COVID-19 in Pregnant Patients

Overview

COVID-19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is an enveloped virus with a nonsegmented, single-stranded, positive-sense RNA genome. The virus can use the angiotensin-converting enzyme (ACE) 2 for cell entry. ACE 2 is an integral-membrane protein that serves many important physiologic functions. The spike protein of the virus can bind to ACE 2. After ligand binding, the virus enters cells via receptor-mediated endocytosis. ACE 2 is highly expressed in alveolar cells, providing the entry site for the virus. ACE 2 also serves a role in lung protection; therefore, viral binding to this receptor deregulates a protective pathway, leading to viral pathogenicity. There are some concerns that ACE inhibitors may exacerbate SARS 2 infection by upregulating the number of ACE 2 receptors, but this seems to be a theoretical risk only, and some studies have shown that patients taking ACE inhibitors or angiotensin receptor blockers (ARBs) actually do better than patients not taking these drugs.

Close to 90% of patients with COVID-19 severe enough to warrant hospitalization have comorbidities. Risk factors include hypertension, obesity, chronic lung disease, diabetes, and cardiovascular disease. Physiological and mechanical changes in pregnancy increase a woman’s susceptibility to infections in general, particularly when her cardiorespiratory system is affected, and may encourage rapid progression to respiratory failure. Furthermore, the pregnancy bias toward T-helper 2 (Th2) system dominance, which protects the fetus, leaves the mother vulnerable to viral infections, which are more effectively contained by the Th1 system.

COVID-19 affects multiple organ systems, including the cardiovascular system. It has been associated with multiple direct and indirect cardiovascular complications, including myocardial injury, myocarditis, arrhythmias, and venous thromboembolism. Other organs or organ systems affected by COVID-19 include the lungs, gastrointestinal tract, liver, and skin. Lung injury in severe cases usually presents as SARS. Acute kidney injury may range from azotemia to acute tubular necrosis and usually presents at 2 to 3 weeks postinfection. Patients may manifest hematuria or proteinuria. Thrombotic complications are also common. Venous thromboembolic disease occurs in up to 31% of critically ill COVID patients. Disseminated intravascular coagulation can also occur. Anticoagulation with low-molecular-weight heparin is advised. Neurologic impacts caused by COVID-19, such as encephalopathy, agitation, confusion, and corticospinal tract signs, also have been reported.

Myocardial injury as assessed by increased troponin has been reported in many patients with severe COVID-19. Higher cardiac troponin levels are associated with a worse prognosis and death. Severe cardiac injury manifested by changes on electrocardiography and echocardiography is seen in 7% to 17% of patients. Patients with COVID-19 may present as though they are having an acute ST-elevation myocardial infarction. Chinese studies have reported arrhythmias in about 17% of patients with COVID-19, but at this time, data about specific arrhythmia types are not available. Congestive heart failure has been reported in up to 23% of hospitalized patients with COVID. It is unclear whether this is caused by an exacerbation of an underlying cardiac dysfunction or a new cardiomyopathy. There are concerns that COVID-19 may cause long-term impairment of left ventricular dysfunction in some patients.