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Pharmacologic treatment for pulmonary arterial hypertension (PAH) remains suboptimal and mortality rates are still high, even with pulmonary vasodilator therapy. In addition, we have only an incomplete understanding of the pathobiology of PAH, which is characterized at the tissue level by fibrosis, hypertrophy and plexiform remodeling of the distal pulmonary arterioles. Novel therapeutic approaches that might target pulmonary vascular remodeling, rather than pulmonary vaso-reactivity, require precise patient phenotyping both in terms of clinical status and disease subtype. However, current risk stratification models are cumbersome and not precise enough for choosing or assessing the results of therapeutic intervention. Biomarkers used in patients with left heart failure, such as troponin-T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are elevated in PAH patients but tend to simply reflect increased circulating plasma volumes and elevated right heart pressure, rather than conveying information about disease mechanism.
In this issue of Heart, Calvier and colleagues (see page 390) propose galectin-3 as a useful biomarker in PAH. The rationale for this hypothesis is that elevated aldosterone levels induce an increase in serum levels of galectin-3, a β-galactoside-binding lectin expressed by circulating myocytes, endothelial cells and other cardiovascular cell types. Among other effects, activation of the aldosterone/galactin-3 pathway promotes fibrosis, suggesting that elevated levels will correlate with the severity of PAH due to increased pulmonary arteriolar remodeling. To test this hypothesis, serum levels were measured in a total of 57 patients – 41 with idiopathic PAH (iPAH) and 16 with PAH …
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