Almost all infants studied showed a minimal septal defect and only one infant had dyspnea and showed a large membranous VSD. All atrial septal defects had < 4 mm in diameter which are very likely to decrease in size or completely close on follow-up. However a small or moderate ventricular septal defect may still be significant if it causes aortic insufficiency or outflow tract obstruction as in the case of double chamber right ventricle. The size alone does not necessarily mean it is not hemodynamically significant. Furthermore it is not known if Zika exposed infants have the same spontaneous regression or closure rate of minor CHD as described in a normal population. Infants with small muscular VSDs might be easily missed without colour Doppler echocardiography. Muscular VSD closed earlier than perimembranous VSD and a recently review observed that all muscular VSD < 3.0 mm closed before the age of 3 years old. This corroborates our finding that only one of the 103 infants studied had signs and symptomns of CHD.
This is the first time that CHD was assessed in infants with presumed congenital Zika syndrome. Currently there are no reports or autopsy evidence of any cardiac defects associated with presumed congenital Zika syndrome. Many others malformations have been described in the presumed congenital Zika syndrome, especially the central nervous system manifestations. As congenital Zika syndrome has many similarities with congenital Rubella syndrome it would be important to rule out cardiac involvement. This study seems to add a new contribution by showing apparently an increased rate of CHD in infants with congenital Zika infection. As we are reporting preliminary findings in a few infants, our results need to be confirmed by others studies.
Currently studies on the relationship between Zika virus infection and heart involvment are lacking. Other Flavivirus such as dengue virus have been associated with myocarditis and pericarditis -. We did not find in our studied infants evidence of pericardium or myocardium involvement in echocardiography, besides these infants did not have any clinical manifestation. Recently Krittanawong et al highlight the potential cardiovascular complications of Zika virus infection and suggested a prompt cardiovascular screening in suspect cases of Zika virus infection.
Our observational study has some limitations. At first we could not make serological diagnosis in all studied infants; 80 infants did not perform this test because this exam was not available at that time. However Zika virus IgM antibody was detected in cerebrospinal fluid samples of 23 infants and all infants had microcephaly and neuroimages alterations compatible with congenital Zika infection. Besides the current outbreak of microcephaly associated with Zika infection during pregnancy in Brazil especially in the Northeast region where IMIP is located makes the diagnosis of congenital Zika infection quite plausible. Second, stillbirths were not studied and this exclusion may underestimate the CHD prevalence in congenital Zika syndrome.