BackgroundRadiological practices are the first anthropic sources of ionizing radiation exposure of the population. However, a review of recent publications underlines inadequate doctors’ knowledge about doses imparted in medical practices and about patient protection that might explain unnecessary radiological prescriptions. We investigated the knowledge of the physicians of Pavia District (Italy) on the risk of radiation exposure.MethodsA cross sectional study was performed involving the Medical Association of Pavia District. Data were collected with a self-administered questionnaire, available on-line with private login and password.ResultsFour hundred nineteen physicians fulfilled the questionnaire; 48% of participants reported training about radiation protection. The average percentage of correct answers on the knowledge on ionizing radiation was 62.29%, with a significantly higher result between radiologist. Around 5 and 13% of the responders do not know that, respectively, ultrasonography and magnetic resonance do not expose patients to ionizing radiations. Only 5% of the physicians properly identified the cancer risk rate associated to abdomen computed tomography.ConclusionsThe findings show a quite good level of the general knowledge about ionizing radiations, higher that reported in literature. Nevertheless, we believe the usefulness of training on the risk linked to radiation exposure in medicine for physicians employed in every area.Electronic supplementary materialThe online version of this article (doi:10.1186/s12913-017-2358-1) contains supplementary material, which is available to authorized users.

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Background: The detection of subclinical/silent atrial fibrillation (SAF) in the general population is of the utmost importance, given its potential adverse consequences. Incident AF has been observed in 30% to 70% of patients with implanted devices, but its prevalence may indeed be lower in the general population. The prospective, multicentric, observational Silent Atrial Fibrillation ANCE Research Initiative (SAFARI) study aimed at assessing the SAF prevalence in a real-world outpatient setting by the means of a small, wearable, prolonged ECG Holter monitoring (>5 days) device (CGM HI 3-Lead ECG; CGM TELEMEDICINE, Piacenza, Italy). Methods: Patients ≥ 55 years of age at risk for AF were screened according to the inclusion criteria to undergo prolonged 3-lead ECG Holter monitoring. SAF episodes were classified as follows: Class A, <30 s; Class B, 30 to 299 s; and Class C, ≥300 s. Results: In total, 119 patients were enrolled (64 men; median age 71 (IQR 55–85) years). At a median of 13.5 (IQR 5–21) days of monitoring, SAF episodes were found in 19 patients (16%). A total of 10,552 arrhythmic episodes were registered, 6901 in Class A (n = 7 patients), 2927 in Class B (n = 3), and 724 in Class C (n = 9), (Class A vs. B and C, p < 0.001). This latter group had multiple (all-class) episodes, and two patients had >1000 episodes. There were no clinical, echocardiographic, or laboratory findings able to discriminate patients with SAF from those in sinus rhythm in univariate and multivariable analyses; of note is that the Class C patients showed a higher diastolic blood pressure, resting heart rate, and indexed LA volume. Conclusions. Over a median of 13 days of Holter monitoring, the SAFARI study confirmed the usefulness of small wearable devices in detecting SAF episodes in real-world outpatients at risk for, but with no prior history of, AF.

Background Gliflozins proved effectiveness in reducing hospitalization and mortality in patients with heart failure and reduced ejection fraction (HFrEF). Recent studies showed how SGLT2-i improve loading condition and afterload by increasing extracellular Na excretion, downregulating RAAS and reducing vascular resistances. This latter aspect seems the result of a combined action on endothelial cells and vascular tone: experimental studies hypnotized that SGLT2-i may inhibit Na-H exchanger on endothelial cells and directly interact with PKG pattern and K+ channels determining vasodilation. On the other hand, 40 to 72% of patients with HFrEF are estimated to have postcapillary pulmonary hypertension. Of note, increased Pulmonary Artery Systolic Pressure (PASP) and Pulmonary vascular resistances (PVR) are associated with a worse outcome among HFrEF patients. However, effect of gliflozins on pulmonary artery pressures have never been investigated. Aim This pilot study aims to assess whether Gliflozins may have positive effects on pulmonary artery by a non-invasive evaluation. Materials and methods We retrospectively analysed transthoracic echocardiograms (TTE) of 24 patients with HFrEF who added gliflozins on top of optimal medical therapy. ETT before and after three months of Dapagliflozin therapy were compared, with particular attention to PASP and right chambers dimension and function. Results At three months, no significant differences in Left Ventricle (LV) dimensions were found (116 ml/mq vs 101.61, p=0.096), while there was an improvement in LV Ejection Fraction (27.9% vs 30,04 p=0.040). E wave velocity and mean E/e’ significantly decreased (respectively 52.9 vs 37,11 p=0.03 and 11.2 vs 8.01 p&lt;0.01). Pulmonary valve Acceleration Time (PV AT) significantly increased from 74.54 (± 22.2) to 101.8 ± 24.74 (p&lt;0.01) while no significative difference in mean PASP (30.48 vs 23.75, p=0.058) and FAC (36.2 vs 38.78, p=0.133) were observed. Left atrial volume indexed (LAVi) was also found to decrease significantly (p&lt;0.01). Discussion Gliflozins positive action on cardiac remodeling, preload and afterload are well known. However, as long as we know, there are no studies investigating Gliflozins effects on pulmonary vascular resistances and pressures. We observed a significative improvement on pulmonary pressures when gliflozins are added on top of OMT. One could speculate that reduction in mean E/e’ and, particularly, in E wave velocity, may be the expression of decrease LA pressure and LA volume due to LV function improvement with decrease in LA overload. In this context, a drop in postcapillary pressures may explain the increase in PV AT, which is an indirect sign of pulmonary pressures. In respect to PASP, which was also reduced, but significantly, PV AT may be more sensitive, explaining the difference in significance of these two results. No significative relation between PV AT increase and E wave velocity, mean E/e’ ratio and LAVi decrease was found, nevertheless a larger population may be required. Further studies, with a larger numerosity, are need to confirm our hypothesis. Conclusion Gliflozins, on top of OMT, appear to improve pulmonary pressures by reducing left atrial pressures after three months of therapy at a non-invasive evaluation.