COVID-19-associated myocardial injury

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Main article: COVID-19

For COVID-19 frequently asked inpatient questions, click here

For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed rizvi, M.B.B.S[[2]]

Synonyms and Keywords: Novel coronavirus, COVID-19, Wuhan coronavirus, coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, COVID-19, 2019-nCoV, 2019 novel coronavirus, cardiovascular finding in COVID-19, myocardial injury in COVID-19, COVID-19-associated myocardial injury, SARS-CoV2-associated myocardial injury, COVID-19 myocardial injury.

Overview

Coronavirus disease 2019 (COVID-19) is a rapidly expanding global pandemic which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is associated with significant morbidity and mortality. It has been seen to cause myocardial injury, usually in patients requiring hospitalization in more severe cases of SARS-CoV 2 infection. COVID-19 associated myocardial injury is a broad term that is used to describe any cause of myocardial tissue death induced by the SARS-CoV-2 virus. This includes acute coronary syndrome, cardiomyopathy and acute heart failure (with or without cardiogenic shock) and myocarditis. Diagnosis is largely based on an elevated high sensitivity troponin I (hs-TnI) level of > 99th percentile of the upper limit of normal. The exact prevalence of COVID-19 associated myocardial injury is around 5000-38,000 per 100,000 hospitalized individuals worldwide.

Historical Perspective

  • January 2, 2020 - first observational study of 41 patients with COVID-19 pneumonia showed that 5 (12%) of the 41 patients had elevated hs-TnI ( high sensitivity troponin) level above the defined threshold (28 pg/ml) [4]
  • To view the full historical perspective of COVID-19, click here.

Classification

Following careful clinical evaluation, patients with cTn increases indicative of myocardial injury, including those with COVID-19, should be classified as [5]

  • Chronic myocardial injury
  • Acute non-ischemic myocardial injury
  • Acute myocardial infarction (MI).

Chronic myocardial injury:[6]

  • Chronic myocardial injury, a term that applies to patients with chronic stable (<20% change) cTn increases, can be frequently encountered in patients with COVID-19 as the patients are of older age and they have high prevalence of chronic cardiovascular disease.

Acute non-ischemic myocardial injury:[7]

  • Acute non-ischemic myocardial injury, a term that applies to patients with dynamic rising and/or falling cTn concentration without clinical evidence of myocardial ischemia, is probably the predominant mechanism for cTn increases in patients with COVID-19.

Acute myocardial infarction (MI): [8]

  • Symptoms of acute myocardial ischemia;
  • New ischemic electrocardiographic (ECG) changes;
  • Development of pathological Q waves;
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology;
  • Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy
    • To view the classification of COVID-19, click here.

Pathophysiology

The pathophysiology of COVID-19 acute myocardial injury depends on the underlying cause of myocardial tissue death. However, the overall trigger is an exaggerated inflammatory response (hyperinflammation) in response to viral infiltration into cells. SARS-CoV-2 virus gains entry via the ACE-2 (Angiotensin Converting Enzyme 2) receptor that is found abundantly in myocardial tissue and endothelium of blood vessels.

Proposed pathophysiological mechanisms of COVID-19 associated myocardial injury:


Hyperinflammation and cytokine storm:

Role of ACE-2 Receptor :

Pathophysiology of Acute myocardial injury

Causes

Differentiating COVID-19 associated Acute myocardial injury from other Diseases

COVID-19 associated AMI vs non COVID-19 AMI
Causes Similar features Features specific to COVID-19
Acute coronary syndrome

-         STEMI, NSTEMI,[30]

Unstable Angina

-         Type I & II MI

Chest pain

Shortness of breath

Diaphoresis

EKG changes

Elevated troponin I level

Evidence of coronary occlusion by imaging/PCI

Clinical evidence of SARS-CoV2 infection[31]

-         Fever

-         Cough

-         Dyspnea

-         Bilateral ground glass opacities on chest imaging

-         Positive SARS-CoV2 PCR

(Patients may have nonspecific symptoms such as fatigue and malaise without specific symptoms of cardiac disease)

Acute Heart failure[32] Chest pain/pressure

Shortness of breath

Orthopnea

Pulmonary edema

Jugular venous distention

Peripheral edema

Elevated BNP

Depressed ventricular function on echocardiography

Myocarditis[33] Chest pain

Fatigue

S3,S4 or summation gallop

Elevated troponin I

EKG abnormalities

Absence of coronary occlusion

AMI- acute myocardial injury; BNP – Brain Natriuretic peptide; MI – myocardial infarction; NSTEMI - non ST Elevation Myocardial Infarction; PCIpercutaneous intervention; STEMI - ST elevation Myocardial Infarction

Epidemiology and Demographics

Study Site/

Location

Sample size (n) Age (years) Pre-existing cardiac disease Definition of myocardial injury used in study Percent with myocardial injury
Huang et al [34] Wuhan, China 41 Median 49.0 15% cardiovascular disease

15% hypertension

Cardiac injury=troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography 12
Shi et al[35] Wuhan, China 416 Median 64.0 (range 21.0–95.0) 4% chronic heart failure

11% coronary heart disease 31% hypertension

Cardiac injury=troponin I above 99th percentile upper reference limit, regardless of new abnormalities on electrocardiography or echocardiography 19.7
Zhou et al [36] Wuhan, China 191 Median 56.0 8% coronary heart disease

30% hypertension

Cardiac injury=high-sensitivity troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography 17
Guo et al[37] Wuhan, China 187 Mean 58.5±14.7 4% cardiomyopathy

11% coronary heart disease 33% hypertension

Myocardial injury=troponin T above 99th percentile upper reference limit 27.8
Wang et al [38] Wuhan, China 138 Median 56.0 15% cardiovascular disease

31% hypertension

Cardiac injury=troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography 7.2


Incidence

Prevalence

  • The prevalence of myocardial injury (as reflected by elevation in cardiac troponin levels) is variable among hospitalized patients with COVID-19 and is known to be approximately 5,000-38,000 per 100,000 hospitalized individuals worldwide.[39]
  • Reported frequencies range from 5% to 38%[40] [41] [42]
  • In a series of 416 patients with COVID-19 who were hospitalized in Wuhan, China, 19.7 percent had high-sensitivity troponin I (hs-TnI) above the 99th percentile upper reference limit on admission.[43]

Case-fatality rate/Mortality rate

Age

Race

  • As of June 12, 2020, age-adjusted hospitalization rates are highest among non-Hispanic American Indian or Alaska Native and non-Hispanic black persons, followed by Hispanic or Latino persons. CDC
    • Non-Hispanic American Indian or Alaska Native persons have a rate approximately 5 times that of non-Hispanic white persons,
    • Non-Hispanic black persons have a rate approximately 5 times that of non-Hispanic white persons,
    • Hispanic or Latino persons have a rate approximately 4 times that of non-Hispanic white persons

Gender

Region

Risk Factors

Screening

Natural History, Complications, and Prognosis

Complications

Prognosis

Diagnosis

Initial Evaluation of Suspected Acute Myocardial Injury in COVID-19
History [51]
Physical exam
  • No specific findings in ACS
EKG changes
Laboratory evaluation
Imaging studies
[51]



Diagnostic approach to chest pain in COVID-19 [52]

For chest pain diagnostics click here

History and Symptoms

Physical Examination

Laboratory Findings

  • Cardiac Biomarkers:
    • The upper reference limit for the high-sensitivity troponin I (hs-TnI) test (0.04ng/mL), is based on the 99th percentile of measurements reported in healthy population without the occlusion of coronary arteries.[55][56]
    • In the recently published retrospective study of 191 COVID-19 patients from two separate hospitals in China, the incidence of elevation in high-sensitivity cardiac troponin I (cTnI) (>28 pg/ml) was 17%, and it was significantly higher among non-survivors (46% versus 1%, p<0.001).
    • Furthermore, elevation of this biomarker was noted to be a predictor of in-hospital death (univariable OR 80.07, 95% CI [10.34–620.36], p<0.0001). The most abrupt increase in cTnI in non-survivors was noted beyond day 16 after the onset of disease. In the same study, the incidence of acute cardiac injury was 17% among all-comers, but significantly higher among non-survivors (59% versus 1%, p<0.0001).[57]
    • CK-MB >2.2 ng/mL
    • Guo et al11 provide additional novel insights that TnT levels are significantly associated with levels of C-reactive protein and N-terminal pro-B-type natriuretic peptide (NT-proBNP), thus linking myocardial injury to severity of inflammation and ventricular dysfunction[58]
Inflammatory biomarkers:

Electrocardiogram

X-ray

  • There are no specific X-ray findings in COVID-19 associated myocardial injury.
  • To view the x-ray findings on COVID-19, click here.

Ultrasound/Echocardiography

  • There are no specific ultrasound/ echocardiographic findings related to COVID-19-associated acute myocardial injury
  • To view the echocardiographic findings on COVID-19, click here.

CT Scan

  • There are no specific CT scan findings related to COVID-19-associated acute myocardial injury.
  • To view the CT scan findings on COVID-19, click here.

MRI

  • There are no specific MRI findings related to COVID-19-associated acute myocardial injury.
  • To view the MRI findings on COVID-19, click here.

Other Imaging Findings

  • There are no other imaging findings related to COVID-19-associated acute myocardial injury.
  • To view other imaging findings on COVID-19, click here.

Other Diagnostic Findings

  • There are no other diagnostic studies related to COVID-19-associated acute myocardial injury.
  • To view other diagnostic studies for COVID-19, click here.

Treatment

Medical Therapy

Surgery

  • There is no established surgical intervention for the treatment of COVID-19-associated acute myocardial injury.

Primary Prevention

  • There are no available vaccines against COVID-19 and studies are going on for finding an effective vaccine.
  • Other primary prevention strategies include measures to reduce the occurrence of myocardial injury among COVID-19 patients. Recent studies have suggested the use of medications improving microcirculation, especially for the high-risk group such as males, smokers, diabetic patients, and patients with established cardiovascular disease comorbidities.[61]
    • For Risk factors associated with COVID-19 please click here

Secondary Prevention

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