Chest
Original ResearchPulmonary Arterial HypertensionSitaxsentan for the Treatment of Pulmonary Arterial Hypertension: A 1-Year, Prospective, Open-Label Observation of Outcome and Survival
Section snippets
Patients
Two hundred twenty-nine patients aged 12 to 78 years in WHO functional class II-IV with idiopathic PAH (IPAH) or PAH associated with connective tissue disease (PAH-CTD) or PAH associated with a congenital heart defect (PAH-CHD) were enrolled in STRIDE-2X. Additional inclusion criteria have been published previously.7 The study was conducted according to ethical principles stated in the Declaration of Helsinki (1996) and applicable guidelines on good clinical practice. The protocol was approved
Demographics
The sitaxsentan and bosentan treatment groups in the analysis population were comparable with regards to baseline characteristics (Table 1). Patients ranged in age from 14 to 78 years (mean, 54 years), and approximately 77% were female. Approximately 60% of patients had IPAH, 30% had PAH-CTD, and 10% had PAH-CHD. Baseline characteristics of patients in predefined subgroups were similar.
The overall treatment population of 229 patients was randomized to sitaxsentan (n = 145) or standard-dose
Discussion
We report 1-year results with the selective ET-A receptor antagonist sitaxsentan coupled with 1-year outcomes with the nonselective ET-A/ET-B receptor antagonist bosentan in a broad class of PAH patients (inclusion of IPAH [approximately 60%] and associated PAH conditions, ie, PAH-CTD [approximately 30%] and PAH-CHD [approximately 10%] with baseline functional class II-IV). It is important to recognize that although the STRIDE-2X study looked at patients who initiated treatment with sitaxsentan
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2020, Clinica Chimica ActaEndothelin antagonism and uric acid levels in pulmonary arterial hypertension: Clinical associations
2014, Journal of Heart and Lung TransplantationCitation Excerpt :Briefly, patients with PAH were randomized 1:1:1:1 to receive sitaxentan 50 or 100 mg or matched placebo orally once daily, or open-label bosentan 125 mg twice daily for 18 weeks. STRIDE-2X was an open-label extension of STRIDE-2.18 Patients were eligible if they completed the STRIDE-2 trial or had prematurely discontinued placebo or sitaxentan 50 mg in STRIDE-2 because of lack of clinical response.
Relationship between baseline ET-1 plasma levels and outcome in patients with idiopathic pulmonary hypertension treated with bosentan
2013, International Journal of CardiologyHemodynamic Stability After Transitioning Between Endothelin Receptor Antagonists in Patients With Pulmonary Arterial Hypertension
2013, Canadian Journal of CardiologyPrognostic factors in severe pulmonary hypertension patients who need parenteral prostanoid therapy: The impact of late referral
2012, Journal of Heart and Lung TransplantationCitation Excerpt :This bias could justify the results obtained, because incident cases have a worst prognosis than prevalent patients.26 The good survival in the open-label phase of the randomized controlled study has created the wrong conclusion that oral therapy represents a definite cure for PAH, but survival is satisfactory only when other drugs are promptly added in case of clinical worsening, which is a common experience during oral monotherapy.10,12–16 In real-world clinical practice, most PAH patients are still dying on monotherapy, with only a few being escalated to parenteral prostanoids, as documented by specialty pharmacy service providers,27 confirming a delayed use of prostanoids usually not available in the non-expert centers.
The authors have no conflicts of interest to disclose.
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