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: Sara Zand, M.D.[2] 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). Myocardial injury presented by high level of cardiac troponin is a common manifestation in COVID-19. The exact pathogenesis of myocardial injury in COVID-19 is not clear yet. However, systemic inflammation, hypoxemia, vasopressor requirement, thrombophilia have been proposed as the underlying mechanisms of myocardial injury. Factors associated with myocardial injury including age, creatinine, multisystem organ failure were similar in both COVID-19 and non COVID-19 patients. Myocardial injury was less common in severe COVID-19 in comparisson with ARDS without COVID-19. However, it was associated with poor outcome in critically ill COVID-19 patients and increased risk of intubation and death. So, Myocardial injury can be the manifestation of underlying critically illness and multisystem organ dysfunction, especially concomitant renal dysfunction, as well as thrombotic complications among COVID-19 patients.

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,[27]

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[28]

-         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[29] Chest pain/pressure

Shortness of breath

Orthopnea

Pulmonary edema

Jugular venous distention

Peripheral edema

Elevated BNP

Depressed ventricular function on echocardiography

Myocarditis[30] 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 [31] 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[32] 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 [33] 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[34] 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 [35] 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.[36]
  • Reported frequencies range from 5% to 38%[37] [38] [39]
  • 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.[40]

Case-fatality rate/Mortality rate

Age

Race

Gender

Risk Factors

Predictors of elevated troponin level in hospitalized COVID-19 were:[42]

Screening

Natural History, Complications, and Prognosis


Complications

Prognosis

  • A retrospective analysis of the cause of death in Chinese patients infected with COVID-19 revealed that 40% of patients died at least in part because of myocardial injury and circulatory collapse.[45]
  • In another study, patients hospitalized for COVID-19 infection developed cardiac injury in roughly 20% of cases; thus leading to greater than 50% mortality.[46]
  • Older patients with preexisting cardiovascular comorbidities and diabetes are prone to develop a higher acuity of illness after contracting SARS-CoV-2 associated with higher risk of myocardial injury and a markedly higher short-term mortality rate.[47]

Diagnosis

Initial Evaluation of Suspected Acute Myocardial Injury in COVID-19
History [49]
Physical exam
  • No specific findings in ACS
EKG changes
Laboratory evaluation
Imaging studies
[49]



Diagnostic approach to chest pain in COVID-19 [50]

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.[53][54]
    • 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).[55]
    • 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[56]
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

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

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

The mainstay of therapy in myocardial injury is:[59]

Surgery

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

Primary Prevention

Secondary Prevention

References

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