Conference Roundup

HYPERINFLAMMATION AFFECTS TROPONIN LEVELS IN COVID-19 PATIENTS

Troponin levels may be affected by beta natriuretic peptide (BNP), interleukin (IL)-6, and D-dimer concentrations among patients with COVID-19. These findings were presented during the American College of Cardiology Annual Meeting, held May 15 to May 17, 2021.

Patients with severe COVID-19 are at risk for having a hyperinflammatory response such as a cytokine storm. Recent data suggest that some patients with COVID-19 experience cardiovascular damage. It remains unclear whether troponin levels during the course of a SARS-CoV-2 infection may be affected by markers of inflammation.

To assess the relationship of COVID-19 and troponin, patients (N=586) admitted to Hackensack University Medical Center in New Jersey between February and June of 2020 who underwent at least 2 troponin assessments were retrospectively reviewed for hyperinflammatory responses and clinical outcomes.

Mortality was associated with age, hypertension, coronary artery disease, heart failure, previous percutaneous cardiac intervention, use of beta-blockers or statins, hemodialysis, shock, concentrations of C-reactive protein, concentrations of IL-6, and change in troponin levels (all P <.05).

Maximum troponin level correlated with BNP (correlation coefficient [r], 0.55; P <.05), D-dimer (r, 0.42; P <.05), and IL-6 (r, 0.30; P <.05) concentrations. Baseline troponin level was also correlated with BNP (r, 0.54; P <.05), D-dimer (r, 0.43; P <.05), and creatinine (r, 0.43; P <.05) concentrations.

This study was limited by its retrospective design because there was no predetermined protocol for assessing troponin at set timepoints during patient hospitalization.

These findings suggest the hyperinflammatory response may contribute to troponin perturbation over the disease course of COVID-19. The response to increased inflammation associated with severe SARS-CoV-2 infections may contribute to multiorgan dysfunction and lead to long-term sequelae.

Additional studies of troponin levels among patients hospitalized with COVID-19 are needed to assess whether reductions in the inflammatory response may decrease troponin levels and subsequent cardiac injury.

EFFECTS OF ASPIRIN THERAPY ON THROMBOTIC COMPLICATIONS IN PATIENTS WITH COVID-19

Antiplatelet therapy with aspirin does not protect patients with COVID-19 from thrombotic events or mortality, according to a study presented during the American College of Cardiology Annual Meeting, held May 15 to May 17, 2021.

COVID-19 has been found to be associated with an increased risk for thrombotic events such as stroke, myocardial infarction (MI), and venous thromboembolism (VTE). It is unknown what influence activated platelets may have on COVID19-associated thrombosis and whether antiplatelet therapies may be of benefit in patients with SARS-CoV-2 infection.

The Cleveland Clinic team in Ohio evaluated the protein expression of both angiotensin-converting enzyme 2 (ACE2; n=20) and TMPRSS2 (n=20) in healthy human platelets via immunoblotting and confirmed the results via confocal microscopy (ACE2, n=6; TMPRSS2, n=3). For comparison, the authors evaluated the same protein expressions in patients (n=10, each) with coronary artery disease.

To determine if antiplatelet therapy protects against MI, VTE, or death, researchers conducted a review of 22,072 patients who were tested for COVID-19 and matched them with 248 COVID-19-positive patients who were not exposed to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) during treatment.

Both ACE2 and TMPRSS2 were found to be present on human platelets. No association was shown between the expression of ACE2 (r2=.004; P =.79) or TMPRSS2 (r2=.058; P =.30) and age. A numerically higher expression of ACE2 and TMPRSS2 was seen in patients with coronary artery disease vs patients in the control group. In the propensity-matched analyses of aspirin use, no difference was found in the incidence of MI and VTE. However, aspirin therapy was associated with increased risk for thrombotic stroke (3.6% vs 0.40%; P =.036), as well as the composite endpoint of MI, VTE, and stroke (9.3% vs 2.8%; odds ratio [OR], 3.52; 95% CI, 1.48-8.40; P =.005). NSAID therapy was similarly associated with risk for the composite endpoint (3.8% vs 1.6%; OR, 2.49; 95% CI, 0.58-1.62; P =.046). Neither aspirin therapy (OR, 0.52; 95% CI, 0.51-1.41; P =.52) nor NSAID therapy (OR, 0.97; 95% CI, 0.58-1.62; P =.90) were associated with mortality.

The investigators concluded, "Human platelets express the requisite SARSCoV-2 receptors to permit viral access, but antiplatelet therapy consisting of aspirin does not protect from thrombotic events or mortality." ■

Aspirin therapy does not protect against MI, VTE, and stroke in patients with COVID-19.

A Case of Sudden-Onset Dysphagia During Lunch, Unresolved by PPIs

A patient presenting with sudden-onset dysphagia and vomiting initially is diagnosed with GERD but does not respond to PPIs. What is your diagnosis?

© GORAN BJELAKOVIC / MEDICALIMAGES.COM

The prevalence of EoE is estimated at 57 per 100,000 people.

A24-year-old man presents to the emergency department (ED) complaining of suddenonset dysphagia that began 2 hours earlier while he was eating lunch. He states that it feels as though something is “stuck in his throat.” He explains that he tried to drink a glass of water to relieve the feeling but immediately vomited. He is now fearful of eating and drinking. The patient denies any previous episodes of dysphagia and reports no odynophagia, nausea, abdominal pain, heartburn, dyspepsia, weight loss, chest pain, or shortness of breath. He denies a medical history of gastroesophageal re ux disease (GERD) and peptic ulcer disease. He has no known food or drug allergies and is not taking any medications. The patient denies use of alcohol, illicit drugs, and tobacco.

Physical Examination

The patient’s vital signs are normal: blood pressure, 118/63 mm Hg; pulse, 95 beats per minute; respiratory rate, 18 breaths per minute; temperature, 97.8 °F; and oxygen saturation, 100%.

On physical examination, the patient is alert and oriented x4. He appears uncomfortable but is in no acute distress. Cardiac examination reveals S1 and S2 heart sounds, with regular rate and rhythm without murmurs. The patient’s lungs are clear to auscultation. His neck is symmetrical with no masses. He has a palpable and nontender thyroid. His trachea is midline and palpable in the suprasternal notch. His abdomen is nondistended and nontender, with active bowel sounds. No organomegaly is present.

Initial Diagnosis and Follow-up

No laboratory or diagnostic tests are ordered. Based on the initial assessment, the ED physician diagnoses the patient with GERD and prescribes a liquid proton pump inhibitor (PPI). The patient is hesitant to take the medication for fear of vomiting, but the doctor reassures him that this is not likely to occur.

Twenty minutes after taking the PPI, the patient experiences no improvement of dysphagia. However, because of the patient’s ability to swallow the prescribed medication, the physician determines that no further workup is needed. The patient is sent home and assured that symptoms will resolve soon.

Early the next morning, the patient returns to the ED with unresolved dysphagia. He states that he vomited 30 minutes after leaving the ED. The gastroenterology team is consulted and they perform a esophagogastroduodenoscopy (EGD).

The EGD reveals a food bolus impaction and esophageal stricture located in the distal third of the esophagus. Mild esophagitis also is noted throughout the esophagus. Given these findings, biopsies are obtained for histology. The results indicate a diagnosis of eosinophilic esophagitis (EoE).

Outcome

During the initial EGD, the food impaction is removed and the esophagus is treated with dilation. The patient is discharged home with a prescription for omeprazole 40 mg daily and is referred to an allergist.

Allergy testing reveals allergic reactions to dairy, shellfish (shrimp, crab, lobster, clams, mussels, oysters, and scallops), bananas, and sweet potatoes. The allergist suggests diet modification and corticosteroids as treatment options. Given the potential long-term side effects of corticosteroids, the patient decides that an elimination diet and a daily PPI is the best treatment option for him.

Two years after being diagnosed with EoE, the patient returns to the gastroenterologist after experiencing another episode of dysphagia. Repeat EGD reveals no stricture but shows diffuse faint corrugated mucosa throughout the esophagus, suggesting worsening disease. Further questioning of the patient reveals that the esophageal findings and recurrent symptoms likely are because of his nonadherence with his diet plan.

Discussion

Eosinophilic esophagitis is a chronic immune-mediated disease that is increasingly encountered in clinical practice.1 The disease is characterized by infiltration of eosinophils and other inflammatory cells into the esophageal epithelium.1 This causes tissue remodeling and fibrosis of the esophagus, leading to symptoms of esophageal dysfunction. A strong correlation has been found between the development of EoE in patients with a personal or family history of atopic disease, specifically asthma, eczema, and food allergies.1 This correlation makes it important to obtain a detailed history to identify possible risk factors for developing EoE. In this case, the patient presented with no medical history of atopic disease, which made this a more challenging diagnosis.

A wide variety of symptoms are associated with EoE. Adults can present with dysphagia, heartburn, food impaction, chest pain, odynophagia, and vomiting.1,2 Although these symptoms are common in patients with EoE, they are not exclusive to the disease and can occur with other gastrointestinal disorders.

Differentiating EoE and GERD Gastroesophageal reflux disease occurs when the lower esophageal sphincter relaxes, allowing reentry of acid and food into the esophagus, which causes injury and inflammation.3 Patients with GERD can present with symptoms of heartburn, dysphagia, chest pain, reflux, abdominal pain, and nausea.3 The similarity between symptoms of EoE and GERD makes distinguishing these 2 diseases clinically challenging (Table).1-3

The patient in this case presented with dysphagia, a common symptom found in patients with both diseases, and was initially misdiagnosed with GERD. The prevalence of EoE is significantly lower than that of other esophageal diseases, occurring in 57 per 100,000 people.4 The lower prevalence and the nonspecific symptoms associated with EoE may contribute to its frequent misdiagnosis.

TABLE. Comparison of EoE vs GERD1-3

Eosinophilic Esophagitis GERD

Age of onset Infancy, early adulthood Middle-late adulthood

Common symptoms

Endoscopic findings Dysphagia, heartburn, chest pain, odynophagia, vomiting Heartburn, reflux, dysphagia, chest pain, nausea, abdominal pain

White exudates, longitudinal furrows, fixed rings, edema, strictures Normal tissue, erythema, erosions, ulcers, strictures

Histology ≥15 eosinophils/hpf <7 eosinophils/hpf

Treatment Diet modification, inhaled corticosteroids (swallowed), PPIs Antacids, diet modification, H2 receptor blockers, lifestyle modifications, PPIs

Complications Strictures, food impactions, “crepe paper esophagus” Barrett esophagus, esophageal adenocarcinoma

EoE, eosinophilic esophagitis; GERD, gastroesophageal reflux disease; H2, histamine; hpf, high-power field; PPI, proton pump inhibitor