Impact of COVID-19 on the Cardiac System: Mechanisms and Prognosts by Biomarkers
COVID-19, cardiac system, biomarkers, angiotensin II converting enzyme (ECA2).
n December 2019, a new coronavirus called severe acute respiratory syndrome - coronavirus 2 (Sars-CoV-2), named by the COVID-19 World Health Organization (WHO), appeared in China's Wuhan province. Widespread globally, it was considered a pandemic with approximately 154 million cases and more than 3 million deaths worldwide. Its symptoms include headache, fever, cough and shortness of breath, the latter considered the main symptom. However, studies show a relationship between Sars-CoV-2 and the heart muscle, given that patients with heart problems seem to have a worse prognosis of the disease. The virus uses angiotensin-converting enzyme 2 (ACE2) receptors to invade human cells, such as cardiomyocytes, by disrupting the axis of the renin angiotensin aldosterone system (RAAS) thereby contributing to an increase in angiotensin II levels due to lack of ECA2 counter-mechanism. The response of the organism of these patients to the virus leads to a systemic inflammation in which there is an increase in inflammatory markers such as C-reactive protein (CRP), Interleukin 6 (IL-6) and ferritin. Increased dosages of cardiac biomarkers such as troponin, N-terminal pro-B natriuretic peptide type (NT-proBNP), creatine kinase (CKMB) and myoglobin confer a poor prognosis for the evolution of COVID-19, usually associated with the onset of acute heart failure , myocarditis and arrhythmias. Cardiovascular complications worsen the body's response to the virus, leading to shock, multiple organ failure and death.