hypothesis that a relationship exists between respiratory-induced blood pressure variability (BPV) and transductal shunting in premature infants with respiratory distress. Ten premature infants (27-32 weeks gestation) with respiratory distress ventilated in the synchronised, positive-pressure mode were examined. The interrelations between blood pressure and transthoracic impedance were described using time and frequency domain analysis. Haemodynamic effects of left-to-right transductal shunting were assessed using Doppler echocardiography (ratio of diastolic flow to systolic flow in the subdiaphragmatic aorta). The dependence of blood pressure fluctuations on the respiratory cycle was seen consistently in both time-domain and cross-spectral analysis. The amplitude of these fluctuations varied between infants. In the time domain, the beat-to-beat pressure difference was 0.69-4.1 mmHg for diastolic and 0.99-5.24 mmHg for systolic blood pressure. There was a positive linear relationship between the respiratory-related BPV indicators and the extent of left-to-right transductal shunting ( r=0.86 for diastolic and 0.80 for systolic pressure, P<0.01). Respiratory-related BPV was not correlated to the indicators of left ventricle preload. It is concluded that respiratory related BPV involves both diastolic and systolic blood pressure and is correlated to the magnitude of left-to-right transductal shunting in the population studied.

This paper presents research regarding the monitoring of the brain and the adequacy of anesthesia during surgery. Particular variables are derived from EEG and ECG signals and are correlated to anesthetic gas (sevoflurane) concentration, in pediatric anesthesia. The methods used for parameter extraction are based on change detection theory and time-frequency representation. Preliminary results show that the expired anesthetic gas concentration modulates both the heart rate variability and the duration of the burst suppression. Monitors of the central nervous system and autonomic nervous system activities can be expected to be based on these variables.

Changes in myocardial loading conditions influence the ventricular action potential via mechanoelectric feedback, a mechanism impaired in pathology. In vivo the QT interval of the electrocardiogram which reflects the action potential duration allows appropriate determination of its modifications. The effects of changes in cardiac loading conditions (load reduction with trinitrin; volume loading with Plasmion) on regional function and ventricular local electrogram were investigated in conscious dogs before (control) and after 4 weeks of rapid pacing (dilated cardiomyopathy, DCM). In controls both interventions increased heart rate. Trinitrin increased end-diastolic wall thickness (EDWth, P<0.001) and reduced absolute QT interval duration (P<0.05). Plasmion decreased EDWth (P<0.001) and increased left ventricular end diastolic pressure (LVEDP, P<0.001) without QT interval alteration. However, the corrected QT interval was unchanged in both interventions. In DCM, trinitrin did not change the QT interval. Plasmion increased LVEDP (P<0.01) and prolonged QT and corrected QT intervals (P<0.01) despite the tachycardia. In controls the changes in cardiac loading conditions did not modify the QT interval, suggesting intact endogenous regulation of repolarization. The impaired adaptation observed in DCM contributed to an increase in QT interval following volume loading. In this model, a prolonged repolarization after abrupt volume loading may result from enhanced or disclosed mechanoelectric feedback.

Kinetics of phosphoryl transfers from PCr to gamma-ATP and from beta-ATP to beta-ADP were measured by magnetization transfer in an in vivo 31P NMR experiment in working rat skeletal hind leg muscles. Two groups were examined. One group was submitted to a 6-week training program of treadmill running. The other group was composed of sedentary animals. Metabolic oxidative capacity and mechanical performance were improved greatly by training as shown previously. Phosphoryl transfer of PCr-->gamma-ATP or beta-ATP-->beta-ADP total fluxes were identical in resting trained and untrained muscles. Under stimulation, the flux of creatine kinase transfer was significantly inhibited by 23% compared with resting level in untrained muscles; by contrast, it was not inhibited and maintained at the high resting level in trained muscles. Thus physiological changes probably linked to a decrease of the production of anions, which could inhibit creatine kinase, were able to maintain creatine kinase flux. The flux of beta-ATP to beta-ADP transfer were enhanced largely in working muscles from 1.4+/-0.8 and 2+/-0.8 at rest to 4+/-1.6 and 6.6+/-2.7 mM s(-1) for untrained and trained muscles respectively; the effect was more pronounced in trained than in untrained muscles. These results showed an acceleration of phosphoryl turnover in working muscles after training, which could contribute to improve oxidative and mechanical performances. Such kinetic measurements of phosphoryl conversion may provide information on ATP turnover in pathophysiologic situations where ADP accumulates because of impaired ATP synthesis (mitochondrial myopathies, lower perfusion level).