COVID-19 & MYOCARDIAL CELL INJURY, COVID-19 myocardial injury in survivors myocardial injury and covid-19 possible mechanisms can covid-19 cause heart

 

COVID-19 & MYOCARDIAL CELL INJURY

 

The common term "myocardial injury" (M.inj) include ALL conditions that lead to cardiomyocyte death.  M.inj can be recognized by the presence of at least one cardiac troponin reading > 99^th percentile upper reference limit (URL). High-sensitivity cardiac troponin levels are sensitive markers of M.inj; however, some ptns with cardiac pathology that cause cardiomyocyte death may express troponin levels < 99^th percentile URL. Possible causes of M.inj that can be seen with COVID-19 may include:

1)    Myocarditis,

2)    Hypoxic injury,

3)    Stress (takotsubo) cardiomyopathy,

4)    Ischemic injury related to cardiac microvascular damage or epicardial coronary artery dis. (plaque rupture or demand ischemia),

5)     Rt heart strain (cor pulmonale), &

6)    Systemic inflamm response syndrome (cytokine storm).

However, the contribution of each of these putative causes to myocardial injury in this setting has not been recognized. Thus far, viral myocarditis caused by SARS-CoV-2 hs not bn definitively confirmed by myocardial histologic & viral genome analysis. To approve that COVID-19 is a new causative of viral myocarditis may necessitate:

1)    Recognition of histologic criteria of active myocarditis,

2)    Identification of SARS-CoV-2 genome in heart tissue,

3)    Recognition of viral particles in the cardiomyocytes, &

4)    Exclusion of other cardio-tropic viruses.  

 

Myocardial injury (raised cardiac troponin) is common among ptns hospitalized with COVID-19, but the real cause of M.inj hv not bn clarified, and its contribution to incident HF has not been well defined. Greater frequency & magnitude of troponin rise can be observed with more severe disease and worse outcome.  Incident HF can be commonly observed in hospitalized ptns with COVID-19. HF in COVID-19 may be induced by acute illness in ptns with preexisting known or undiagnosed heart disease (e.g., CAD or HT heart disease) or incidental acute myocardial injury (e.g., AMI, stress cardiomyopathy, etc..). Most ptns with COVID-19 with clear evidence of myocardial injury present with the typical Sms & Sns of SARS-CoV-2 infection (e.g. fever, cough, SOB, & bilateral infiltrates on radiological studies). A minority of ptns with COVID-19 with evidence of M.inj may present with classic cardiac Sms (e.g. chest pain or palpitations).  

 

 

The pattern of cardiac troponin rise in hospitalized ptns with COVID-19 includes mild limited elevation (the most common one), a moderate time-limited rise (approaching or exceeding 99^th percentile URL), and a progressive one with moderate rise followed by a progressive rise along an elevation of other biomarkers consistent with cytokine storm. If the clinical picture is suggestive of acute coronary syndrome (ACS), proper evaluation is warranted to determine if urgent intervention is needed. Most ptns with COVID-19 with no suspected ACS, with mild troponin rise, and without acute HF can be clinically monitored with no need cardiac imaging. For ptns who develop new onset HF, echocardiogram may be performed to determine regional & global ventricular & valvular malfunction as decided by a cardiologist decisions and is expected to hv a significant reflection on management or has an impact patient's outcome.

 

As there’s no established treatment for clinically suspected myocarditis, routine evaluation for myocarditis is NOT recommended in COVID-19 ptns. Evaluation for myocarditis by endo-myocardial biopsy (with or without prior cardiac MRI) may be appropriate in selected cases if a treatable myocarditis is suspected (e.g., giant cell myocarditis) or with finding of intense unexplained biventricular malfunction, unexplained cardiogenic shock, or unexplained life-threatening arrhythmia with normal coronary arteries (with/without troponin elevation) to confirm a definitive diagnosis of myocarditis and identify its etiology. As biopsy-proven myocarditis is widely prevalent in young ptns but rarely seen in elderlies, clinical suspected myocarditis should be higher, and the threshold to t proceed to an endo-myocardial biopsy should be lowered in young ptns without CVS comorbidities. Optimal management for M.inj seen with COVID-19 has not been recognized. So, management of M.inj, including those with clinically suspected myocarditis (with or without CVS MRI confirmation), include supportive care (including management of HF, control for arrhythmias and prohibition of cardio-toxins).

 

REFERENCES

v  Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol 2020; 5:802.

v  Creel-Bulos C, Hockstein M, Amin N, et al. Acute Cor Pulmonale in Critically Ill Patients with Covid-19. N Engl J Med 2020; 382:e70.

v  Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol 2020; 17:259.

v  Tersalvi G, Vicenzi M, Calabretta D, et al. Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms. J Card Fail 2020; 26:470.

v  Inciardi RM, Lupi L, Zaccone G, et al. Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol 2020; 5:819.

v  Zeng JH, Liu YX, Yuan J, et al. First case of COVID-19 complicated with fulminant myocarditis: a case report and insights. Infection 2020; 48:773.

v  Hu H, Ma F, Wei X, Fang Y. Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin. Eur Heart J 2020.

v  Fried JA, Ramasubbu K, Bhatt R, et al. The Variety of Cardiovascular Presentations of COVID-19. Circulation 2020; 141:1930.

v  Tavazzi G, Pellegrini C, Maurelli M, et al. Myocardial localization of coronavirus in COVID-19 cardiogenic shock. Eur J Heart Fail 2020; 22:911.

v  Kim IC, Kim JY, Kim HA, Han S. COVID-19-related myocarditis in a 21-year-old female patient. Eur Heart J 2020; 41:1859.