To the Editor:

Biomarkers can be reliable substitutes for clinical endpoints in pulmonary arterial hypertension (PAH), and need to be quantified rapidly at a low cost for a routine use. Heresi and colleagues reported significantly decreased circulating levels of high-density lipoprotein (HDL) cholesterol in subjects with PAH, which were associated with worse clinical outcomes (1). This association, which was independent of other cardiovascular risk factors and insulin resistance, required confirmation in an independent sample of patients before monitoring HDL cholesterol can be routinely recommended.

We recently conducted a multicenter prospective cohort study of 110 incident cases of PAH enrolled between 2003 and 2006 and followed up for 3 years (2). For each patient, 24-ml venous blood samples were immediately transferred to the Annemasse French Blood Service biobank. In May 2011, plasma microstraws, stored at −180°C, from 107 patients were sent via an express carrier in dry ice to the Grenoble University Hospital, in France, for HDL cholesterol quantification using a Vista Lab System (Siemens, Saint-Denis, France). The demographic, clinical, and baseline cardiorespiratory data of the 107 patients are listed in Table E1 in the online supplement, together with the characteristics of the subgroup of 74 patients with idiopathic, heritable, and drug- or toxin-related PAH.

The mean HDL cholesterol levels were 0.46 g/L (standard deviation [SD], 0.09, normal values > 0.4 g/L) in all patients and 0.47 (SD, 0.08) in the subgroup of 74 patients with idiopathic, heritable, and drug-induced PAH. Such levels were higher than those reported by Heresi and coworkers, but comparable to those observed by Zamanian and colleagues (3). We did not find any significant association between HDL cholesterol and 3-year mortality (Table 1).

The HDL cholesterol measurement is worldwide standardized, and technical differences cannot explain the discrepancy. Our cohort slightly differs in that we included only incident patients at the time of right heart catheterization, not under targeted therapies, whereas in the Heresi and coworkers study, data collection was both prospective and retrospective. An issue is the stability of HDL cholesterol at −180°C in microstraws for a long period of time (5–8 years). However, the levels measured were within the normal range and were similar to those of Zamanian and colleagues. In addition, when kept between −19° and −21°C, HDL cholesterol concentrations remained stable for more than 18 months (4). In conclusion, we do not confirm the prognostic value of HDL cholesterol in a multicenter prospective cohort study of patients with incident PAH. Our data do not support its widespread use as a marker in PAH prognostic assessment.

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