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the World Health Organization declared coronavirus disease 2019 (COVID-19) a pandemic. The presence of underlying cardiovascular disease (CVD) confers the highest mortality with COVID-19. Thus, patients with CVD must be considered a particularly at-risk population. [1][2][3][4][5] Community transmission, patient-to-patient transmission and health care worker infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are overwhelming health services worldwide. [4][5][6] High quality cardiac care must minimise risk of viral transmission to patients and health care workers. It should adapt resources in the context of reduced access to hospital beds and personal protective equipment (PPE). This consensus statement reviews and summarises data on SARS-CoV-2 infection in pre-existing CVD and acute cardiovascular manifestations of COVID-19, and makes recommendations for cardiac service provision during the pandemic. Development process for the recommendationsA group of CVD experts, drawn from the Cardiac Society of Australia and New Zealand (CSANZ), the Australian and New Zealand Society of Cardiac and Thoracic Surgeons, the National Heart Foundation of Australia and the High Blood Pressure Research Council of Australia, convened in March 2020. Key opinion leaders in cardiology, cardiothoracic surgery and public health with broad geographic representation were consulted. We searched major databases (EMBASE, MEDLINE and PubMed) to identify relevant systematic reviews, randomised controlled trials and clinical case series in English from January 2020 to 25 March 2020. As the majority of studies relating to COVID-19 and CVD at the time of writing were observational in nature, results must be interpreted with caution. Given data limitations, consensus documents produced by international cardiology societies from December 2019 to March 2020 were reviewed. [7][8][9] Experts from key areas (electrophysiology and pacing, interventional cardiology, imaging, cardiothoracic surgery, nursing, hypertension, prevention and rural) generated key recommendations from their respective councils and groups. In addition, social networking platforms (eg, WhatsApp) involving CSANZ board members, cardiology heads of department and key opinion leaders were used to identify relevant resources, guidance documents and protocols. An online living document was shared to facilitate wide input. The full draft underwent peer review by the listed authors as well as external experts in each subspecialty field of cardiology before agreement and acceptance of the final document. Pre-existing cardiovascular disease and COVID-19Patients with COVID-19 and pre-existing CVD are at increased risk of severe disease and death. [1][2][3][4][5] A meta-analysis of eight studies and over 46 000 patients in China reported that hypertension, diabetes and CVD were the most common comorbidities. 5 Baseline CVD conferred the highest odds of any comorbidity for developing severe versus mild COVID-19 (odds ratio [OR], 3.42; 95% CI, 1.88-6.22). Hypertension ...

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Debate continues in the medical literature on the role of the renin angiotensin system (RAS) in Coronavirus disease 2019 (COVID-19) pathophysiology and the implications for the use of cardiovascular drugs acting on the RAS. Could these drugswhich include angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptors blockers (ARBs)be harmful or potential key therapeutic agents in COVID-19? And, could potentially helpful measures be available and in plain view on the pharmacy shelf? KeywordsCOVID 19 Renin angiotensin system Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Neprilysin Vitamin D

The Challenges Rural and remote Australians and New Zealanders have a higher rate of adverse outcomes due to acute myocardial infarction, driven by many factors. The prevalence of cardiovascular disease (CVD) is also higher in regional and remote populations, and people with known CVD have increased morbidity and mortality from coronavirus disease 2019 (COVID-19). In addition, COVID-19 is associated with serious cardiac manifestations, potentially placing additional demand on limited regional services at a time of diminished visiting metropolitan support with restricted travel. Inter-hospital transfer is currently challenging as receiving centres enact pandemic protocols, creating potential delays, and cardiovascular resources are diverted to increasing intensive care unit (ICU) and emergency department (ED) capacity. Regional and rural centres have limited staff resources, placing cardiac services at risk in the event of staff infection or quarantine during the pandemic.

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Objective: To determine whether the process of reverse left ventricular remodelling in response to carvedilol is dependent on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR) in response to carvedilol. Design: Retrospective analysis of serial echocardiograms in 257 patients with chronic systolic heart failure at baseline and at 12-18 months after starting carvedilol. Reverse left ventricular remodelling was determined by changes in left ventricular end diastolic dimension (LVEDD), end systolic dimension (LVESD), and fractional shortening (LVFS). Setting: Heart failure clinic within a university teaching hospital. Main outcome measures: Changes in LVEDD, LVESD, and LVFS. Results: LVEDD and LVESD decreased by 2.6 (0.4) mm and 4.9 (0.5) mm, respectively (mean (SEM)), and LVFS increased by 4.3 (0.5)% (all p < 0.0001 v baseline). Simple regression revealed no significant relation between BHR or HRR and the changes in LVEDD, LVESD, or LVFS. Stratification of patients into high and low BHR groups (above and below the mean) or according to the baseline heart rhythm (sinus rhythm v atrial fibrillation) showed no differences between groups in the extent of reverse left ventricular remodelling. Improvements in left ventricular function and dimensions were associated with significant improvements in New York Heart Association functional class. Conclusions: The benefits of carvedilol in terms of reverse left ventricular remodelling and symptomatic improvement in patients with chronic heart failure are independent of BHR, heart rhythm, and the HRR that occurs in response to carvedilol.