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Patients with heart failure with reduced ejection fraction (HFrEF) who received the sodium-glucose co-transport 2 inhibitor, dapagliflozin, in the DAPA-HF (Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure) study have a significant reduction in worsening heart failure (HF) and cardiovascular death. It is uncertain what proportion of patients admitted to a large regional cardiac centre with decompensated heart failure would be eligible for dapagliflozin post-discharge based on their characteristics at discharge.

The DAPA-HF study criteria were retrospectively applied to a cohort of 521 consecutive patients referred to the inpatient HF service in a tertiary cardiac centre in South West Wales between April 2017 and April 2018. Inclusion criteria: left ventricular ejection fraction (LVEF) <40%, New York Heart Association (NYHA) class II–IV symptoms and an elevated N-terminal pro-B-type naturietic peptide (NT-proBNP). Exclusion criteria: systolic blood pressure (SBP) <95 mmHg, estimated glomerular filtration rate (eGFR) <30 ml/min/1.73 m² or type 1 diabetes mellitus. We did not have complete NT-proBNP data for the cohort, as it was not routinely measured at the time in our institute.

There were 478 patients, mean age 78 ± 13 years, 57% male and 91% NYHA class II–IV symptoms, were included in the analysis. Of these, 247 patients had HFrEF, 219 (46%) patients met the inclusion criteria, 231 (48%) were excluded as LVEF was >40%, and 48 (10%) were excluded with NYHA class I symptoms. Of the 219 patients who met the inclusion criteria, 13 (5.9%) had a SBP <95 mmHg, 48 (22%) had eGFR <30 ml/min/1.73 m², leaving 136 (28.5% of total and 55% of those with HFrEF) who met DAPA-HF study criteria.

In our study, 28.5% of all heart failure admissions and 55% of patients with HFrEF would be eligible for dapagliflozin post-discharge according to the DAPA–HF study entry criteria.

Takotsubo cardiomyopathy (TCM) was first described about 30 years ago. It has been attributed to the sudden catecholamine surge in relation to severe stress, which can cause multi-vessel coronary spasms and myocardial apical ballooning. Football supporters are prone to develop severe stress due to sudden changes in match results. This case presents a football supporter of Sheffield United (the Blades) who was admitted to the hospital with cardiac sounding chest pain following a last minute goal by the opposing team. The necessary investigations were carried out including coronary angiogram and echocardiogram. He was diagnosed with TCM following a left ventricular angiogram demonstrating the typical appearance of the octopus pot.

Increased demand for transcatheter aortic valve implantation (TAVI) procedures for patients with severe aortic stenosis has not been matched with a proportional increase in available resources in recent years. This article highlights the importance of developing integrated care pathways for TAVI, which incorporate standardised protocols for permanent pacemaker implantation (PPI) to ensure best practice, increase service efficiency and reduce rates of PPI post-TAVI.

During the recent ‘first wave’ of the COVID-19 pandemic, the National Health Service (NHS) has triaged planned services to create surge capacity. The primary prevention implantable cardioverter-defibrillator (ICD) was in a grey area of triage guidance, but it was suggested as a procedure that could be reasonably stopped. Recent reports have highlighted deaths of patients awaiting ICDs who may have been deferred during the pandemic. In our trust we reorganised our device service and continued to implant primary prevention ICDs during the ‘first wave’ and, here, report that most patients wished to proceed and underwent uncomplicated implantations. One patient later died from COVID-19, although the transmission site cannot be definitively concluded. With strict adherence to public health guidance and infection prevention strategies, we believe that ICD implantation can be performed safely during the pandemic, and this should be standard practice during subsequent surges.

Cardiorenal syndrome has attracted an enormous amount of attention, particularly in the last decade. A lot of research has been conducted in pathophysiology, haemodynamic manifestations, therapeutic options, and clinical outcomes.^1,2 In practice, however, cardiorenal syndrome remains clinically challenging for both cardiologists and nephrologists. Cardiorenal syndrome covers a wide range of structural and functional disorders of both the heart and kidneys. Typically, the acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other. The interaction between the two organs may well be in multiple interfaces, such as haemodynamic cross-talk between the failing heart and the response of the kidneys and vice versa, alterations in neurohormonal markers, as well as inflammatory molecular characteristics.² Much of the credit for the initial description of cardiorenal syndrome is attributed to Robert Bright who, in 1836, described the interdependent relationship between the kidney and the heart based on his observations on significant cardiac structural changes seen in patients with advanced kidney disease.³ The formal definition of cardiorenal syndrome and its classifications were established more recently,^1,2,4 although uncertainty remains still. The classification appears to be attractive and easily applicable in clinical practice, but its value in aiding treatment or prevention strategy has yet to be ascertained.⁴