Anatomical complexity does not predict outcomes after COVID-19 in adults with congenital heart disease

Abstract

Few could have guessed the global devastation of COVID-19 when it was first reported more than a year ago. Community spread has been a major route of transmission as COVID-19 has a lower case fatality rate (2.3%) but much greater infectivity compared with previous outbreaks (severe acute respiratory syndrome, 2002–2003; Middle Eastern respiratory syndrome, 2012–ongoing). Most patients experienced mild infection (81%), while 5% developed critical illness. Risk factors for death that have been identified include age, disease severity and comorbidities such as cardiovascular disease, diabetes, hypertension, chronic respiratory disease and cancer. Patients with congenital heart disease (CHD) were perceived to be especially vulnerable to infection due to their fragile physiology, particularly those with moderate to severe complex anatomy such as repaired tetralogy of Fallot, status post atrial or arterial switch procedure or Fontan circulation. 3 Data to quantify this risk have been limited—until now. In this issue of Heart, Schwerzmann et al describe the clinical course of 105 patients with CHD with COVID-19 infection, based on either a positive biochemical test (by PCR or ELISA) or strong clinical suspicion (based on symptoms and chest CT findings). This was a collaboration between 25 centres in nine countries, as part of the European Collaboration for Prospective Outcome research in Congenital Heart Disease. It is the largest multicentre cohort study thus far and the first publication of its kind. The authors aimed to identify patient characteristics associated with ‘complicated’ infection, which they defined as either death or hospitalisation requiring noninvasive/invasive ventilation and/or inotropic support after COVID-19 infection. In total, 73/105 patients (70%) had mild disease, while 13 patients (12%) experienced a complicated infection (online supplemental table S1). At study conclusion, 91 patients (87%) had recovered; 9 cases (9%) were ongoing; and 5 patients (5%) had died. Two patients with Eisenmenger syndrome chose palliative care after diagnosis, which is an important reminder of the importance of advance care planning for patients with CHD. Cyanotic CHD (highest risk), Body Mass Index (BMI) of >25 kg/m and ≥2 nonCHDrelated comorbidities (see online supplemental table S1 and figure 1B for a full list) were identified as independent risk factors for complicated infection. Age was significant in univariate analysis but was omitted from multivariate analysis by study design because its OR was less than 5. Interestingly, other CHDrelated features were not associated with complicated infection: underlying anatomical disease complexity (simple, moderate or complex) and main defectrelated problems (valvular problem, heart failure, arrhythmia or pulmonary arterial hypertension) were not statistically significant in univariate analysis, though the study may have been underpowered for these analyses. Also, rather than using a unifying definition for comorbidities such as heart failure or renal failure, study authors relied on the discretion of individual clinicians at each study centre. Finally, it is unclear how many patients had a genetic syndrome in the entire cohort as only one patient with a complicated infection had this reported as a comorbidity in the authors’ table 4.