As the Coronavirus disease 2019 (COVID-19) pandemic progresses, we begin to uncover more information regarding the treatment of these patients and the impact COVID-19 has on the body. First discovered in December 2019, COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). (Lippi) Despite primarily thought of as a respiratory disease, COVID-19 infects the cardiovascular system with almost equal voracity.(Fei Zhou et al.) Specifically, one cardiovascular outcome of COVID-19 disease is thrombosis with symptoms including large vessel clots and deep vein thrombosis/pulmonary embolism (DVT/PE). (Phend) Understanding the link between the cardiovascular system and COVID-19 is important as the high mortality rate observed among COVID-19 patients may be partly due to unrecognized pulmonary embolism (PE) and pulmonary in situ thrombosis. (Lodigiani)
COVID-19 patients with pre-existing cardiovascular conditions represent large proportions of patients with symptomatic infections. These patients experience disproportionately worse outcomes with a 5 to 10-fold increase in mortality. (Liu) There is also a significant number of patients presenting with COVID-19 infections with no history of pre-existing cardiovascular conditions who develop cardiovascular complications, such as heart failure, myocarditis, pericarditis, vasculitis, and cardiac arrhythmias. (Liu)
The first clinical observation noted with COVID-19 patients that present with DVT/PE is elevated levels of the biomarker D-dimer. Patients who experienced an increase in D-dimer levels (>1 μg/mL), correlated to a mortality risk 18-times higher than those will levels under 1 μg/mL. (Fei Zhou et al.) Survivors of COVID-19 pneumonia have also experienced significantly lower D-dimer levels than deceased patients. (Tang)
Hospitalized patients with COVID-19 were characterized by substantial levels of in-hospital mortality and a high rate of thromboembolic complications. Rapidly increasing D-dimer levels were observed in deceased patients. (Lodigiani) r\Risk factors related to COVID-19, and the subsequent mortality from the disease, include older age, neutrophilia, higher SOFA (Sequential Organ Failure Assessment) score, and coagulation dysfunction (e.g., D-dimer). (Fei Zhou et al.) , (Wu)
In addition, COVID-19 results in severe cardiac injury which can manifest itself in elevated levels of cardiac troponin I (cTnI) and natriuretic peptides (BNP and NT-proBNP). Abnormal cTnI values (>99th percentile) in some patients hospitalized with COVID-19 were associated with more severe complications, worse outcomes and about 10-times higher mortality rate. (Lippi, Shi) Troponin and natriuretic peptides, together with the presence of underlying cardiovascular diseases or cardiovascular risk factors, are highly prognostic for ICU admission, ventilation and death. (Liu) In the clinical course of patients with COVID-19, detectable hs-cTnI (high sensitivity troponin I) was observed in most patients, and hs-cTnI was significantly elevated in more than half of the patients that died. (Januzzi)
Investigations have shown a correlation between COVID and cardiovascular symptoms, and it is clear that high levels of D-dimer and troponin are correlated with a high mortality risk. The early presence of cardiac injury and stress, as evidenced by biomarkers of elevated troponin and/or natriuretic peptides, are important to ascertain especially in higher risk patients. (Liu) If clinicians are reluctant to measure cardiac troponin in these patients, the consequence may be to ignore the plethora of ischemic and non-ischemic causes of myocardial injury related to COVID-19, which may be directly or indirectly associated with poor outcomes. (Chapman)