Case Report: Multiple fetal cardiac rhabdomyomas with aortic outflow tract involvement and preserved cardiac function

Background Multiple fetal cardiac rhabdomyomas can present a challenging anatomical appearance even when cardiac function remains preserved. Serial assessment of ventricular performance, rhythm, and both ventricular outflow tracts is central to individualized surveillance. Case presentation A 28-year-old gravida 2 para 1 woman was referred at 23 weeks of gestation. Fetal echocardiography identified eight masses in total, including a dominant 22 × 10 mm lesion involving the left ventricular outflow tract (LVOT); the remaining lesions measured approximately 6–8 mm. Cardiac rhythm was assessed using M-mode and pulsed-wave Doppler. Spectral Doppler examination of both the aortic and pulmonary outflow tracts was performed at 30, 32, and 34 weeks and at term. Serial assessment showed no ventricular dysfunction, clinically significant outflow obstruction, sustained arrhythmia, hydrops, or pericardial effusion. Prenatal mechanistic target of rapamycin (mTOR) inhibitor therapy was not administered. Planned cesarean delivery at 39 weeks resulted in a 2,920-g male neonate with Apgar scores of 8 and 9 at one and five minutes. Precautionary inpatient observation continued until postnatal day 22, considering clinical concern and distance from home. At one month, the dominant mass measured 24.1 × 11.9 mm, with preserved biventricular systolic function, a peak aortic outflow tract velocity of 114.98 cm/s (approximately 1.15 m/s), and a peak instantaneous Doppler gradient of 5.29 mmHg. A 12-lead ECG obtained at one month of age showed sinus rhythm at 150 beats/min without arrhythmia or atrioventricular block on the recorded tracing. Genetic testing was not obtained; pediatric and neurological follow-up was recommended. Conclusion This case illustrates the importance of integrating tumor anatomy with repeated assessment of cardiac function, rhythm, and outflow physiology. Substantial tumor burden did not produce documented hemodynamic deterioration during the reported period. Follow-up limited to one month and the absence of molecular confirmation preclude conclusions about long-term cardiac or tuberous sclerosis complex-related outcomes.