ABSTRACT
As the world progressively recovers from the acute stages of the coronavirus disease 2019 (COVID-19) pandemic, we may be facing new challenges regarding the long-term consequences of COVID-19. Accumulating evidence suggests that pulmonary vascular thickening may be specifically associated with COVID-19, implying a potential tropism of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) virus for the pulmonary vasculature. Genetic alterations that may influence the severity of COVID-19 are similar to genetic drivers of pulmonary arterial hypertension. The pathobiology of the COVID-19-induced pulmonary vasculopathy shares many features (such as medial hypertrophy and smooth muscle cell proliferation) with that of pulmonary arterial hypertension. In addition, the presence of microthrombi in the lung vessels of individuals with COVID-19 during the acute phase, may predispose these subjects to the development of chronic thromboembolic pulmonary hypertension. These similarities raise the intriguing question of whether pulmonary hypertension (PH) may be a long-term sequela of SARS-COV-2 infection. Accumulating evidence indeed support the notion that SARS-COV-2 infection is indeed a risk factor for persistent pulmonary vascular defects and subsequent PH development, and this could become a major public health issue in the future given the large number of individuals infected by SARS-COV-2 worldwide. Long-term studies assessing the risk of developing chronic pulmonary vascular lesions following COVID-19 infection is of great interest for both basic and clinical research and may inform on the best long-term management of survivors.
ABSTRACT
Myocarditis has been discovered to be a significant complication of coronavirus disease 2019 (COVID-19), a condition caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. COVID-19 myocarditis seems to have distinct inflammatory characteristics, which make it unique to other viral etiologies. The incidence of COVID-19 myocarditis is still not clear as a wide range of figures have been quoted in the literature; however, it seems that the risk of developing myocarditis increases with more severe infection. Furthermore, the administration of the mRNA COVID-19 vaccine has been associated with the development of myocarditis, particularly after the second dose. COVID-19 myocarditis has a wide variety of presentations, ranging from dyspnea and chest pain to acute heart failure and possibly death. It is important to catch any cases of myocarditis, particularly those presenting with fulminant myocarditis which can be characterized by signs of heart failure and arrythmias. Initial work up for suspected myocarditis should include serial troponins and electrocardiograms. If myocardial damage is detected in these tests, further screening should be carried out. Cardiac magnetic resonance imagining and endomyocardial biopsy are the most useful tests for myocarditis. Treatment for COVID-19 myocarditis is still controversial; however, the use of intravenous immunoglobulins and corticosteroids in combination may be effective, particularly in cases of fulminant myocarditis. Overall, the incidence of COVID-19 myocarditis requires further research, while the use of intravenous immunoglobulins and corticosteroids in conjunction requires large randomized controlled trials to determine their efficacy.
ABSTRACT
BACKGROUND AND OBJECTIVES: Reports comparing the characteristics of patients and their clinical outcomes between community-acquired (CA) and hospital-acquired (HA) COVID-19 have not yet been reported in the literature. We aimed to characterise and compare clinical, biochemical and haematological features, in addition to clinical outcomes, between these patients. METHODS: This multi-centre, retrospective, observational study enrolled 488 SARS-CoV-2 positive patients - 339 with CA infection and 149 with HA infection. All patients were admitted to a hospital within the University Hospitals of Morecambe Bay NHS Foundation Trust between March 7th and May 18th, 2020. RESULTS: The CA cohort comprised of a significantly younger population, median age 75 years, versus 80 years in the HA cohort (P = 0·0002). Significantly less patients in the HA group experienced fever (P = 0·03) and breathlessness (P < 0·0001). Furthermore, significantly more patients had anaemia and hypoalbuminaemia in the HA group, compared to the CA group (P < 0·0001 for both). Hypertension and a lower median BMI were also significantly more pronounced in the HA cohort (P = 0·03 and P = 0·0001, respectively). The mortality rate was not significantly different between the two cohorts (34% in the CA group and 32% in the HA group, P = 0·64). However, the CA group required significantly greater ICU care (10% versus 3% in the HA group, P = 0·009). CONCLUSION: Hospital-acquired and community-acquired COVID-19 display similar rates of mortality despite significant differences in baseline characteristics of the respective patient populations. Delineation of community- and hospital-acquired COVID-19 in future studies on COVID-19 may allow for more accurate interpretation of results.