Study links allergy molecule to worsening heart function in PAH
Worse right heart function tied to higher IgE levels in blood
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Higher blood levels of immunoglobulin E (IgE), an immune molecule typically linked to allergies, are associated with worse right heart function in people with pulmonary arterial hypertension (PAH), according to a study.
While the left side of the heart pumps oxygen-rich blood to the body, the right side pumps blood into the lungs. In PAH, this task becomes increasingly difficult as lung vessels narrow and stiffen.
The study found that patients with higher IgE levels tended to have more severe symptoms, greater limitations in physical activity, and signs that the right side of the heart was struggling to pump blood effectively into the lungs.
The findings suggest that the body’s immune system may contribute to accelerating heart failure in PAH. IgE holds potential “as a diagnostic biomarker for PAH-related right heart failure, and anti-IgE therapy may represent a promising therapeutic strategy that warrants further investigation,” the researchers wrote.
The study, “Association of Immunoglobulin E With Right Ventricular Dysfunction in Pulmonary Arterial Hypertension,” was published in Pulmonary Circulation.
IgE’s role in remodeling the arteries
PAH is a form of pulmonary hypertension characterized by the narrowing of the pulmonary arteries, the blood vessels that transport blood through the lungs. This restricts blood flow across the lungs, causing high blood pressure and making the right side of the heart work harder to pump blood.
Recent studies have suggested that IgE, an immune molecule usually associated with allergic diseases, may play a role in remodeling the pulmonary arteries and the right ventricle, the heart’s lower-right chamber that pumps deoxygenated blood to the lungs for oxygenation.
The researchers set out to investigate whether elevated IgE levels were associated with right ventricular dysfunction in PAH.
The study enrolled 30 patients with idiopathic (of unknown cause) PAH, and 30 age- and sex-matched individuals with normal cardiac function and no cardiopulmonary disease. Most patients were women (56.7%), with a mean age of 41.3.
Blood IgE levels were significantly higher in PAH patients than in controls (859 vs. 430 nanograms [ng]/mL) and were associated with the levels of NT-proBNP, a marker of heart damage.
IgE levels were also markedly higher in patients with higher symptom severity and more physical activity limitations, classified as World Health Organization (WHO) functional class III, than in those without physical activity limitations (WHO functional class I).
Further analysis demonstrated that IgE levels were significantly higher in patients with higher right ventricular wall thickness and size, and those with right ventricular dysfunction. These parameters were assessed by echocardiography, an imaging test to assess the heart’s structure and function. Higher IgE levels were also associated with higher blood pressure in the pulmonary arteries and right ventricle.
Blood IgE levels were also significantly associated with right ventricular–pulmonary artery coupling, assessed by the TAPSE/sPAP ratio, an echocardiographic marker that assesses how well the right ventricle can pump against the pressure in the pulmonary artery.
Patients were further separated based on their TAPSE/sPAP ratio into those with adaptive remodeling and those with maladaptive remodeling. Adaptive remodeling means the right ventricle adapts and compensates to increased pressure in the pulmonary artery by increasing contractility, while maladaptive remodeling occurs when the right ventricle fails to adapt to rising pressure in the lungs, which can signal worsening disease.
IgE blood levels were also significantly higher in patients with maladaptive right ventricular remodeling than in those in the adaptive phase.
“These findings suggest that elevated serum IgE is linked to the progression of [right ventricle] dysfunction in PAH,” the researchers wrote, adding that they also “introduce a new perspective for exploring immune‐related mechanisms in PAH‐associated right heart failure.”
