key: cord-0791863-up7ept00
authors: Tutor, Austin; Unis, Graham; Ruiz, Brent; Bolaji, Olayiwola Akeem; Bob-Manuel, Tamunoinemi
title: Spectrum of Suspected Cardiomyopathy due to COVID-19: A Case Series
date: 2021-07-03
journal: Curr Probl Cardiol
DOI: 10.1016/j.cpcardiol.2021.100926
sha: d66fc3d73692da26df0ca094d60f589ef7f1e984
doc_id: 791863
cord_uid: up7ept00

INTRODUCTION: : The effects of COVID-19 on the cardiovascular system remains understudied given the early stage of the pandemic. Several case series and case reports have been published on COVID-19 related cardiomyopathies; however, there is often a lack of baseline echocardiographic data confirming a normal cardiac health prior to infection. Here we examine four patients with preserved left ventricular systolic function on prior echocardiogram who developed de novo cardiomyopathies which following COVID-19 infection. METHODS AND OUTCOMES: : The study comprised of four individuals with an average age of 80.5 years, 75% of which were white males. 50% of cases were suspected to have Takotsubo CM vs. myocarditis while the remaining half were diagnosed as myocarditis. Left ventricular systolic function dropped from a normal range to an average of 30% during COVID-19 infection in these individuals. Moreover, half of the cases later died. CONCLUSION: : In conclusion, the COVID-19 pandemic has demonstrated its ability to cause several serious cardiovascular complications with associated worsening of prognosis. Repeat TTE showed recovery of systolic function in 50% of the patients included. There does not appear to be any correlation between COVID-19 related treatments, age, or level of inflammatory markers in those who recovered systolic function versus those who remained depressed. Given the minimal literature on this topic, it is evident more information is needed to help advance treatment and understanding of COVID-19 induced cardiomyopathies; particularly if the vaccination fails to protect against novel strains of COVID-19 and the virus becomes endemic.

The effects of COVID-19 on the cardiovascular system remains understudied given the early stage of the pandemic. Current research suggests COVID-19 can cause a broad spectrum of cardiac injuries and cardiomyopathies (CM) such as myocarditis, stress, or ischemic. Numerous mechanisms have been purposed which include direct myocardial injury from the cytokine storm, down regulation of angiotensin converting enzyme 2 (ACE2) receptors, and supply/demand mismatch (1). Many are felt to be related to the severe inflammatory response; however, this link remains an area of intense research. Regardless of the cause, COVID-19 associated CM can severely worsen morbidity and mortality during active infection and have unclear long-term implications; therefore, more research is needed to direct therapy.

Several case series and case reports have been published on COVID-19 related cardiomyopathies; however, there is often a lack of baseline echocardiographic data confirming a normal cardiac health prior to infection. Here we examine 4 patients with preserved LVEF on prior echocardiogram who developed de novo cardiomyopathies following COVID-19 infection. Also, we demonstrate that some of these patients regained their systolic function following resolution of their acute illness suggesting a reversible cardiomyopathy in patients managed promptly. U/L, lactic acid 1.5 mmol/L, mildly elevated LFT's, troponin 0.079 ng/ml. CXR showed bilateral multifocal infiltrates. Patient was initially started on empiric community acquired pneumonia treatment with azithromycin. Hydroxychloroquine was held for concern of QT prolongation. Shortly after admission he became hypotensive and was moved to the ICU for vasopressor requirements.

Subsequently, started on broad spectrum antibiotics and steroids. Repeat EKGs showed diffuse twave inversions. Peak troponin 3.170 ng/ml. Cardiology was consulted due to initial concern of NSTEMI as cause of hypotension. Stat TTE showed LVEF of 30%, severely depressed LV systolic function, and global hypokinesis with akinesis of the apex and basal sparing. Given no chest pain, diffuse EKG pattern and TTE findings, there was a high likelihood for secondary myocarditis or Takotsubo CM. On hospital day 7, was weaned off oxygen and discharged home. Upon discharge, he was continued on a beta blocker and ACE inhibitor, both prescribed prior to admission. Repeat owing to the fact that the entry protein, ACE2, is heavily expressed in heart, vascular, and pulmonary tissue (1). Acute myocardial injury, defined as an elevation in cardiac troponins, was common in hospitalized patients with COVID-19. In one review, between 8-62% of hospitalized patients demonstrated elevated troponins with a wide range (3, 4) . It was found to be strongly associated with worse clinical outcomes initially from Wuhan and confirmed in other studies (1,5).

Since this discovery, COVID-19 has been associated with numerous cardiovascular complications ranging from acute myocardial injury, arterial thrombosis, myocarditis, tachyarrhythmias, and acute cardiomyopathies (1,2). The diverse cardiovascular complications of COVID-19 are well highlighted in the above 4 cases.

Myocarditis was included in the differential diagnosis of all our cases; however, given the wall motion abnormalities seen on echo in Cases 1 and 3, Takotsubo CM was suspected. Takotsubo cardiomyopathy (TTS) has been previously documented as associated with COVID-19 infection.

Among COVID-19 patients receiving TTE, echocardiogram findings suggestive of stress cardiomyopathy was noted in 1.5%-5.6% of patients (6, 7) . A recent systematic review compilating 27 reported cases associated with COVID-19 was recently published which delineated a number of imaging characteristics including a proposed pathophysiologic mechanism for cytokine storm induced TTS (8) . Additionally, patients with COVID-19 induced TTS were found to have higher mortality than patients with matched cardiovascular risk factors (8) . In this case series, one of the two patients with suspected TTS expired; however, Case 3 had eventual recovery of systolic function. Of note, both cases of suspected TTS had significant elevation of troponin levels compared to the other patients, which may indicate a higher level of inflammation and myocardial damage, leading to a more severe cardiomyopathy such as TTS.

COVID-19 induced myocarditis is thought to occur via non-ischemic pathophysiology. Prior studies with endomyocardial biopsies have yielded classic T cell mediated inflammatory infiltrate and further characteristic MRI findings (11) . Patients include in prior reports had drastically elevated biomarkers, global wall motion abnormalities, and require inotropic support for cardiogenic shock which frequently developed (11) . Due to this similarity in presentation to stress cardiomyopathy, diagnosis must be made meticulously as inotropic support in TTS would worsen prognosis. In this case series, patients 2 and 4 appeared to have findings more consistent with myocarditis. Both patients had no focal ischemic changes on EKG, minimally elevated troponins, no angina, and a newly depressed LVEF. Unfortunately, given the COVID-19 positive status and early timing of the pandemic, our facility was limiting MRI use for COVID-19 patients; therefore, no definitive diagnosis of myocarditis could be established. Of the myocarditis patients, only Case 4 had recovery of systolic function; Case 2 did not have recovery of LVEF which may be secondary to patients age, deconditioning, and comorbid medical conditions. All patients in this case series were evaluated by cardiology and thought to not have acute coronary syndrome given the above-mentioned findings of non-localizing EKG and echo findings in absence of anginal type chest pains. Furthermore, 75% of the patients had follow up TTEs and EKGs with no noted wall motion abnormalities in coronary distribution or pathologic q-waves, respectively.

In conclusion, the COVID-19 pandemic has demonstrated its ability to cause several serious cardiovascular complications with associated worsening of prognosis. Here we presented four patients with suspected myocarditis or Takotsubo CM and varying outcomes. Repeat TTE showed recovery of systolic function in 50% of the patients included. Of these, both were restarted on goal directed medical therapy with exception of Case 4 where ACEi/ARB was held due to acute on ESRD. There does not appear to be any correlation between COVID-19 related treatments, age or level of inflammatory markers in those who recovered systolic function versus those who remained depressed. This may be partly due to concurrent comorbidities. Given the minimal literature on this topic, it is evident more information is needed to help advance treatment and understanding of COVID-19 induced cardiomyopathies; particularly if the vaccination fails to protect against novel strains of COVID-19 and the virus becomes endemic.

All authors have no conflict of interest to disclose.

COVID-19 and Cardiovascular Disease: From Bench to Bedside

What We Know in 2021

Characterization of Myocardial Injury in Patients With COVID-19

Cardiac Troponin for Assessment of Myocardial Injury in COVID-19: JACC Review Topic of the Week

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Indications for and Findings on Transthoracic Echocardiography in COVID-19

Global evaluation of echocardiography in patients with COVID-19

Takotsubo Syndrome a Rare Entity in COVID-19: a Systemic Review-Focus on Biomarkers, Imaging, Treatment, and Outcome

International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology

Cardiovascular Manifestations of COVID-19