Severe COVID-19 infection in young patient with hypertension on ACE inhibitor

A 30-year-old female patient with a past medical history of asthma, morbid obesity (BMI 39.5), and hypertension on an angiotensin-converting enzyme (ACE) inhibitor presented with a 6-day history of fever (Tmax 38.9°C), cough, and shortness of breath. Laboratory studies were remarkable for lymphopenia (0.6×10³/µL, normal range 0.9×10³/µL – 3.3×10³/µL), elevated serum creatinine (1.3 mg/dL, normal range 0.6 mg/dL – 1.2 mg/dL), elevated aspartate aminotransferase (73 IU/L, normal range 13 IU/L – 39 IU/L), elevated c-reactive protein (8.6 mg/dL, normal range 0 – 1 mg/dL), elevated procalcitonin (2.39 ng/mL, normal < 0.1 ng/mL), elevated interleukin-6 (197 pg/mL, normal ≤ 5 pg/mL), elevated cardiac troponin I (142 ng/L, normal < 15 ng/L), and mildly elevated d-dimer (570 ng/mL, normal < 500 ng/mL). She reported a history of contact with a COVID-positive co-worker and no recent travel. Influenza A/B RT-PCR were negative. She developed acute respiratory distress and was emergently intubated.

AP chest X-ray after emergent intubation demonstrates bilateral upper-lobe predominant patchy and confluent airspace opacities (Fig. 1).

CTA chest performed on presentation demonstrates bilateral patchy and diffuse ground-glass opacities with a more focal consolidative process in the right lower-lobe and upper-lobe predominant air bronchograms. There was no evidence of acute or chronic pulmonary embolism (Figs. 2a-e).

Prone portable PA chest X-ray on second day of admission demonstrates persistent airspace opacities, cardiomegaly and haziness of the cardiac borders (Fig. 3).

A. Background
Coronavirus disease-19 (COVID-19) is a novel viral pandemic that has been reported to have a more severe course in older patients and those with comorbidities including hypertension [1, 2]. The virus invades cells by binding to the angiotensin-converting enzyme 2 (ACE2) receptor, which is expressed in epithelial cells in the lung, heart, kidney, intestine, and blood vessels [3]. It has been theorised that patients taking ACE inhibitors could have increased risk of severe infection due to upregulated ACE2 receptor expression, though there has not yet been conclusive clinical or experimental data [4–6].

B. Clinical Perspective
Dyspnoea from COVID infection has been reported a median of 7 days after symptom onset and elevated d-dimer has been associated with decreased survival [1].  D-dimer is an acute phase reactant which may be elevated in the setting of active infection/inflammation, and is not specific for acute pulmonary embolism, though cases of concomitant COVID infection and acute pulmonary embolism have been reported [7, 8]. Acute kidney injury has been reported in up to 19% of COVID patients admitted to the intensive care unit [9].

C. Imaging Perspective
Radiographic and computed tomography (CT) imaging may be initially normal in COVID infection, with up to 50% of patients having normal CT imaging within the first two days of symptom onset [10]. Early CT findings include multi-lobar, peripheral-predominant, patchy ground-glass opacities with or without consolidations. Additional findings can include air bronchograms, a halo sign, and crazy paving pattern [11].  

D. Outcome
COVID-19 RT-PCR was positive. The patient was initiated on hydroxychloroquine, azithromycin, and tocilizumab, positioned prone for severe ARDS, and developed worsening acute kidney injury with serum creatinine of 3.0.

E. Teaching Points
Patients of all ages with comorbidities including hypertension have an increased risk of developing severe COVID disease. Serum d-dimer elevation is not specific to pulmonary embolism, though cases of concomitant COVID infection and acute pulmonary embolism have been reported. ACE inhibitors could have theoretical increased risk of severe infection due to upregulated ACE2 receptor expression, though conclusive data has not yet been reported.

Written patient consent for this case was waived by the Editorial Board. Patient data may have been modified to ensure patient anonymity.