| Abstract [eng] |
Based on the studies reviewed in this thesis, COVID-19 is associated with cardiovascular diseases as well as structural alterations of the myocardium, both through direct cardiac injury and indirectly through affecting multiple organ systems, which may worsen underlying cardiac diseases or even cause cardiovascular diseases through vascular dysfunction or inflammation. COVID-19 disease has been associated with coagulation abnormalities both clinically and histopathologically, and evidence suggests vascular inflammation and endothelial dysfunction could occur due to COVID-19 infection. Importantly, the major pathophysiological trigger for organ dysfunction, including cardiovascular manifestations, is an imbalanced immune system response. Myocardial injury in association with COVID-19 has been recognized as a significant predictor of mortality in patients. This highlights the importance of establishing prognostic markers and novel treatments to decrease the incidence of myocardial injury. In addition, the downregulation of the Angiotensin-converting enzyme 2 (ACE2) receptor as a defense mechanism and consequent unwanted downregulation of myocardial protective effects provides an interesting topic for further research as a possible therapeutic target or a marker of complications. However, it seems that while initially COVID-19-myocarditis was reported fairly frequently, the prevalence of myocarditis fulfilling diagnostic criteria is rare, while inflammation of the myocardium on imaging and histopathology is more common. As myocardial inflammation without myocarditis has been reported in imaging and histopathological studies consistently, more research is required to assess its effect on developing cardiac comorbidities in the future. Other structural alterations such as hypertrophy and fibrosis of the myocardium have been reported on autopsies and imaging, but to determine whether they are directly due to COVID-19 infection, or due to underlying cardiac pathology, is still undetermined. Further research is required to determine the causality between COVID-19 and the aforementioned structural changes in the myocardium. Long-term studies on the relationship between COVID-19 and the risk of developing cardiovascular diseases after initial infection are limited, but recent studies with relatively large patient cohorts have been able to demonstrate an increased 12-month risk of cardiovascular disease, even in patients without prior known comorbidities. |
