COVID-19 is a disease caused by the new coronavirus discovered in 2019, which may lead to a severe acute respiratory syndrome and has a major impact on public health worldwide, being declared a pandemic by World Health Organization. In Italy, and especially in the region of Lombardia, the healthcare system has faced a huge overload, which led to significant consequences on cardiology resources. The accessibility to cardiology care units has been drastically reduced, and scheduled interventions, such as elective primary percutaneous coronary interventions, have been significantly delayed. During this time, there was a global concern regarding the management of the SARS-CoV-2 pandemic, but also the management of main cardiovascular emergencies. Under usual circumstances, the differential diagnosis of myocardial injury does not confront many difficulties. Unfortunately, there are several limitations in the management of patients with SARS-CoV-2 infection in the current pandemic state. The aim of the present manuscript is to provide an overview on the main causes of myocardial injury during the COVID-19 pandemic.

Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) has been defined as clinical presentation of an acute coronary syndrome with laboratory evidence of myocardial necrosis, but with coronary stenosis of less than 50% on coronary angiography. On the other side, myocarditis is an inflammatory response triggered by viral, bacterial, fungal, lymphocytic, eosinophilic, or autoimmune myocardial injury, which may be associated with elevated myocardial necrosis serum biomarkers. We present the case of a young male patient with acute chest pain, ST-segment elevation, and high-sensitivity troponin levels of 22,162 ng/L.

Environmental factors may have an important role in the development of coronary heart disease. However, it is not clearly understood yet how the genetic factors interplay with the environmental ones in the onset of acute myocardial infarction. The early onset of coronary artery disease in cases with a positive family history suggests a certain role of genetic predisposition, but the open question remains: could environmental differences contribute to this predisposition? This case report describes similar coronary angiographic findings of two brothers who developed acute myocardial infarction in their early 40s, after being exposed to different environmental risk factors.

The novel coronavirus disease first appeared in Wuhan (China) is an infectious disease spreading throughout the world, causing life-threatening conditions in vulnerable or even healthy individuals. The great impact of this virus on healthcare urges physicians to investigate all aspects of the disease in order to overcome its complications. A particularly investigated aspect of the SARS-CoV-2 infection is represented by the coagulation disorders among infected and critically ill patients. Several studies observed modified blood coagulation parameters such as D-dimers, fibrinogen, and coagulation times. Moreover, the severe thrombotic complications, mainly pulmonary embolism, could be responsible for the high mortality and poorer outcomes of COVID-19 infected patients. The aim of this article is to present the current knowledge related to thrombosis predisposition in patients infected with the new coronavirus.