BackgroundA small minority of people with coronavirus disease 2019 (COVID-19) develop a severe illness, characterised by inflammation, microvascular damage and coagulopathy, potentially leading to myocardial injury, venous thromboembolism (VTE) and arterial occlusive events. People with risk factors for or pre-existing cardiovascular disease may be at greater risk. ObjectivesTo assess the prevalence of pre-existing cardiovascular comorbidities associated with suspected or confirmed cases of COVID-19 in a variety of settings, including the community, care homes and hospitals. We also assessed the nature and rate of subsequent cardiovascular complications and clinical events in people with suspected or confirmed COVID-19. Search methodsWe conducted an electronic search from December 2019 to 24 July 2020 in the following databases: the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, covid-19.cochrane.org, ClinicalTrials.gov and EU Clinical Trial Register. Selection criteriaWe included prospective and retrospective cohort studies, controlled before-and-a er, case-control and cross-sectional studies, and randomised controlled trials (RCTs). We analysed controlled trials as cohorts, disregarding treatment allocation. We only included peerreviewed studies with 100 or more participants, and excluded articles not written in English or only published in pre-print servers.COVID-19 and its cardiovascular e ects: a systematic review of prevalence studies (Review)

Aims Healthcare services worldwide have been significantly impacted by the COVID-19 pandemic. Recent reports have shown a decline in hospitalization for emergency cardiac conditions. The impact of the COVID-19 pandemic on hospitalization and particularly mortality due to acute heart failure has not been thoroughly described. Methods and results In this single-centre observational study, we examined referrals to the acute heart failure team over a period of 16 weeks (7 January to 27 April 2020) spanning the ongoing COVID-19 pandemic; 283 patients referred to our acute heart failure services over the study period were included on the basis of typical symptoms, raised BNP, and echocardiogram. There was a substantial but statistically non-significant drop in referrals with 164 referred in the 8 weeks before the first UK death due to COVID-19 on 2 March 2020 (BC), compared with 119 referred after (AC) in the subsequent 8 weeks, representing a 27% reduction overall (P = 0.06). The 30 day case fatality rate was increased from 11% in the BC group compared with 21% in the AC group (risk ratio = 1.9, 95% confidence interval 1.09-3.3). Age, gender, length of stay, left ventricular ejection fraction, and N-terminal pro-brain natriuretic peptide were similar between the groups. Admission creatinine, age, and AC cohort status were found to be univariable predictors of mortality. On multivariate Cox regression analysis, only age (hazard ratio 1.04, P = 0.03) and AC cohort status (hazard ratio 2.1, P = 0.017) remained significant predictors of mortality. On sensitivity analysis, this increased mortality was driven by COVID-19 positive status. Conclusions There was a reduction in referral of patients with acute heart failure with significant increase in mortality in the 8 weeks following the first reported UK death due to COVID-19. The observation of increased mortality does not appear related to a change in population in terms of demographics, left ventricular ejection fraction, or N-terminal pro-brain natriuretic peptide. The observed increased mortality appears to be related to the coexistence of COVID19 infection with acute heart failure. The study highlights the need for widespread preventative and shielding measures particularly in this group of patients especially in the light of the second wave. Longer follow-up with inclusion of data from other centres and community heart failure services will be needed.

Clinically relevant abnormalities were found in 11.5% of patients with pLUTS, rUTI, or pain, supporting recently published NICE guidelines recommending cystoscopy in patients with pLUTS or rUTI. Of the 17 patients who were investigated for pain, none was found to have clinically relevant abnormalities; further studies are needed to define the clinical utility of FC in these cases.

Background  The Gerbode defect is a rare abnormal communication between the left ventricle (LV) and right atrium (RA). The lesion is either congenital or acquired. Acquired defects are largely iatrogenic or infective in origin. We present two cases of acquired Gerbode defects with similar clinical presentations but very different outcomes. Case summaries Patient 1 A 64-year-old male presented with features of decompensated cardiac failure and a low-grade temperature. Dehiscence of a recently implanted bioprosthetic aortic valve and high-velocity LV to RA jet (Gerbode defect) was found on echocardiography. Blood cultures grew Staphylococcus warneri and the diagnosis of infective endocarditis was established. The patient was treated with intravenous antibiotics and the aortic valve and Gerbode defect were successfully surgically repaired. Patient 2 An 81-year-old male presented after being found on the floor at home. On admission, he was clinically septic with evidence of decompensated heart failure. No clear infective focus was initially found. Transthoracic echocardiography revealed severe left ventricular impairment, with a normal bioprosthetic aortic valve. He was treated with intravenous antibiotics, but later deteriorated with evidence of embolic phenomena. Repeat echocardiography revealed a complex infective aortic root lesion with bioprosthetic valve dehiscence and flow demonstrated from the LV to RA. Unfortunately, the patient succumbed to the infection and cardiac complications. Discussion  The Gerbode defect is a rare but important complication of infective endocarditis and valve surgery. Care needs to be taken to assess for Gerbode defect shunts on echocardiogram, especially in the context of previous cardiac surgery.

Objectives: The purpose of this audit was to ascertain whether troponin tests are requested appropriately for acute admissions via A&E and EAU at the John Radcliffe Hospital, Oxford. Troponin tests are not 100% specific, and commencing the ACS protocol is not without risks. Inappropriate tests could result in minimally positive levels, and starting antiplatelets in these situations could lead to unnecessary complications.Methods: Data was collected on two 24-hour periods for all admissions to A&E and EAU (Emergency Assessment Unit). Admissions were monitored on the electronic whiteboard and follow-up was through a combination of reading notes and using 'Case Notes'. The primary outcome was whether troponin tests were requested appropriately. Criteria for appropriateness of requests were decided after meeting with cardiologists. The secondary outcome was whether the troponin tests were requested within an appropriate time frame, i.e. at admission and at 12 hours.Results: A total of 55 patients had troponin tests. Mean age was 72.3 years. Nine requests came via EAU and the majority through A&E. Of these 55 patients, 40% had a troponin requested inappropriately, the majority of which were requested by the nursing staff. Mean time for the first troponin test was 63.5 minutes. Repeat troponins were requested at a range (5 hours to 13 hours). Three patients were actually started on ACS protocol inappropriately. The cost of inappropriate tests totaled £320. Conclusion:Although there were no adverse events in the patients that were sampled during this audit, the ACS protocol was started inappropriately in three patients. Cutting down inappropriate troponin tests in the acute setting could, by extrapolation, amount to savings of £58,400 per annum. We presented this audit at several local and regional meetings, and came up with recommendations to put in place within our hospital. Our intervention in the form of checklists, posters and widespread teaching, improved results considerably, with only 5% inappropriate tests requested in the second audit cycle.

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We present the case of a 23-year-old student admitted with fever, night sweats and splenomegaly. These non-specific signs and symptoms posed a diagnostic challenge which was further complicated by a history of recent foreign travel. The range of potential diagnoses required a variety of investigations in order to reach the final diagnosis. The incidental finding of an incompetent bicuspid aortic valve and an inflamed gallbladder further clouded the diagnostic process. Despite treatment with broad spectrum antibiotics, the patient continued to deteriorate. Serological testing finally provided a diagnosis of visceral leishmaniasis. The patient subsequently developed haemophagocytic lymphohistiocytosis, a life-threatening immune hyperactivity state that very rarely complicates leishmaniasis infection. With the use of amphotericin B and high-dose steroids, the patient made an excellent recovery.

Aims. Previous studies have suggested that intravenous administration of adenosine improves myocardial reperfusion and reduces infarct size in ST-elevation myocardial infarction (STEMI) patients. Intracoronary administration of adenosine has shown conflicting results. Methods. In this retrospective, single-centre, blinded clinical study, we assessed whether selective intracoronary administration of adenosine distal to the occlusion site immediately before initial balloon inflation reduces microvascular obstruction (MVO) as assessed with cardiac magnetic resonance imaging (MRI). Using contrast-enhanced sequences, microvascular obstruction (MVO) was calculated. We found 81 patients presenting with STEMI within 12 h from symptom onset who were eligible for the study. In 80/81 (100%) patients receiving the study drug, MRI was performed on Day 1 after primary angioplasty. Results. The prevalence of MVO was reduced in the patients treated with intracoronary adenosine, (45%) compared to 85% of patients who were administered intravenous adenosine (P = 0.0043). We found that the size of MVO in patients receiving intracoronary adenosine was significantly reduced compared to 0.91 g in the intravenous-treated group (P = 0.027). There was no statistically significant difference in TIMI flow and clinical outcomes after primary PCI. Conclusion. We found significant evidence that selective high-dose intracoronary administration of adenosine distal to the occlusion site of the culprit lesion in STEMI patients results in a decrease in microvascular obstruction.