A prospective, randomized study of inhaled prostacyclin versus nitric oxide in patients with residual pulmonary hypertension after pulmonary endarterectomy

被引:25
|
作者
Abe, Shinichiro [1 ]
Ishida, Keiichi [1 ]
Masuda, Masahisa [2 ]
Ueda, Hideki [1 ]
Kohno, Hiroki [1 ]
Matsuura, Kaoru [1 ]
Tamura, Yusaku [1 ]
Watanabe, Michiko [1 ]
Matsumiya, Goro [1 ]
机构
[1] Chiba Univ, Grad Sch Med, Dept Cardiovasc Surg, Chuo Ku, 1-8-1 Inohana, Chiba 2600856, Japan
[2] Chiba Med Ctr, Dept Cardiovasc Surg, Chuo Ku, 4-1-2 Tsubakimori, Chiba 2600042, Japan
关键词
Chronic thromboembolic pulmonary hypertension; Pulmonary endarterectomy; Residual pulmonary hypertension; Inhaled prostacyclin; Inhaled nitric oxide; CARDIAC-SURGERY; HEART-TRANSPLANT; CONTROLLED-TRIAL; DOUBLE-BLIND; ILOPROST; HYPOXEMIA; THROMBOENDARTERECTOMY; DYSFUNCTION; EXPERIENCE;
D O I
10.1007/s11748-016-0724-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pulmonary endarterectomy (PEA) is an effective treatment for chronic thromboembolic pulmonary hypertension (CTEPH), but postoperative residual hypertension leads to in-hospital mortality. Inhaled epoprostenol sodium (PGI(2)) and NO are administered for pulmonary hypertension after cardiothoracic surgery. This prospective study provides the first comparative evaluation of the effects of inhaled PGI(2) and NO on pulmonary hemodynamics, systemic hemodynamics, and gas exchange in patients developing residual pulmonary hypertension after PEA. Thirteen patients were randomized to receive either NO (n = 6) or PGI2 (n = 7) inhalation when pulmonary hypertension persisted after weaning from cardiopulmonary bypass. Hemodynamic and respiratory variables were measured before inhalation of the agent (T0); 30 min (T1), 3 h (T2), and 6 h after inhalation (T3); and the next morning (T4). The NO dose was started at 20 ppm and gradually tapered until extubation, and PGI(2) was administered at a dose of 10 ng kg(-1) min(-1). In both groups, mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) significantly decreased over time until T4 (mean PAP: p < 0.0001; PVR: p = 0.003), while mean systemic arterial blood pressure significantly increased (p = 0.028). There were no significant between-group differences in patient characteristics, cardiac index, left atrial pressure, or ratio of arterial oxygen tension to fraction of inspired oxygen. There were no in-hospital deaths. Both inhaled PGI(2) and NO significantly reduced PAP and PVR without adverse effects on systemic hemodynamics in patients who developed residual pulmonary hypertension after PEA. Inhaled PGI(2) can be offered as alternative treatment option for residual pulmonary hypertension.
引用
收藏
页码:153 / 159
页数:7
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