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Pulmonary valve stenosis (PVS) is a congenital heart defect where the pulmonary valve leaflets thicken or fuse, narrowing the valve opening and restricting blood flow from the right ventricle to the pulmonary arteries. This forces the right ventricle to pump harder, potentially leading to hypertrophy over time.

Most cases are detected in infancy via a heart murmur during routine exams, though mild forms may remain asymptomatic until adulthood. Symptoms in moderate-to-severe PVS include fatigue, shortness of breath, chest pain, fainting (especially post-exercise), cyanosis, poor weight gain in infants, and abdominal distention. Rarely, it is associated with syndromes like Noonan or Tetralogy of Fallot.

Diagnosis involves echocardiography to assess valve gradient and severity, with ECG and cardiac catheterization for confirmation. Mild cases require monitoring; moderate-severe ones need intervention.

Primary treatment is percutaneous balloon valvuloplasty, inflating a balloon to stretch the valve, often curative. Severe cases may require surgical valvotomy or valve replacement. Medications like prostaglandins, diuretics, or antiarrhythmics support associated defects. Post-treatment, regular follow-up prevents recurrence.
This illustration depicts normal versus stenotic pulmonary valve anatomy, highlighting restricted outflow.