BEST PRACTICES :: CARDIAC BIOMARKERS
Short and long-term effects of the COVID pandemic on cardiovascular patients
By Sean-Xavier Neath, MD, PhD T
he COVID-19 pandemic has created a number of diagnostic challenges for clinicians and laboratorians world-wide. Even during the relatively quiet “off-peak” periods of acute
COVID, there remain the challenges of helping the large group of patients left with the shrapnel of “long Covid.” Kaufman and Meyer, in a recent edition of this journal,1
present an excellent
overview of the evolving long-term health consequences of COVID-19. This article will focus on the cardiovascular elements of acute COVID and long COVID with an emphasis on how deployment of known cardiovascular biomarkers can help aid in the identification, risk-stratification and treatment of patients. While COVID-19 is primarily thought of as a respiratory
illness, it became apparent early in the pandemic that the cardiovascular system is not spared from the effects of the disease. This makes sense mechanistically as the virus gains entry to human cells via the angiotensin-converting enzyme2 (ACE2), which is ubiquitously present in the body, including the cardiovascular epithelium. Additionally, it became quickly clear that patients with preexisting cardiovascular conditions were at higher risk for going on to develop severe COVID-19 disease.2
Similarly, patients hospitalized with severe COVID-19
even without pre-existing cardiovascular disease have had a significantly higher rate of cardiovascular complications such as myocardial infarction, heart failure, vascular thrombotic events, and myocarditis. Interestingly, myocarditis and heart failure can also be seen as rare but serious complications of mRNA COVID-19 vaccines absent any active viral infection, particularly in younger men.3
In all these patient groups,
there is diagnostic and prognostic utility of cardiovascular biomarker management using necrosis markers (cardiac troponin), natriuretic peptides (BNP or nt-proBNP), and thrombosis markers (d-dimer). Throughout the pandemic, a number of biomarkers have
been identified to risk stratify patients presenting to the ER with COVID. In particular, either a troponin or a d-dimer
28 JUNE 2022
MLO-ONLINE.COM
value twice the upper limit of normal is associated with severe disease.5
Mueller and colleagues have published an overview of
cardiovascular biomarkers in patients with COVID that helps differentiate some of the nuances in interpretation needed in patients with COVID.6 Troponin should be measured in hospitalized patients with
COVID, and repeated if abnormal or if new clinical criteria arise. In non-critically-ill patients with COVID-19, modest elevations (up to 3 times the ULN) are often due to prior cardiac disease or myocardial ischemia related to respiratory failure. Higher concentrations (>3x ULN) are more likely to be due to the presence of specific acute cardiac disease such as myocardial infarction, myocarditis, or takotsubo syndrome. Natriuretic peptides (NPs), such as BNP, nt-proBNP or MRpro-ANP should be measured if heart failure is suspected on clinical grounds. In patients who are not critically ill, NPs cut- offs for heart failure “rule-in” maintain high positive predictive value, even in patients with pneumonia. In contrast, currently recommended NP cut-offs should not be applied in critically ill in patients with ARDS or septic shock, as most critically-ill patients have substantial elevations in BNP/NT-proBNP, due to overwhelming hemodynamic decompensation. D-dimers are generated by cleavage of fibrin monomers by plasmin, therefore, signal thrombus formation and resulting fibrinolysis. A d-dimer value lower than its assay specific cut-off has a high-negative predictive value to help rule out venous thromboembolism in low-risk patients. In more seri- ously ill patients, d-dimer can be used for the diagnosis and monitoring of disseminated intravascular coagulation associ- ated with sepsis or shock. During the outbreak of COVID-19, a coagulopathy has been commonly observed in hospitalized patients that can be identified by d-dimer values. One mecha- nistic explanation is that severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) has a high affinity to endothelial cells and may induce ‘endotheliitis’, which
Photo by
DragosCondrea@Bigstockphoto.com
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