COVID-19 affects not only the respiratory system, but also the cardiovascular system. The damage to the cardiovascular system in COVID-19 is multifactorial and several mechanisms are involved, including direct invasion, inflammation, thrombosis, autoantibody synthesis, and oxygen imbalance. The inflammation causes the release of cytokines, especially interleukin-6, and damage to cardiomyocytes. The overproduction of cytokines leads to an abnormal inflammatory response called a cytokine storm, which is believed to be the culprit in cardiovascular events in COVID-19 patients.
Cardiovascular disease is common in patients with COVID-19, and these patients are at increased risk of morbidity and mortality. There is still no data on cardiac dysfunction due to myocardial damage in patients recovering from COVID-19. Most often, this is normal heart function after complete recovery. But often there are myocardial damage and an increased level of troponin as a marker of the severity of the disease associated with a cytokine storm, hypoxia, vasopressors and blood clotting disorders. It is important for every physician to make a differential diagnosis between decompensated heart failure complicated by pulmonary infection and COVID-19 infection. Monitoring and influencing myocardial injury is extremely important in critically ill patients.
Treatment of COVID-19 patients with cardiovascular complications is mostly supportive. The role of pharmacological blocking of the reninangiotensin-aldosterone system in patients with cardiovascular disease and COVID-19 infection requires further research as the relationship appears to be very complex. To date, professional cardiological societies do not recommend canceling ACE inhibitors or agiotensin II receptor antagonists for patients taking these drugs for other indications. Special care should be taken about the potential cardiovascular side effects of the various therapies used to treat viral infections. When using them, daily monitoring of the QT interval on the ECG is proposed.
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