Page 76 - Mesenchymal Stem cells, Exosomes and vitamins in the fight aginst COVID

Intravascular Mesenchymal Stem Cells to Treat Organ Failure and Possible Application in COVID-19

and mechanical ventilatory support when indicated respiratory syndrome coronavirus 2 (SARS-CoV-2) vi-
(11). The National Institute of Health treatment rus infects type II alveolar epithelial cells and causes
guidelines recommend the cautious use of Remde- COVID-19. After infection, COVID-19 progresses to a
sivir, hydroxychloroquine, convalescent plasma, and viral replicative phase of this disease that clinically
interleukin-6 inhibitors, and state that they must be may present as mild flu-like symptoms. This phase
used mostly in the setting of clinical trials. The lack is followed by a massive release of proinflamma-
of treatment options leads to a desperate need for tory cytokines causing heightened inflammatory
novel therapies in patients afflicted with serious reaction and increased activity of immune cells. This
complications from COVID-19. Mesenchymal stem causes recruitment of inflammatory cells, such as
cells (MSCs), also known as medicinal signaling cells, macrophages, to the lungs and disrupts the junctions
mostly through their paracrine activity secrete growth between alveolar epithelial cells and capillary endo-
factors, cytokines, and chemokines resulting in tissue thelial cells. Eventually an alveolar-capillary barrier is
regeneration and improved organ function. Here we formed causing influx of proteinaceous fluid into the
want to explore the possibility of MSCs in treating alveoli. Injury to the alveolar epithelial cells causes
severe complications from COVID-19 to decrease mor- accumulation of fluid in the alveoli that interferes
bidity and mortality. with normal gas exchange, subsequently causing
impaired oxygenation leading to hypoxemia. Wide-
Pathophysiology of Multiorgan spread pulmonary inflammation also induces the
Complications with COVID-19 hypoxic state and produces excessive extracellular
Even though respiratory compromise is the major calcium levels leading to myocyte apoptosis contrib-
clinical manifestation of COVID-19, cardiovascular uting to extensive pulmonary injury .
and other organ involvement may be responsible for
eventual poor outcome. Autopsy reports have also Cardiovascular Complications in Patients
shown direct myocardial injury due to viral load on with COVID-19
cardiomyocytes, with systemic surge of inflammation The most common cardiovascular complication
appearing to be contributing to cardiovascular and in COVID-19 is acute myocardial injury marked by
other multiorgan injury. Even though the most domi- elevated cardiac enzymes, specifically elevated car-
nant clinical manifestation of COVID-19 starts with re- diac troponin I (cTnI). The overall incidence of acute
spiratory symptomatology with a mild flu-like illness, cardiac injury with elevated troponin (cTnI) varies
in some cases it progresses to potentially lethal ARDS between 8% and 12% (14). The incidence of acute
or life-threatening pneumonia, and preexisting car- cardiac injury has consistently shown to be a nega-
diovascular disease risk factors enhance vulnerability tive prognostic marker in patients with COVID-19
to COVID-19, leading to deadly outcome. . A study by Wang et al (15) in 138 patients with
COVID-19 reported 16.7% incidence of arrhythmia.
Respiratory Complications of COVID-19 The incidence was much higher (44.4%) in those re-
The pulmonary complication pneumonia, charac- quiring ICU admission as compared with those not
terized by cough, fever, and dyspnea, and bilateral requiring ICU admission (8.9%).
infiltrates seen on imaging studies, is the most fre-
quent and serious manifestation of COVID-19 infec- Pathophysiology of Cardiac Complications
tion. Fortunately, most patients will only experience The respiratory tract is the prime target for
mild symptoms of the disease, and some patients may SARS-CoV-2; however, the cardiovascular system is
experience rapid progression of their symptoms in involved in many different ways . The hyperinflam-
a few days. The study by Chen et al (12) found that matory response due to cytokine surge, hemophago-
in those patients who developed ARDS, 65% rapidly cytic lymphohistiocytosis, and increased myocardial
worsened and died from multiple organ failure. Wu demand in the setting of acute infection can lead
et al (13) reported that ARDS was frequently associ- to rupture of the atherosclerotic plaque leading to
ated with older age (> 65 years), diabetes mellitus, acute myocardial infarction. The blood pressure ab-
and hypertension. Imaging studies of these patients normalities and cardiac arrhythmia of multifactorial
showed bilateral lower zone consolidation in 10 to 12 etiology, myocarditis, and hypoxic state due to ARDS,
days from the onset of symptoms. The severe acute may lead to reduced ejection fraction and heart en-

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