Updated: April 10, 2020
Definition and incidence
- Definition: The definition differs in studies and is non-specific. More recent studies define as troponin > 99th percentile upper limit of normal; earlier studies include abnormal ECG or echocardiographic findings (Zhou et al, Lancet, 2020; Shi et al, JAMA Cardiology, 2020).
- Incidence: Incidence of 7-22% in hospitalized patients with COVID-19 in China (Ruan et al, Intensive Care Med, 2020; Wang et al, JAMA, 2020; Chen et al, Lancet, 2020; Shi et al, JAMA Cardiology, 2020; Guo et al, JAMA Cardiology, 2020).
- The mechanism is unknown, though several have been proposed, based on very limited data outside of case series and reports (Ruan et al, Intensive Care Med, 2020; Hu et al, Eur Heart J, 2020; Zeng et al, Preprints, 2020; Inciardi et al, JAMA Cardiology, 2020)
- Possible direct toxicity through viral invasion into cardiac myocytes (i.e., myocarditis)
- Acute coronary syndrome and demand ischemia
- Stress cardiomyopathy (i.e., Takotsubo’s)
- Myocardial suppression in the setting of profound inflammatory response/cytokine storm (Siddiqi & Mehra, Journal Heart Lung Transpl, 2020)
Time course and prognostic implication
- Troponin rise and acute cardiac injury may be late manifestations of COVID-19.
- Troponin increased rapidly from ~14 days from illness onset, after the onset of respiratory failure (Zhou et al, Lancet, 2020).
- Among non-survivors, a steady rise in troponin I levels was observed throughout the disease course from day 4 of illness through day 22 (Zhou et al, Lancet, 2020).
- ACI is associated with ICU admission and mortality
- ACI is higher in non-survivors (59%, n=32) than survivors (1%, n=1) (Zhou et al, Lancet, 2020).
- ACI is higher in ICU patients (22%, n=22) compared to non-ICU patients (2%, n=2) (Wang et al, JAMA, 2020)
- Cardiology Consultation
- The following clinical scenarios should prompt cardiology consultation:
- Malignant and unstable arrhythmias
- A marked rise in cardiac biomarkers (including hsTnT >200 ng/L)
- Concern for myocarditis
- Concern for ACS
- New heart failure or new reduction in LVEF
- Undifferentiated or suspected mixed or cardiogenic shock
- Cardiovascular Testing
- Please see cardiovascular testing in the Diagnostics section
- Case series report the occurrence of unspecified arrhythmias in 17% of hospitalized patients with COVID-19 (n=23 of 138), with higher rate in ICU patients (44%, n=16) compared to non-ICU patients (7%, n=7) (Wang et al, JAMA, 2020). In one study of 189 hospitalized patients in Wuhan, China, the rate of VT/VF was 5.9% (n=11) (Guo et al, JAMA Cardiology, 2020).
- Telemetry, 12-lead EKG, cardiac troponin, NT-proBNP, TFT
- ScvO2 if central line present (ScvO2 <60%, trigger for further workup or cardiology consultation).
- POCUS to assess LV and RV function with uploaded images
- Obtain formal TTE and consider cardiology consultation if abnormalities of any of the above
- Atrial fibrillation/atrial flutter
- Beta blockade if no evidence of heart failure or shock
- If significant heart failure or borderline BPs, use amiodarone. There is no known increased concern for amiodarone lung toxicity
- If unstable, synchronized DCCV with 200 Joules biphasic
- Ventricular tachycardia (VT)
- Unstable/pulseless: initiate ACLS
- Cardiology consult (may represent evolving myocardial involvement)
- Amiodarone 150mg IV x 1 or lidocaine 100mg IV x 1
- There is no current available data on the incidence of ACS in COVID. However, we presume that due to the presence of ACE2 receptors on the endothelium, and the known increased risk of ACS in influenza that there is a possible increased incidence of ACS among COVID-19 patients.
- The incidence of ACS is about 6 times as high within seven days of an influenza diagnosis than during the control interval - incidence ratio 6.05 (95% CI, 3.86 to 9.50) (Kwong et al, NEJM, 2018).
- Elevated troponin/ECG changes alone may not be able to discriminate between:
- Coronary thrombosis
- Demand-related ischemia
- Toxic myocardial injury (e.g. sepsis)
- Determination of ACS will rely on all evidence available:
- Symptoms (if able to communicate): New dyspnea, chest pain, anginal equivalents
- Regional ECG changes
- Rate of change of Troponin changes (i.e., steep rise suggests ACS)
- Echo findings (e.g., new RWMA): When in doubt, request a cardiology consult.
- When in doubt, request a cardiology consultation
- Medical management of ACS should be coordinated with cardiology
- Treat with full dose aspirin, clopidogrel (if not bleeding), heparin, oxygen (if hypoxemic), statin, nitrates (if hypertensive), and opioids (if persistent pain during medical management).
- Beta blockers should be used with caution given possible concomitant myocarditis/decompensated heart failure.
- As of the time of this writing, the cath lab will take COVID-19 patients, even if ventilated.
- If resources become constrained and door-to-balloon time is no longer adequate, cardiology may decide to use lytic medications for COVID-19 STEMI patients in lieu of PCI.
- Myocarditis and pericarditis are potential manifestations of COVID-19 and source of Acute Cardiac Injury, based on case reports/case series (Ruan et al, Intensive Care Med, 2020; Zeng et al, Preprints, 2020; Hu et al, Eur Heart J, 2020; Inciardi et al, JAMA Cardiology, 2020). One case report had cMRI proven myocarditis and a concomitant reduction in LVEF to 35% with rapid resolution after antiviral treatment and systemic glucocorticoids (Inciardi, et al, JAMA Cardiology, 2020).
- Likely no role for endomyocardial biopsy
- cMRI should be discussed on a case-by-case basis with a cardiology consult team.
- Supportive for heart failure and direct viral treatments
- The use of steroids and anti-inflammatory medications such as Colchicine and Ibuprofen should also be discussed with the cardiology consult team as this literature is evolving.
- The literature available on COVID-19 in patients with a history of heart transplantation is limited. Currently, there are two published case series from China (Zong-Li et al, Journal of Heart Lung Transplantation, 2020; Fei Li et al, Journal of Heart Lung Transplantion, 2020). In one case series of two patients, one severe and one mild, both recovered.
- In heart transplant patients presenting with symptoms, positive for SARS-Co-V-2 and no pulmonary findings (normal CXR, none to mild CT findings, no hypoxia)
- Exclude co-infection (e.g. CMV) and bacterial infection (procalcitonin >0.5ng/ml)
- Maintain baseline immunosuppression (avoid over-immunosuppression)
- Continue ACEi/ARB//Statins
- Do not augment steroids
- Check troponins and NT-proBNP, monitor CRP and other indices of inflammation (platelets, LDH, ferritin, d-dimer)
- In heart transplant patients with proven COVID-19 pneumonia (CT findings and hypoxemia)
- Hold MMF/AZA/SRL
- Consider holding tacrolimus if renal dysfunction or diarrhea (where levels are expected to rise); in others consider decreasing dose by 50%
- Use low dose IV steroids as main immunosuppression (do not exceed 0.5-1mg/kg methyprednisolone)
- Exclude co-infection as above (including CMV, pneumocystis and fungal infections) and use empiric antimicrobials in consultation with ID teams
- It is reasonable to add antiviral therapy via clinical trials (IV remdesivir) or other trial-based treatments
- Special circumstances
- With evidence of hyper-inflammation (d-dimer > 1,000, low platelets, markedly high CRP, ferritin > 1,000, IL-6 > 40) would strongly consider tocilizumab (8mg/kg IV over 60 minutes) early rather than late in the disease course
- Follow cardiac allograft function closely (check troponins, TTE for increased LV wall thickness or decline in allograft function, QRS amplitude decrease, raised filling pressures clinically, significantly elevated NT-proBNP) and consider tocilizumab with higher dose steroids (1 mg/kg methylprednisolone); in a case-by-case basis may consider use of IVIG (10-20 mg/kg over 2-3 days)
- Once recovery ensues restart CNI at usual dose and adjunctive (MMF) at 50% of baseline dose until viral recovery is seen (2 negative NAT), then return to baseline as tolerated. There is uncertain benefit to switch to mTOR (known benefit in CMV suppression)