Pharmacotherapeutic modifications in cardiopulmonary patients during COVID-19 outbreak

ABSTRACT

Severe acute respiratory syndrome coronavirus (SARS-CoV-2), has a well-established host cell entry mechanism by the angiotensin-converting enzyme2 (ACE2 receptor) most commonly found in epithelial cells of blood vessels, respiratory tract including lungs, intestines and kidney. Cardiopulmonary disorders were the most important comorbidities for COVID-19 patients. Recent studies conducted in Wuhan, China (the epicenter of the COVID19 outbreak) showed that an alarming 1,099 patients with polymerase chain reaction (PCR) confirmed COVID19 had serious illnesses such as hypertension, diabetes mellitus both types, diseases coronary heart disease (CAD), kidney and cerebrovascular disease. Chronic inflammation and respiratory tract infections are usually treated with fluoroquinolones and corticosteroids. Fluoroquinolones increase the QT interval and threaten the evolution of arrhythmias and overuse of chloroquine or hydroxychloroquine in COVID-19;expanding the threat of developing arrhythmias;on the other hand, corticosteroids mask the immune response resulting in worsening of the condition. While inhibitors cause respiratory depression, it increases the severity in COVID-19 patients. Based on available pharmacological data, there are no studies showing that calcium channel blocker increases ACE2 expression. Therefore, calcium channel blockers may be a suitable alternative treatment in these patients. Macrolides (azithromycin) may be a better choice than fluoroquinolones, as they are reported to be more effective in reducing secondary infection in COVID-19, paracetamol can be used than ibuprofen and diclofenac in COVID-19 patients. It is suggested that by modifying pharmacotherapy, the severity in cardiopulmonary patients during this COVID-19 outbreak can be reduced.