1.     Introduction
The COVID-19 infection is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2)1. SARS-CoV2 as well as other coronaviruses have been verified to transit into their host human cells via angiotensin-converting enzyme 2 (ACE2). ACE2 is a type I integral membrane protein with many vital physiologic functions which is highly expressed in alveolar and cardiovascular cells2,3.In the published clinical studies of COVID-19, patients with acute cardiac injury4, shock, and arrhythmia were present in 7.2%, 8.7%, and 16.7% respectively. Thus, cardiac injury has also attracted attention in COVID-19 pneumonia.
Echocardiography is the choice of method in detecting cardiac structure and function. Left ventricular global longitudinal strain (LVGLS) is beneficial for both diagnosis and risk stratification in patients with cardiac diseases5. In the published cases, COVID-19 infected patients showed an enlarged left ventricle, diffuse myocardial dyskinesia with a decreased left ventricular ejection fraction (LVEF), pulmonary hypertension, as well as a reduced pulmonary artery systolic pressure (PASP), tricuspid annular plane systolic excursion (TAPSE) 6and a lower inferior vena cava (IVC) collapse rate. In addition, cardiac tamponade and pericardiocentesis could also happen in these patients7. Besides that, there is lack of the cohort echocardiography study to explore different cardiac performance of different severity of disease by standard and strain echocardiography in patients with COVID-19.
Therefore, this study aimed to observe 1. Different cardiac function of patients in ICU and general ward by standard and strain echocardiography. 2. the cardiac function change in follow-up of severe patients in ICU with COVID-19.
2.     Methods