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2020 ; 5
(5
): 537-542
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The Heart in COVID-19: Primary Target or Secondary Bystander?
#MMPMID32292847
Libby P
JACC Basic Transl Sci
2020[May]; 5
(5
): 537-542
PMID32292847
show ga
In the throes of the current coronavirus disease-2019 (COVID-19) pandemic,
interest has burgeoned in the cardiovascular complications of this virulent viral
infection. As troponin, a biomarker of cardiac injury, often rises in
hospitalized patients, its interpretation and actionability require careful
consideration. Fulminant myocarditis due to direct viral infection can certainly
occur, but in patients with increased oxygen demands due to tachycardia and fever
and reduced oxygen delivery due to hypotension and hypoxemia, COVID-19 disease
can cause myocardial injury indirectly. Cytokines released during the acute
infection can elicit activation of cells within pre-existing atherosclerotic
lesions, augmenting thrombotic risk and risk of ischemic syndromes. Moreover,
microvascular activation by cytokines can cause not only myocardial injury but
can also harm other organ systems commonly involved in COVID-19 infections
including the kidneys. Dealing with the immense challenge of COVID-19, confronted
with severely ill patients in dire straits with virtually no rigorous evidence
base to guide our therapy, we must call on our clinical skills and judgment.
These touchstones can help guide us in selecting patients who might benefit from
the advanced imaging and invasive procedures that present enormous logistical
challenges in the current context. Lacking a robust evidence base,
pathophysiologic reasoning can help guide our choices of therapy for individual
clinical scenarios. We must exercise caution and extreme humility, as often
plausible interventions fail when tested rigorously. But act today we must, and
understanding the multiplicity of mechanisms of myocardial injury in COVID-19
infection will help us meet our mission unsupported by the comfort of strong
data.