Echocardiographic evaluation in patients with myocardial injury during COVID-19 infection

During COVID-19 infection, cardiovascular system is affected by direct viral invasion, activation of immune system characterised by release of interferon ϒ, macrophage activation, endothelial activation with expression of cell adhesion molecules and increased vascular permeability.
Elevated cardiac troponin level could be found in significant proportion of patients presenting with COVID-19. In presented work, more than a half of the patients with elevated troponin had myocardial injury that could be visualised with TEE.
Having in mind high infectious potential and easy transmission of the virus it is of paramount significance to make proper indication for further diagnostics such as TTE, and balance protection of the health care providers and benefit for the patients. Appropriate diagnostics should be directed towards specific therapy, including early application of steroids, iv. immunoglobulins, antivirals, implementation of invasive procedures and active mechanical life support.
Patients undergoing echocardiography need to be clearly defined by clinical indications - cardiac biomarkers, troponin concentration and BNP level may improve selection of the patients. In patients with symptoms of heart failure and elevated BNP, NT pro BNP and troponin, bedside TTE is very useful in accessing haemodynamic, LV function, acute valvular disease, and lung echocardiography could reveal the presence of lung B lines.
Troponin elevation could be present in various pathologic states other than acute coronary syndrome, and myocarditis is the real threat. Some signs such as: myocardial thickening, tissue oedema caused by permeability disorder and shift of the fluids and proteins from intravascular to extravascular compartment, LV and/or RV dysfunction, pericardial effusion can be seen on echocardiography, which is the first line, bedside available technique in every hospital. Magnetic resonance imaging is a superior method for diagnosing myocarditis, but not accessible in most cases in index hospitalization.
During COVID-19 infection, inflamed and dysfunctional endothelium becomes proadhesive and prothrombotic. Acute coronary syndrome in COVID-19 is facilitated by systemic inflammation and may present as STEMI, NSTEMI, MINOCA, myocardial infarction type 2, or even as stress cardiomyopathy.
Sequence of events could lead to plaque destabilisation in epicardial artery and its rupture, but inflammation per se could also provoke endothelial vasoconstriction and thrombosis, thus creating many forms of acute coronary syndrome.
Pneumonia, systemic infection, fever, tachycardia, hypoxia cause myocardial supply-demand imbalance with elevation of biomarkers, leading to myocardial infarction type 2. Cytokine storm can cause severe microvascular dysfunction contributing to myocardial infarction with non- obstructive coronary arteries.
In present paper, total occlusion of epicardial coronary artery, requiring PCI was present in seven (2.3%) patients and was associated with chest pain and regional wall motion abnormality.
High pre-test probability and ECG changes should raise concern and direct therapy toward invasive diagnostic.
According to the EACVI Position paper of imaging in hospitalised COVID-19 patients, transthoracic echocardiography should be wisely used in patients necessitating proper diagnosis that will guide further therapy, minimising the exposure and risk of health professionals.