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 > 99th 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 < 99th 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 99th 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).
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