Myocardial injury, as defined by an increased troponin level, can occur due to both ischemic and nonischemic processes. Myocarditis would be an example of a nonischemic event.
A severe, acute respiratory infection causing hypoxia, especially due to COVID-19, can cause this myocardial injury.
Elevated troponin levels have been described in patients infected with COVID-19, with significant differences between patients who died during hospitalization and those who survived to discharge.
A recent meta-analysis of 4 studies showed that elevated troponin levels were higher in patients who suffered severe COVID-19-related illness compared with infected patients whose clinical course was mild.
Reports even suggest that myocardial injury does not only include elevation of cardiac biomarkers over the 99th percentile of the upper reference limit, but also electrocardiographic and echocardiographic alterations. This scenario is highly prevalent in patients with severe disease and worse prognosis.
Cohort studies in China estimate that such injury occurs in 7% to 17% of hospitalized patients. Additionally, it is much more significant in patients who required intensive care (22.2% vs. 2% in mild cases; p < 0.001) and even more so among patients who died (59% vs. 1%; p < 0.001).
These troponin levels can be exacerbated in patients with renal insufficiency.
Prior studies on other coronavirus species (MERS-CoV) have demonstrated evidence of acute myocarditis in magnetic resonance imaging, and myocardial inflammation and damage have been reported with COVID-19.
Besides type II infarction cases (due to supply and demand mismatch), we have patients with “classic” cardiovascular manifestations.
The profound inflammatory response and hemodynamic changes may trigger atherosclerotic plaque rupture, and a subsequent type I infarction, in susceptible patients.
There is prior evidence indicating that, in patients with influenza or non-influenza-related viral infections (including those due to other coronavirus species), the risk for acute myocardial infarction can be multiplied several times over.
Another problem related to the current pandemic is potential overlapping symptomatology between acute coronary syndromes and COVID-19 infection, including electrocardiographic changes. Up to half of the patients infected with COVID-19 experiencing angina symptoms and electrocardiographic changes who were brought to the cath lab had no obvious culprit lesion.
Título original: Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the Coronavirus Disease 2019 (COVID-19) Pandemic.
Referencia: Elissa Driggin et al. https://doi.org/10.1016/j.jacc.2020.03.031.
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