In December, 2019 the koronavirusny disease of 2019 (COVID-19) was for the first time described to Wuhan (China) at the patients complaining of the symptoms reminding flu symptoms. The virus was allocated and identified as a new strain of a coronavirus which received the name SARS-CoV-2 (the coronavirus causing a heavy acute respiratory syndrome). The death rate from COVID-19 is on average estimated at 1%, generally because of a heavy acute respiratory syndrome and multiorgan insufficiency.
Traditionally pay less attention to cardiovascular complications of COVID-19 though about myocarditis cases at patients with COVID-19 it is reported, and myocarditis was recognized as a cause of death of some patients with COVID-19. Myocarditis is the inflammation of a muscle of heart characterized by availability of inflammatory infiltrate and injury of a myocardium without his ischemia. The virus nature of myocarditis is most widespread in the developed countries. This pathology at COVID-19 usually affects directly a myocardium, but there is a risk of developing of arrhythmia, with progressing to fulminantny heart failure and cardiogenic shock.
Now it is supposed that the pathophysiology of viral myocarditis represents a combination of direct cellular damage and the cytotoxicity caused by T lymphocytes which can be increased by a syndrome of a tsitokinovy storm. Interleukin-6 (IL-6), apparently, is the main mediator of a tsitokinovy storm in which it manages pro-inflammatory answers of immune cells, including T lymphocytes. This process causes activation of T lymphocytes and further release of inflammatory cytokines which stimulate development of a large number of T lymphocytes that leads to positive feedback of immune activation and injury of a myocardium. It is considered that the cardiotropism of T lymphocytes results from interaction of the growth factor of hepatocytes (HGF) produced by heart and with-Met (HGF receptor on naive T lymphocytes).
It is also necessary to note that not one SARS-CoV-2 can cause myocarditis, this ability also other coronaviruses have. In spite of the fact that coronaviruses of the person are the insignificant reason of all cases of viral myocarditis, they can the myocarditis reason at patients of all age groups. Virus RNA of a coronavirus of a Middle Eastern respiratory syndrome (MERS-CoV) and SARS-CoV which are close relatives of SARS-CoV-2 were found in tissues of heart of the infected animals that allows to assume that these coronaviruses have cardiotropism. Besides, it was proved that some proteins of a coronavirus do them very infectious for cells of the person.
The prevalence of myocarditis among patients with COVID-19 is not clear, partly because in the first reports diagnostic methods of assessment of myocarditis often were not specified. Some researchers claimed that they to 7% of death connected with COVID-19 were connected with myocarditis. But it only the assumption which cornerstone unconfirmed myocarditis is so this indicator could be overestimated. But, on the other hand, it agrees to one of reports, 24.5% of patients with COVID-19 have the coinfection caused by other viruses. Proceeding from it, it is possible that many cases of the myocarditis caused by COVID-19 are passed due to the lack of diagnostics of SARS-CoV-2.
Arrhythmia is considered one of clinical manifestations of COVID-19. Researches showed that a cardiopalmus was observed on average at 7.3% of patients. Moreover, it was reported that arrhythmia was the cause of the transfer to intensive care unit at 44.4% of patients with COVID-19. The exact nature of arrhythmia usually is not reported therefore it is difficult to estimate whether there was arrhythmia earlier or is secondary in relation to other states, such as disturbance of electrolytic balance. Thus, the actual prevalence of arrhythmia at patients with COVID-19 remains to the unknown. Nevertheless, as it is well known, arrhythmia can arise also owing to myocarditis.
Clinical manifestations of the myocarditis caused by SARS-CoV-2 differ occasionally. Some patients can have rather easy symptoms, such as fatigue and asthma whereas others report about a stethalgia or to feeling of a prelum in a thorax at loading. In hard cases patients can have symptoms of right ventricular heart failure, including supertension in a jugular vein, peripheral hypostasis and pain in the right top quadrant of a stomach. The most obvious manifestation is the fulminantny myocarditis defined as dysfunction of ventricles and heart failure 2–3 weeks later after infection with a virus.
Treatment of myocarditis includes introduction of inotrop and/or vazopressor and mechanical ventilation of the lungs, mechanical support of blood circulation, such as extracorporal membrane oxygenation, auxiliary ventricular device or intra aortal balloon counterpulsation.