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Background In April 2020, formal face-face cardiology training was put on pause due to COVID-19. We adapted by utilising a video-conferencing platform to continue some form of Cardiology education on a national scale, and maintain morale. This programme, known as CardioWebinar, has continued ever since. We looked to study the effectiveness of delivering virtual Cardiology education 1 year into the COVID pandemic. Methods Expert speakers throughout the UK were sought after via social media and ‘word of mouth.’ Weekly webinars were organised and advertised (Canva posters) on social media (Twitter), as well as via the British Cardiovascular Society and British Junior Cardiologists’ Association (BJCA) media links. Each webinar was scheduled mid-week at 17:30 (UK). Interested attendees registered for free using an online ticketing platform (Eventbrite). Webinars were delivered using an online video conferencing platform (Zoom) which required a £14.99 monthly subscription. Each webinar consisted of a 40-minute presentation followed by Q&A (20mins). All webinars were recorded and later accessible for free on the BJCA TV Gallery. A Learning Management System (LMS) was used to collect feedback after each session and generate certificates of attendance for attendee appraisal. We systematically reviewed the LMS feedback of live attendees from 6 consecutive webinars delivered between Jan-Feb 2021. We further surveyed our most recent (March 2021) attendees (145 participants) via an extended questionnaire through the LMS exploring their experiences of our virtual education. Results 55 CardioWebinars have been delivered since April 2020. The speakers have been predominantly Consultant Cardiologists from the UK. Some of the recordings have had >1000 views. Other than the video platform subscription, no cost was incurred in the delivery of this entire programme.We collected feedback from 392 respondents (~65 live attendees per webinar) from each session between Jan-Feb 2021. The sessions were rated as ‘very good-excellent’ by 97%. We collected a further 145 responses from March 2021 attendees to an extended questionnaire. 90% rated the whole series as ‘very good –excellent’ in supporting their cardiology education during the Covid pandemic, and 84% felt the programme sufficiently covered even the more challenging areas of the Cardiology curriculum (e.g aortopathies). 90% of the respondents felt that their work-life schedule allowed them to join the live webinars at this time. The respondents where predominantly from the UK (91%), though included an international audience (9%). Whilst 74% of attendees were cardiology trainees, the remaining 26% included physiologists, nursing staff, consultants and other junior doctors. 99% felt that virtual education should continue to play a formal part in their training after the COVID pandemic. Conclusion Webinars allow everyone interested in cardiac care across the world the opportunity to hear experts teach, and without a travel cost. They are cheap and easy to organise. Whilst the ‘social’ aspect of training is limited, this study suggests that webinars will remain an integral part of the post-Covid era. Conflict of Interest Nil

Formal face-to-face cardiology teaching was halted due to the COVID-19 pandemic, and innovation in digital education was required to fill the training gap. We created ‘CardioWebinar’ to deliver free, accessible, high-quality teaching to help maintain trainee morale and fill this gap. We hoped that by maintaining and improving knowledge we would indirectly improve patient care. This programme consisted of weekly live consultant-delivered webinars covering the breadth of cardiology, all recorded and available online for viewer convenience. In this article, we explore the advantages and challenges of webinars in cardiology, using CardioWebinar as a case study. One advantage of webinars is the ease of delivery. Webinars need minimal administrative support and can be advertised on social media and through mailing lists. The event itself has no hotel fees, venue hire, catering or travel costs. Teaching can be organised relatively swiftly and at minimal cost. This simplicity has allowed CardioWebinar to deliver over 60 webinars in 15 months, watched by >15 000 people. Webinars …

Introduction Sodium-glucose cotransporter 2 (SGLT2) inhibitors are known to reduce the risk of cardiovascular events in patients with type 2 diabetes (T2DM). The recent ground-breaking DAPA-HF trial has shown similar results in patients with heart failure with reduced ejection fraction (HFrEF) regardless of whether they have T2DM. Guidelines on their use in HFrEF patients are widely anticipated. Our study aims to identify the proportion of cardiology patients who may benefit from SGLT2 inhibitors in a central London teaching hospital. Methods We retrospectively analysed two patient cohorts from August 2019 to January 2020: 1) Inpatient (IP) Cardiology referrals (452 patients), and 2) Inpatient Heart Failure Service referrals (68 patients). Using four large-scale cardiovascular outcome trials - EMPA-REG, CANVAS, DECLARE-TIMI 58 and DAPA-HF; we generated a set of screening criteria for the suitability of SGLT2 inhibitors in patients with T2DM and HFrEF, and applied them to our cohorts (Table 1). Results Over the 6 month period, 452 patients were referred for an IP Cardiology review; 191 (42%) of these patients had T2DM or HFrEF. Using our criteria, 101 (53%) of these 191 patients would be suitable, representing 22% of all Cardiology referrals. Only 5 patients were already on SGLT2 inhibitors. Looking at this more closely, 44% (48/110) of T2DM only patients were suitable for an SGLT2 inhibitor compared to 65% (53/81) of the HFrEF population. In the second patient cohort (IP Heart Failure referrals), half (34/68) of patients were suitable for SGLT2 inhibitors. The trend was broadly similar to the Cardiology referrals cohort, with 37% (7/19) of patients with T2DM only and 71% (27/38) of patients with HFrEF found to be suitable (Figure 1). Of all HFrEF patients who would be suitable for SGLT2 inhibitors, 81% (48/59) were on an angiotensin-converting-enzyme inhibitor, angiotensin-receptor blocker or sacubitril-valsartan; 92% (54/59) were on a beta-blocker; 25% (15/59) were on a mineralocorticoid receptor antagonist and 59% (35/59) were on a diuretic on admission. The main exclusion criteria in our patient cohorts was an estimated glomerular filtration (eGFR) rate below 30 mL/min/1.73m2 of body-surface area. Conclusions Ahead of expected release of guidelines on SGLT2 inhibitor use in patients with HFrEF, we have formulated a set of screening criteria for suitability of SGLT2 inhibitors and applied them to our patient cohorts. The results show that 50% of patients referred to the IP Heart Failure Service and over 20% of patients referred to IP Cardiology may be suitable for SGLT2 inhibitors, which are much higher potential use rates than we had anticipated. This has important ramifications for cardiology services across the country when thinking about who will initiate this new heart failure therapy and in which setting. Conflict of Interest None

Introduction The use of handheld echocardiography (hTTE) is increasing, due to its diagnostic value in a number of clinical scenarios coupled with its availability, portability and relatively low cost1. The well-documented limitations of hTTE compared to standard TTE (sTTE) include operator experience in both image acquisition and interpretation2. Our first aim was to quantify the discrepancy when assessing left-sided cardiac pathology. Secondly, we aimed to identify whether this was amenable to improvement following educational intervention. Methods We retrospectively identified 119 patients who underwent both hTTE and sTTE. Cardiology specialist trainees (STs) performed hTTE and this was compared to sTTE performed by blinded BSE accredited sonographers (gold standard). The parameters assessed and the grading system used is detailed below (table 1). Concordance between hTTE and sTTE was evaluated, both pre- and post-education, by the weighted Kappa statistic. Educational intervention included information given to all cardiology trainees highlighting both the overall cohort performance and confidential individualised feedback. Following this a further 29 patients who underwent both hTTE and sTTE were identified. Results The average error for all parameters was 0.34 with fair agreement (k = 0.38). Figure 1 and Table 2 highlight the average error for each parameter. Where discrepancy existed, hTTE tended to underestimate severity of each parameter, with the exception of LVSF which was equivocal. The greatest discrepancy was seen when grading MR, and of 80 discordant scans, 57 were due to an underestimation (figure 2). The majority of error was in severe MR. As predicted, performance improved through years of training; ST3s consistently had the highest error compared to other grades, particularly when assessing MR. This improved significantly after education (0.66 to 0.33). Preliminary analysis post-education has shown an increase in overall agreement and a reduction in error when grading valvular pathology, but an increase in error when grading LVSD. Conclusion Our results are concordant with previous studies demonstrating that diagnostic accuracy of hTTE is heavily influenced by operator experience. It is less known how much training should be given to operators before hTTE assessment is reliable enough to base clinical decisions upon. However with simple education, we hope to demonstrate that discrepancy between hTTE and sTTE can be reduced. Moving forwards, we plan to introduce a dedicated training day for new ST3 cardiology trainees and observe how this influences performance. The discrepancy and underestimation with hTTE raises the question of clinical implications, particularly of underestimating MR. It may be the case that cardiology trainees should be more prudent when commenting on MR, spend slightly longer obtaining images if MR is present and liaise more closely with medical colleagues informing them about the limitations of HHE. Conflict of Interest None

Objectives This study sought to identify the effect of coronary autoregulation on myocardial perfusion during intra-aortic balloon pump (IABP) therapy. Background IABP is the most commonly used circulatory support device, although its efficacy in certain scenarios has been questioned. The impact of alterations in microvascular function on IABP efficacy has not previously been evaluated in humans. Methods Thirteen patients with ischemic cardiomyopathy (left ventricular ejection fraction: 34 ± 8%) undergoing percutaneous coronary intervention were recruited. Simultaneous intracoronary pressure and Doppler-flow measurements were undertaken in the target vessel following percutaneous coronary intervention, during unassisted and IABP-assisted conditions. Coronary autoregulation was modulated by the use of intracoronary adenosine, inducing maximal hyperemia. Wave intensity analysis characterized the coronary wave energies associated with balloon counterpulsation. Results Two unique diastolic coronary waves were temporally associated with IABP device use; a forward compression wave and a forward expansion wave caused by inflation and deflation, respectively. During basal conditions, IABP therapy increased distal coronary pressure (82.4 ± 16.1 vs. 88.7 ± 17.8 mm Hg, p = 0.03), as well as microvascular resistance (2.32 ± 0.52 vs. 3.27 ± 0.41 mm Hg cm s–1, p = 0.001), with no change in average peak velocity (30.6 ± 12.0 vs. 26.6 ± 11.3 cm s–1, p = 0.59). When autoregulation was disabled, counterpulsation caused an increase in average peak velocity (39.4 ± 10.5 vs. 44.7 ± 17.5 cm s–1, p = 0.002) that was linearly related with IABP–forward compression wave energy (R2 = 0.71, p = 0.001). Conclusions Autoregulation ameliorates the effect of IABP on coronary flow. However, during hyperemia, IABP augments myocardial perfusion, principally due to a diastolic forward compression wave caused by balloon inflation, suggesting IABP would be of greatest benefit when microcirculatory reserve is exhausted.

Left ventricular (LV) dysfunction is often seen in acute coronary syndromes (ACS) and high–risk percutaneous coronary intervention (PCI). Wave intensity analysis (WIA) quantifies energy flux within the circulation. We used WIA to examine the hemodynamic perturbations following ACS and PCI with

Somatostatin-14 (SST) inhibits insulin and glucagon secretion by activating G protein-coupled somatostatin receptors (SSTRs), of which five isoforms exist (SSTR1–5). In mice, the effects on pancreatic β-cells are mediated by SSTR5, whereas α-cells express SSTR2. In both cell types, SSTR activation results in membrane hyperpolarization and suppression of exocytosis. Here, we examined the mechanisms by which SST inhibits secretion from human β- and α-cells and the SSTR isoforms mediating these effects. Quantitative PCR revealed high expression of SSTR2, with lower levels of SSTR1, SSTR3, and SSTR5, in human islets. Immunohistochemistry showed expression of SSTR2 in both β- and α-cells. SST application hyperpolarized human β-cells and inhibited action potential firing. The membrane hyperpolarization was unaffected by tolbutamide but antagonized by tertiapin-Q, a blocker of G protein-gated inwardly rectifying K+ channels (GIRK). The effect of SST was mimicked by an SSTR2-selective agonist, whereas a SSTR5 agonist was marginally effective. SST strongly (>70%) reduced depolarization-evoked exocytosis in both β- and α-cells. A slightly weaker inhibition was observed in both cell types after SSTR2 activation. SSTR3- and SSTR1-selective agonists moderately reduced the exocytotic responses in β- and α-cells, respectively, whereas SSTR4- and SSTR5-specific agonists were ineffective. SST also reduced voltage-gated P/Q-type Ca2+ currents in β-cells, but normalization of Ca2+ influx to control levels by prolonged depolarizations only partially restored exocytosis. We conclude that SST inhibits secretion from both human β- and α-cells by activating GIRK and suppressing electrical activity, reducing P/Q-type Ca2+ currents, and directly inhibiting exocytosis. These effects are mediated predominantly by SSTR2 in both cell types.