Fig. 6: A 34-year-old male from the central rural region of Turkey with a history of childhood surgical repair for congenital heart disease, now presenting with a residual muscular VSD measuring 9.7 mm (arrow) and evidence of progressive pulmonary hypertension.

The patient had not been followed in regular cardiology care for years, and the residual lesion had remained unrecognized until adulthood. Peripheral oxygen saturation was 80%, raising concern for Eisenmenger physiology. Late presentation with hypoxemia and residual lesions highlights the importance of lifelong surveillance in congenital heart disease, which is challenging in LMIC settings. CMR revealed marked right ventricular dilation and dysfunction, with RV EDVI of 331 mL/m², ESVI of 228 mL/m², and an ejection fraction of 31%. The left ventricle showed preserved function (LV EF: 53%), but was also dilated (LV EDVI: 175 mL/m²). Pulmonary regurgitation fraction was significantly elevated at 45%. Importantly, phase-contrast imaging revealed early and mid-diastolic right-to-left shunting across the VSD, a finding highly suggestive of bidirectional or Eisenmenger-level physiology. Flow quantification demonstrated Qp:Qs = 1.8, consistent with significant left-to-right shunting. Pulmonary flow distribution was relatively symmetric (RPA-to-LPA flow ratio is calculated as 48:52%). The RVOT was aneurysmal, classified as Type IV RVOT morphology. This case illustrates the long-term consequences of incomplete follow-up after congenital heart defect repair and emphasizes the role of CMR in accurately characterizing residual lesions, ventricular function, regurgitation severity, and shunt physiology in adult congenital heart disease. CMR cardiac magnetic resonance imaging, EDVI end-diastolic volume index, EF ejection fraction, ESVI end-systolic volume index, LMIC low- and middle-income countries, LV left ventricle, LPA left pulmonary artery, Qp:Qs pulmonary-to-systemic flow ratio, RPA right pulmonary artery, RV right ventricle, RVOT right ventricular outflow tract, VSD ventricular septal defect.