Contemporary approach to understand and manage COVID-19-related arrhythmia

Arrhythmia, one of the most common complications of COVID-19, was reported in nearly one-third of diagnosed COVID-19 patients, with higher prevalence rate among ICU admitted patients. The underlying etiology for arrhythmia in these cases are mostly multifactorial as those patients may suffer from one or more of the following predisposing mechanisms; catecholamine surge, hypoxia, myocarditis, cytokine storm, QTc prolongation, electrolyte disturbance, and pro-arrhythmic drugs usage. Obviously, the risk for arrhythmia and the associated lethal outcome would rise dramatically among patients with preexisting cardiac disease such as myocardial ischemia, heart failure, cardiomyopathy, and hereditary arrhythmias. Considering all of these variables, the management strategy of COVID-19 patients should expand from managing a viral infection and related host immune response to include the prevention of predictable causes for arrhythmia. This may necessitate the need to investigate the role of some drugs that modulate the pathway of arrhythmia generation. Of these drugs, we discuss the potential role of adrenergic antagonists, trimetazidine, ranolazine, and the debatable angiotensin converting enzyme inhibitors drugs. We also recommend monitoring the level of: unbound free fatty acids, serum electrolytes, troponin, and QTc (even in the absence of apparent pro-arrhythmic drug use) as these may be the only indicators for patients at risk for arrhythmic complications.

Unbound Free Fatty Acids and Heart-Type Fatty Acid–Binding Protein: Diagnostic Assays and Clinical Applications

Background: A biomarker that reliably detects myocardial ischemia in the absence of necrosis would be useful for initial identification of unstable angina patients and for differentiating patients with chest pain of an etiology other than coronary ischemia, and could provide clinical utility complementary to that of cardiac troponins, the established markers of necrosis. Unbound free fatty acids (FFAu) and their intracellular binding protein, heart-type fatty acid–binding protein (H-FABP), have been suggested to have clinical utility as indicators of cardiac ischemia and necrosis, respectively. Methods: We examined results of clinical assessments of FFAu and H-FABP as biomarkers of cardiac ischemia and necrosis. Data published on FFAu and H-FABP over the past 30 years were used as the basis for this review. Results: Although little clinical work has been done on FFAu since the initial reports, recent studies documented an association between increased serum FFAs and ventricular dysrhythmias and death in patients with acute myocardial infarction (AMI). Recent data suggest that serum FFAu concentrations increase well before markers of cardiac necrosis and are sensitive indicators of ischemia in AMI. H-FABP is abundant in cardiac muscle and is presumed to be involved in myocardial lipid homeostasis. Similar to myoglobin, plasma H-FABP increases within 3 h after AMI and returns to reference values within 12–24 h. Conclusions: FFAu may have a potential role in identifying patients with cardiac ischemia. H-FABP is useful for detecting cardiac injury in acute coronary syndromes and predicting recurrent cardiac events in acute coronary syndromes and in congestive heart failure patients. Assays are available for both markers that could facilitate further clinical investigations to assess their possible roles as markers of cardiac ischemia and/or necrosis.