key: cord-1037193-rc5nksxf
authors: Loghin, Catalin; Chauhan, Siddharth; Lawless, Sean M.
title: Pseudo acute myocardial infarction in a young COVID-19 patient
date: 2020-04-27
journal: JACC. Case reports
DOI: 10.1016/j.jaccas.2020.04.015
sha: ffc50bbba1bd8bed7df66cb54a5988a5abe6b7ad
doc_id: 1037193
cord_uid: rc5nksxf

Abstract: A 29 year old man tested positive for COVID-19 and developed acute respiratory distress syndrome (ARDS). While mechanically ventilated, his electrocardiogram (EKG) showed inferior ST segment elevations, with normal serial cardiac troponin I and transthoracic echocardiograms. He was treated conservatively, with complete clinical recovery and resolution of his EKG abnormalities.

A 29 year old, morbidly obese man (BMI: 42 kg/m 2 ), presented to an emergency care center after eight days of fever (up to 103°F), myalgias, non-productive cough, sore throat, and malaise. He had been in contact with a family member with upper respiratory symptoms, whom recently traveled by plane. While receiving symptomatic treatment, he returned to the urgent care facility twice, with complaints of worsening dyspnea. His physical examination revealed a young man in obvious respiratory distress, with mild peripheral cyanosis, and corresponding vital signs: respiratory rate: 29/min, O2 saturation: 89% with supplemental O2 flow rate: 4l/min, temperature: 98.8 0 F, blood pressure: 116/88 mm Hg, and heart rate: 104 bpm. His lungs auscultation showed bilateral fine crackles and no evidence of consolidation, whereas the rest of his examination was normal. While in the emergency room, the patient required mechanical ventilation, for rapidly progressing respiratory failure.

The patient had no significant medical history. He never smoked. There was no family history of cardiovascular disease.

Differential diagnosis: An early viral panel PCR was negative for multiple respiratory viruses.

A SARS CoV-2 NAAT test returned positive five days after admission. In the absence of any cardiovascular risk factors, the etiology of the ST segment elevations was initially interpreted as evidence for COVID-19 related myocarditis.

A chest computed tomography study (CT) showed bilateral, multifocal airspace opacities. An initial EKG (Fig 1) showed sinus tachycardia and marked right QRS axis deviation.

Over the following 48 hours, while the patient was acidotic (ph 7.27, base excess: -4 mMol/L), he developed marked ST segment elevations in leads II, III, aVF, and V6 (Fig 2) . Serial cardiac troponin I (cTnI) and myoglobin levels remained normal (< 0.02 ng/mL, and 55.0 ng/mL, respectively). The creatine kinase-myocardial band (CK-MB) was initially elevated (2034 unit/L), and normalized over the subsequent 72 hrs. Repeated transthoracic echocardiograms (TTE) showed normal heart chamber size, no regional wall motion abnormalities, and no pericardial effusion.

Given the very low pretest probability for coronary artery disease (CAD), and the absence of coronary calcifications on the chest CT, a coronary CT angiogram (cCTA) was not indicated, and the patient was not referred for invasive coronary angiography. The patient was treated conservatively, without thrombolytics or initiation of the acute coronary syndrome management protocol.

The COVID-19 pandemic represents the largest worldwide health care challenge to date.

Limited, but rapidly emerging data has documented the role of cardiovascular disease (CVD) in increasing both the risk of infection and the severity of its clinical presentation (1-4). In particular, CVD is associated with a sharp increase in overall mortality, which reaches almost 20% of those hospitalized(5). However, while such an association can be somewhat anticipated (based on existing data from previous outbreaks of influenza and SARS), the incidence of myocardial injury for COVID-19 infection appears to be higher (6) . Furthermore, the definition of COVID-19 associated "myocardial injury" lacks standardization, and is based primarily on elevated (and highly variable) serum levels of cardiac-specific troponins as the single most common defining marker. This myocardial injury has been associated with evidence of left ventricular systolic dysfunction and arrhythmia (2, 5, 7, 8) .

In contrast, our case demonstrates the presence of major, isolated EKG abnormalities in a patient without any other commonly accepted evidence for "myocardial injury". This includes normal results for serial measurements of cTnI and repeated TTE studies, and no arrhythmia other than sinus tachycardia. Accepting electrocardiographic ST segment elevation as representative of "myocardial injury" may be conceptually tempting for the diagnosis of cardiac involvement related to COVID-19 infection. However, the cautious practitioner will remember the poor specificity of ST segment elevation, which is encountered in a variety of conditions that mimic acute myocardial infarction. To further complicate the matter, serum cTnI can also be elevated in a variety of non-cardiac conditions, including sepsis and critical illness.

To our knowledge, this is the first reported COVID-19 patient to demonstrate acute, dynamic ST elevations in inferior leads that were, in our opinion, neither ischemic, nor representing true "myocardial injury" as defined by biochemical markers or echocardiographic changes. We did not interpret the isolated elevation of low specificity CK-MB as evidence for a diagnosis of myocarditis in the context of severe illness, sepsis, and acidosis, with normal myoglobin. Right ventricular supply-demand mismatch was also ruled out by normal serial cTnI serum values. We felt that the hypothesis of non-ischemic EKG changes was further supported by the absence of gross coronary calcifications on the chest CT, a finding associated with very high negative predictive value for coronary artery disease (CAD). Therefore, we attributed the EKG changes to acute, severe right ventricular strain in the setting of COVID-19 related ARDS, a phenomenon described by anecdotal reports of pulmonary embolism.

Worldwide, there are only two reports of COVID-19 patients who presented with acute ST segment elevations, and for both patients the EKG changes were present in the inferior leads (9, 10) . In each case, a diagnosis of myocarditis was supported by elevated cardiac troponins, a moderate decrease of left ventricular ejection fraction, and the absence of flow limiting CAD by invasive coronary angiography. In one of these cases, the diagnosis of myocarditis was complemented by the presence of myocardial edema by cardiac magnetic resonance imaging, as a marker of acute myocardial injury (9) . Our patient, while critically ill and mechanically ventilated, maintained hemodynamic stability, a normal left ventricular ejection fraction, and had no evidence for cardiac arrhythmias. As such, we felt comfortable recommending medical management, and chose not to pursue an invasive coronary angiography or any additional imaging tests, including a cCTA. We perceived these tests to be not indicated in this clinical context, and to have insufficient potential to alter further management decisions.

Moreover, any additional imaging tests would have unnecessarily increased the health care staff exposure, a risk that we have actively tried to diminish.

The evolution of our patient was favorable with vigorous correction of his metabolic abnormalities. An EKG 48 hours later showed near complete resolution of the ST segment elevations (Fig 3) . Following continuous improvement of his respiratory status, he was successfully extubated. Two weeks after hospital discharge, the patient was interviewed by telephone and confirmed a complete clinical recovery.

COVID-19 infection is associated with a high rate of cardiac complications, resulting in acute systolic heart failure and arrhythmias, which contribute to a marked increase in mortality. EKG changes may mimic an acute myocardial infarction, and must be interpreted in clinical context, for a consistent diagnosis, and to determine the true incidence of "myocardial injury" related to COVID-19 infection.

(1) Early and rapid testing is critically necessary in suspected COVID-19 patients to prevent severe evolution. 

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