COVID-19 - Does This Disease Kill Due to Imbalance of the Renin Angiotensin System (RAS) Caused by Genetic and Gender Differences in the Response to Viral ACE 2 Attack?

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 drugs - which 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?

Rural and Remote Cardiology During the COVID-19 Pandemic: Cardiac Society of Australia and New Zealand (CSANZ) Consensus Statement.

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. MAIN RECOMMENDATIONS: Health districts, cardiologists and government agencies need to minimise impacts on the already vulnerable cardiovascular health of regional and remote Australians and New Zealanders throughout the COVID-19 pandemic. Changes in management should include.

Tolerability of carvedilol in patients with heart failure and concomitant chronic obstructive pulmonary disease or asthma.

BACKGROUND: A substantial proportion of the population with congestive heart failure (CHF) has concomitant airway disease. Little information exists on the tolerability of carvedilol in patients with chronic obstructive pulmonary disease (COPD). In this study, we assessed the tolerability and efficacy of carvedilol in patients with CHF and concomitant COPD or asthma. METHODS: Between 1996 and 2000, a total of 487 patients began receiving open-label carvedilol. Forty-three (9%) had COPD (n = 31) or asthma (n = 12). Spirometry supported clinical diagnosis in all, and full pulmonary function testing supported diagnosis in 71%. Sixty percent began carvedilol therapy in the hospital and underwent measurement of peak expiratory flow rates (PEFR) before and after dosing. RESULTS: In patients with COPD, mean forced expiratory volume in one second (FEV(1)) was 62% +/- 13% predicted, reversibility was 4% +/- 4% with bronchodilators, and FEV(1)/FVC was 62% +/- 8%. Mean PEFR was 325 +/- 115 liter/min before the dose and increased by 17% 2 hours after the carvedilol dose (p = 0.04). In patients with asthma, mean FEV(1) was 80% +/- 17% predicted, reversibility was 13% +/- 7%, and FEV(1)/FVC was 74% +/- 11%. Mean PEFR was 407 +/- 161 liter/min before the dose with no significant change 2 hours after the dose. Carvedilol was introduced safely in 84% of patients with COPD, with only 1 patient withdrawn from therapy for wheezing. In contrast, only 50% of patients with asthma tolerated carvedilol. Survival at 2.5 years was 72%. In survivors, left ventricular end-diastolic diameter decreased from 76 +/- 11 mm to 72 +/- 14 mm (p = 0.01), left ventricular end-systolic diameter decreased from 65 +/- 13 mm to 60 +/- 15 mm (p = 0.01), and fractional shortening increased from 14% +/- 7% to 17% +/- 7% (p = 0.05) at 12 months. CONCLUSIONS: Patients with CHF and COPD tolerated carvedilol well with no significant reversible airflow limitation, but patients with CHF and asthma tolerated carvedilol poorly. The effect of carvedilol on left ventricular dimensions and function in patients with concomitant airway diseases was similar to that seen in our general group of patients. Asthma remains a contraindication to beta-blockade.