Arq. Bras. Cardiol. 2024; 121(1): e20230888
How Can COVID-19 Influence the Evolution of Patients with Acute Coronary Syndromes?
This Short Editorial is referred by the Research article "In-Hospital Outcomes of ST-Segment Elevation Myocardial Infarction in COVID-19 Positive Patients Undergoing Primary Percutaneous Intervention".
The pandemic caused by the COVID-19 virus has changed the way we view infectious diseases. In a more intense way than in other situations, COVID-19 was from the beginning related to a greater number of thrombotic events, whether in its acute presentation, with pulmonary microthrombi worsening the hypoxia, or even in its late evolution with a large number of pulmonary embolic events. The interface between the endothelium and the coagulation cascade was modified, and different pro-thrombotic mechanisms were deregulated, with elevated expression of tissue factor, CD40, leukocyte adhesion molecules, pro-inflammatory cytokines, thromboxane, and reduced production of nitric oxide. Along with the lungs, the heart is one of the organs most affected by the disease with global involvement, whether myocardial, arrhythmogenic, or coronary.–
Thus, the study presented by Baytugan et al. describes patients with ST-elevation acute coronary syndrome (ST-ACS) with COVID-19, comparing them with the group without COVID-19 in relation to the clinical outcomes found. Some interesting points should be highlighted, including the fact that it takes longer for patients to present themselves to the hospital. This was very common during the pandemic and certainly worsened outcomes related to ACS. It was also observed that patients with COVID-19 were older and had more comorbidities, such as diabetes and chronic obstructive pulmonary disease. Finally, in an incisive and clear way, patients with COVID-19 developed worse outcomes, such as a greater number of stent thromboses, more cardiogenic shock, and higher mortality. A curious fact was the description of higher troponin levels in the COVID-19 group. More simply, we can relate this to the greater diagnostic delay; however, it is worth highlighting the possibility of direct cardiac aggression caused by COVID-19, in addition to the greater thrombotic and inflammatory load that the disease can cause.
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