Key result
ASD closure in HCM with diastolic dysfunction risks pulmonary edema by removing beneficial LV decompression.
Why the study?
The impact of atrial septal defect closure in patients with hypertrophic cardiomyopathy and its effects on left ventricular preload and diastolic function is unclear.
In patients with hypertrophic cardiomyopathy and diastolic dysfunction, an atrial septal defect may act as a beneficial 'pop-off' valve, and its closure could precipitate pulmonary edema.
ASD closure in pediatric HCM remains unproven; leaves open hemodynamic benefit and requires prospective trials before adoption.
Hypertrophic cardiomyopathy (HCM) affects 0.2% of the general population, with lower frequency in the pediatric population, albeit with higher incidence of associated cardiac defects.1 An atrial septal defect (ASD) can result in a left-to-right shunt that decreases preload to the left ventricle (LV). Eliminating this shunt can be favorable in a hypertrophied LV, allowing for improved filling and decreasing outflow obstruction. In diastolic dysfunction, an ASD can serve as a “pop-off” to decompress the LV, with closure resulting in pulmonary edema and activity intolerance.
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Alnoor et al. (2024) studied Hypertrophic cardiomyopathy with atrial septal defect. Atrial septal defect closure was evaluated. In patients with hypertrophic cardiomyopathy and diastolic dysfunction, an atrial septal defect can serve as a beneficial shunt to decompress the left ventricle, and closure may cause pulmonary edema.
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