Prostacyclin (epoprostenol) and heart-lung transplantation as treatments for severe pulmonary hypertension.

Abstract

Objective-To determine whether epoprostenol (prostacyclin, PGI,) or heartlung transplantation (HLT), or both improves survival of patients with severe pulmonary hypertension. Design-This was a prospective study where the effects of epoprostenol were compared with conventional treatment. Also, the benefits of epoprostenol and HLT were assessed by comparing survival Diagnostic right heart catheterisation was performed with a triple lumen flow directed catheter in all patients on entry to the study."3 A brachial artery cannula was also inserted.In nine of the 44 patients it was not possible to record pulmonary artery wedge pressure. The total pulmonary vascular resistance (mean pulmonary artery pressure/cardiac index) was therefore calculated. A further measurement similar to that in the Mayo clinic study was included. The mixed venous oxygen saturation, together with arterial oxygen saturation were recorded from blood samples. The degree of disability was assessed by the New York Heart Association (NYHA) classification. 14 The capacity to acutely vasodilate the pulmonary vasculature with epoprostenol was assessed in our patients during the catheter study.'5 The infusion rate of epoprostenol was increased step wise every 10 minutes until the

Plasma Brain Natriuretic Peptide as a Prognostic Indicator in Patients With Primary Pulmonary Hypertension

“…In contrast, some patients refractory to vasodilator therapy may ultimately require heart-lung or lung transplantation. 4 Thus, accurate prediction of mortality is important in the treatment of patients with PPH. RV hemodynamic variables obtained by catheterization have been shown to be closely associated with outcome in patients with PPH.…”

Effects of Long-Acting Beraprost Sodium (TRK-100STP) in Japanese Patients With Pulmonary Arterial Hypertension

“…Since lesions are observed in most of the pulmonary vascular system from the tunica intima and media to the adventitia, conventional vasodilators are only effective for the systemic vasculature and show almost no effect on the pulmonary vasculature. The only formulation which shows evidence of exerting a pulmonary vasodilator effect during the chronic period is an endothelin receptor antagonist [25][26][27][28][29][30][31][32][33][34] apart from prostacyclin 22,[35][36][37][38][39][40] and its derivatives. [15][16][17][18]41,42) The 6MW distance is widely used as an indicator of the functional severity of pulmonary hypertension in each individual as a clinical test for efficacy evaluation before and after administration of several pulmonary vasodilators.…”

“…6,37,39,40) From its beneficial effects widely reported by many investigators, intravenous long-term epoprostenol therapy has been established as the recommended technique for the treatment of moderate to severe PAH. 45,46) However, epoprostenol therapy requires continuous intravenous infusion and modified reconstitution of the medication that has to be kept cold prior to infusion, as well as a chronic indwelling catheter and infusion pump, because epoprostenol is unstable at room temperature and has a short half-life of less than 6 minutes in human circulatory blood.…”

Minimizing the Inhaled Dose of NO With Breath-by-Breath Delivery of Spikes of Concentrated Gas

“…The maximal fall in PVR with the vasodilator intravenous prostacyclin (Epoprostenol, PGI 2 ) 16 was compared with NO CD . For the NO min , the duration of the spike of NO/N 2 (100 ppm) was varied until a minimum dose caused a fall in PVRI of Ն10%.…”