Unusual cardiac presentation of congenital cytomegalovirus infection

A 27-year-old woman was referred at 15 weeks' gestation following confirmation of acute cytomegalovirus (CMV) infection. At 6 weeks' gestation she had a mild viral illness and maternal serology showed reactive CMV immunoglobulin (Ig) M and IgG at 0.65 induced systemic resistance (ISR) (NR < 0.2) and 3.15 ISR (NR < 1.1), respectively. Follow-up CMV serology was done at 17 weeks' gestation and was again reactive (IgM, 0.62 ISR; IgG, 2.78 ISR). CMV avidity testing was performed on three maternal samples at 10, 12 and 15 weeks' gestation (avidity 15%, 16% and 21%, respectively), confirming acute CMV infection. A detailed fetal ultrasound examination performed at 15 weeks' gestation demonstrated abnormal findings in the heart, with echogenicity and thickening of the mitral valve and patchy echogenicity of the left ventricle (Figures 1a and b). No other fetal abnormalities were detected. A fetal echocardiogram performed at 16 weeks demonstrated abnormally echogenic and thickened mitral valve leaflets with decreased excursion but no mitral regurgitation. Patchy echogenicity of the papillary muscles and left ventricular endocardium was seen. The echocardiogram was repeated 1 week later by which time the mitral valve appeared normal but the left atrioventricular valvar tension apparatus appeared abnormally bright, compatible with either localized inflammation or a fibrotic process (Figure 1c). The remainder of the myocardium appeared normal. Testing for maternal anti-Ro/SSA and anti-La/SSB antibodies as another potential cause of the abnormal myocardial echodensity was negative. The family elected for termination of pregnancy at 18 weeks' gestation. (a, b) Transvaginal cardiac ultrasound examination at 15 weeks. The mitral valve (MV) is dysplastic and there is patchy echogenicity of the mitral valve leaflets and papillary muscles (PM) in the left ventricle. (c) Four-chamber view of the fetal heart at 17 weeks' gestation. There is increased echogenicity of a mitral valve papillary muscle and its cords (arrow) suggesting myocardial inflammation or fibrosis. The lesion appeared more extensive than a benign echogenic focus and inflammation was confirmed by postmortem histology. LV, left ventricle. A postmortem examination of the products of conception was performed. CMV polymerase chain reaction was performed on tissue of the heart, brain, liver and placenta, and all were positive for CMV. Macroscopic examination of the heart was limited owing to damage that occurred during the termination procedure. A section of myocardium was examined microscopically, and myocytes exhibited eosinophilia and enlarged nuclei consistent with CMV infection. No evidence of endocardial fibroelastosis was seen histologically. Brain microscopy showed scattered cells with typical cytomegalic viral effects. CMV infection is the most common congenital viral infection in humans, with a birth prevalence of 0.7%1, 2. Symptomatic congenital CMV occurs in only 11% of cases but often affects several systems, resulting in a spectrum that includes in-utero growth restriction (IUGR), thrombocytopenia, neonatal hepatitis, chorioretinitis and central nervous system (CNS) abnormalities3. Involvement of the CNS is the predominant cause of adverse outcome4. Abnormal prenatal ultrasonographic findings, including fetal ascites, IUGR, echogenic bowel, microcephaly and intracerebral calcification, are found in approximately 30% of symptomatic fetuses5-7. Ultrasonographic evidence of fetal cardiac involvement in congenital CMV is rare. Large series have reported low rates of cardiac involvement and no cases with similar findings to ours6. The case we describe demonstrates ultrasonographically detectable inflammatory changes in the heart that resemble endocardial fibroelastosis. The marked echogenicity of the left ventricle and thickening of the mitral valve had a different appearance from that of the more common finding of echogenic focus in the heart8. The unique ultrasonographic appearance we report appears to have been caused by CMV-related myocarditis and should raise clinical suspicion of fetal CMV infection. C. P. Barnett*, E. Jaeggi , R. K. Han , O. Nevo**, S. Keating?, P. Shannon?, A. Bitnun , D. Chitayat* ? **, * Division of Clinical and Metabolic Genetics, The Hospital for Sick Children, 555 University Ave, Toronto M5G 1X8, Canada, Division of Cardiology, The Hospital for Sick Children, 555 University Ave, Toronto M5G 1X8, Canada, Division of Infectious Diseases, The Hospital for Sick Children, 555 University Ave, Toronto M5G 1X8, Canada, ? Division of the Prenatal Diagnosis and Medical Genetics Program, Mount Sinai Hospital, Toronto, Canada, ? Department of Laboratory Medicine and Pathology, Mount Sinai Hospital, Toronto, Canada, ** Department of Obstetrics and Gynecology, Mount Sinai Hospital, Toronto, Canada, Pediatric Cardiology, Sunnybrook Health Sciences, Toronto, Canada

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