Study Identifies Factors that May Increase PH Risk After Atrial Septal Defect Repair

Study Identifies Factors that May Increase PH Risk After Atrial Septal Defect Repair

High pulmonary pressure, cardiac medication use, and poor heart function are all risk factors for pulmonary hypertension (PH) in adults after a procedure to repair an atrial septal defect, a hole in the wall (septum) that divides the two upper chambers of the heart, a study reports.

The study, “Risk Factors for Pulmonary Hypertension in Adults After Atrial Septal Defect Closure,” was published in The American Journal of Cardiology.

An atrial septal defect is a birth defect in the heart characterized by blood from the left chamber leaking into the right chamber of the heart, and from there into the lungs.

If the hole in the septum is large, a considerable amount of blood leaks to the right chamber, making the heart and lungs work harder, potentially leading to the development of PH.

A surgery to close the septum is the strategy of choice to prevent PH in these patients. However, the effectiveness of atrial septal defect closure surgery is variable, with studies reporting a PH prevalence varying from 5% to 50% in adults post-surgery.

A team led by researchers at the Erasmus Medical Center in the Netherlands estimated the prevalence of PH in a group of adults before and after atrial septal defect closure. They also investigated how a patient’s characteristics correlate with the risk of PH after surgery.

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In total, the researchers analyzed 198 patients who underwent atrial septal defect closure, either via open heart surgery (110 patients) or a needle-puncture of the skin (88 patients) — a procedure called percutaneous atrial septal defect closure — in the Netherlands between 2000 and 2014.

Most of the patients were women (148 patients), with a median age of 45 years at the time of the procedure.

The researchers analyzed the patients’ echocardiograms before and after the procedure. Median follow-up was 15 months.

Results showed that before closure, PH was prevalent in 13.1% of the patients (26 patients), which decreased to 5% (10 patients) after closure.

Of the 10 patients with PH after closure, seven were suspected to have pulmonary arterial hypertension (PAH), and in three others, PH was linked to a dysfunction in filling the heart’s left ventricle.

Among the 10 patients with PH after closure, seven of them used a combination of PH therapies — a phosphodiesterase-5 inhibitor plus an endothelin antagonist, which are used to relax blood vessels — and two used a phosphodiesterase-5 inhibitor alone.

Researchers identified several parameters significantly associated with PH at follow-up, including PH before closure, patients with heart symptoms belonging to class 3 or 4 in the New York Heart Association Functional Classification — used to classify patients’ risk of heart failure according to the severity of their symptoms — presence of pulmonary disease, cardiac medication use, and certain functional parameters of the heart’s right ventricle function.

The age of patients at closure and the size of the septum hole were not associated with PH after closure.

“Adult patients with low pulmonary pressures before ASD [atrial septal defect] closure are not at risk for the development of PH after ASD closure during a follow-up period of 15 months,” the researchers wrote, adding that “these patients can be reassured and need less frequent follow-up.”

In contrast, “patients with high pulmonary pressures before ASD closure, high NYHA functional class, presence of pulmonary disease, cardiac medication use, and impaired [right ventricular] function at baseline are at risk and therefore require close follow-up after ASD closure,” they concluded.

Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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