乌鸦传媒

An 82-year-old woman presents to a Baltimore hospital after suffering for 5 days with a cough (productive), fever with chills, and intermittent diarrhea. Initial clinical assessment finds her afebrile and hemodynamically stable, with no evidence of respiratory distress.

Her medical history includes hypertension, hyperlipidemia, iron deficiency anemia, and paroxysmal atrial fibrillation. She has been receiving chronic flecainide therapy with tachy-brady syndrome, for which she has an s/p dual-chamber pacemaker (Boston Scientific INGENIO K173 implanted in 2012).

Suspecting that she may be infected with COVID-19, clinicians order a PCR test, which returns positive. She is admitted to the isolation ward for further care and assessment.

An index 12-lead EKG reveals an atrial paced rhythm with diffuse new, prominent T-wave inversions and a prolonged QT interval (>500 ms). The team decides not to start the patient on treatment with hydroxychloroquine and azithromycin, due to potential risks related to QT prolongation and given the relative dearth of safety and efficacy data to support the treatment in COVID-19 patients.

Despite discontinuation of the flecainide treatment, the EKG changes persist. The patient's mild elevation in troponins peaks at 0.037 ng/ml, and she has no anginal symptoms. An initial echocardiogram shows preserved left ventricular function (ejection fraction 55%), a small circumferential pericardial effusion, and apical hypokinesis.

The patient continues to remain hemodynamically stable, and based on her clinical condition, it is determined that mechanical ventilation is not indicated. Clinicians keep her in physical isolation, and manage her conservatively with antipyretics, hydration, and oxygen therapy.

Five days later, a repeat echocardiogram shows a moderately enlarging pericardial effusion with left pleural effusion.

Two days after the second echocardiogram, the patient develops chest tightness and shortness of breath, prompting a third echocardiogram, which reveals further enlargement of the previously observed circumferential pericardial effusion.

Clinicians also note a right ventricular (RV) pacemaker wire "piercing" the RV apex alongside early diastolic collapse of the right ventricle, suggesting echocardiographic tamponade. The medical team follows up with non-contrast chest CT, and imaging shows extension of the RV pacemaker lead beyond the myocardium into the pericardial fat, with bilateral pleural effusions and patchy lung infiltrates.

The findings are compared with those of a previous chest CT from 2019, in which the lead positions are similar; clinicians conclude that this pacemaker lead position may have been longstanding.

However, the new enlarging pericardial effusion, pleural effusions, infiltrates, and EKG changes are strongly suggestive of a viral syndrome. As well, a pacemaker interrogation shows appropriate pacing function of both leads.

The RV lead thresholds are stable at 1.3 V at 0.4 milliseconds pulse width, and R wave sensing is measured at 10.6 millivolts. The impedance range is 450-500 ohms, which has remained stable from the previous year. Given appropriate RV lead-pacing function, the chronicity of the RV lead position on chest CT, and the fact that the patient is not experiencing any chest pain or chest-wall stimulation on high-output RV pacing, the clinicians conclude that there is no definitive evidence to support the suspected RV lead perforation.

The patient undergoes pericardiocentesis based on the echo­cardiographic evidence of tamponade, and 400 cc of straw-colored, serous fluid is removed and assessed. Fluid analysis tests negative by RT-PCR for COVID-19. The patient's leukocyte count is 10³/mm³; glucose is high (over 40 mg/dL), as is protein (3.9 g/dL), suggesting exudate per Light's criteria.

Diagnosis

The patient's clinical presentation, high serum C-reactive protein level of 24.30 mg/L, EKG abnormalities, and wall-motion abnormalities on echocardiogram, along with the exudative character of the pericardial fluid, are highly suggestive of SARS-CoV-2-induced inflammatory ­myopericarditis and pericardial effusion. A follow-up echocardiogram 24 hours after pericardiocentesis shows minimal fluid re-­accumulation, and the patient continues to improve clinically.

Discussion

Clinicians presenting this of a patient with COVID-19 infection complicated by myopericarditis and pericardial effusion with tamponade requiring drainage note that acute myopericarditis and pericardial effusion can occur in patients with COVID-19 infection, even in the absence of severe pulmonary disease.

The team, therefore, urges clinicians encountering such a situation to consider the possibility of myopericardial involvement in patients presenting with cardiac symptoms, EKG abnormalities, or wall-motion abnormalities on imaging, with or without cardiac enzyme elevation.

The virus that causes COVID-19, SARS-CoV-2, most typically presents as a respiratory illness with clinical symptoms of fever (high- or low-grade), cough, pharyngodynia, fatigue, and progressive shortness of breath. A pulse oximeter may also be used to help identify COVID-19 infection, as many patients have been found to be hypoxic on initial assessment.

Also often reported are loss of smell and loss of taste -- anosmia and dysgeusia -- and symptoms typically develop over a period of a week, with rapid progression to respiratory distress around day 8.

There have also been numerous reports of cardiovascular manifestations such as tachycardia, acute arrhythmias, acute cardiac injury, acute-onset heart failure, myocardial infarction, myocarditis, and cardiac arrest.

The case report authors note that this patient presented a diagnostic dilemma because of the sudden onset and severity of the COVID-19 induced cardiac manifestations, along with only mild pulmonary involvement. Diagnosis was further complicated by the presence of a pacemaker, with concern for late RV lead perforation on imaging, albeit without supportive evidence based on functioning lead parameters.

Nevertheless, the authors attribute the patient's acutely enlarging effusion to COVID-19 related inflammatory myopericarditis, with the serous straw-colored, non-bloody, and exudative characteristics associated with pericardial fluid.

The acute myocardial injury caused by SARS-CoV-2 infection may be related to either myocardial angiotensin-converting enzyme-2 receptors or cytokine storm triggered by an imbalanced response by type 1/2 T helper cells.

The patient's life-threatening cardiac tamponade due to myopericarditis induced by SARS-CoV-2 infection, followed by worsening hemodynamic parameters including hypotension and tachycardia, reflects the first mechanism. Pericardiocentesis with removal of 400 cc serosanguinous fluid immediately improved the patient's hemodynamic parameters.

The team urges physician vigilance for COVID-19 induced inflammatory myopericarditis and pericardial effusion with impending tamponade, which may require urgent pericardiocentesis.

In addition, personal protective equipment should be readily available for operators and staff performing emergent, lifesaving procedures on COVID-19 patients. In particular, this case highlights the importance of continued, global preparedness of cardiac catheterization and electrophysiology laboratories during the pandemic, the authors state.

Results of a retrospective, single-center of 138 consecutive patients hospitalized with confirmed novel coronavirus–infected pneumonia in Wuhan, China, from January 1 to January 28, 2020, included the following observations:

• Mean incubation period: 5.2 days (95% CI 4.1 to 7.0)

• 95th percentile of the distribution: 12.5 days

• Mean serial interval: 7.5 days (95% CI 5.3 to 19)

• Estimated basic reproductive number (R₀): 2.2 (95% CI 1.4 to 3.9) (R₀ = the average number of additional individuals that one affected case infects during the course of their illness -- i.e., specifically in a population previously free of infection and unvaccinated)

Adherence to personal protective equipment (PPE) guidelines in the management of COVID-19 patients during cardiac procedures remains a critical element of care. In this case of a hemodynamically stable patient, given the evidence of rapidly enlarging effusion and echocardiographic tamponade, the medical team intervened early in order to maximize adherence to quality parameters and PPE usage.

The authors conclude that in a patient with COVID-19, cardiac involvement may lead to rapid clinical and hemodynamic deterioration unless managed urgently, thus necessitating an invasive approach in some cases.

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