Woodmansey P A, O'Toole L, Channer K S, Morice A H
University Department of Medicine, Royal Hallamshire Hospital, Sheffield.
Heart. 1996 Feb;75(2):171-3. doi: 10.1136/hrt.75.2.171.
Calcium antagonists are the only oral vasodilators shown to influence mortality in primary pulmonary hypertension, but the high doses required are often poorly tolerated. Amlodipine is a novel, relatively well tolerated, calcium antagonist. It has not been previously tested in humans with pulmonary hypertension.
Calcium antagonists are claimed to be of benefit in the 20-30% of patients who respond--that is, whose mean pulmonary artery pressure and pulmonary vascular resistance decreased by 20% after acute administration. Increasing oral doses of amlodipine (up to 40 mg) were given and haemodynamic measurements were obtained by the use of indwelling pulmonary artery catheters 12 h after each dose.
Large teaching hospital, primary referral centre.
Six patients (four women; age range 37-78 years) with pulmonary hypertension (one with primary pulmonary hypertension, five with thromboembolic disease.
Mean pulmonary artery pressure and pulmonary vascular resistance decreased by greater than 20% in two patients, mean pulmonary artery pressure decreased by greater than 20% in one patient with a pulmonary vascular resistance reduction of 19%. Thus, two of six patients responded to amlodipine and one partially responded.
The whole group mean (SEM) pulmonary artery pressure decreased from 47.7 (4.2) to 41.7 (4.4) mm Hg and mean pulmonary vascular resistance from 8.6 (2.1) to 7.1 (1.8) Wood units. Cardiac output rose by a mean (range) of 4% (-20.8 to+20.8), heart rate by 8.8% (-10 to +33), and systemic systolic blood pressure decreased by 12% (-29.2 to -5.8) and diastolic blood pressure by 6.8% (-28.2 to+20.0). There were no symptoms of systemic hypotension.
These results show that oral amlodipine can produce acute pulmonary vasodilatation in patients with pulmonary hypertension. Further studies are required, but amlodipine may prove to be of value in the treatment of primary pulmonary hypertension.
钙拮抗剂是唯一显示可影响原发性肺动脉高压患者死亡率的口服血管扩张剂,但所需的高剂量往往耐受性较差。氨氯地平是一种新型的、耐受性相对较好的钙拮抗剂。此前尚未在肺动脉高压患者中进行过测试。
据称钙拮抗剂对20% - 30%有反应的患者有益,即急性给药后平均肺动脉压和肺血管阻力降低20%的患者。给予递增剂量的口服氨氯地平(最高40毫克),每次给药12小时后通过留置肺动脉导管进行血流动力学测量。
大型教学医院,主要转诊中心。
6例肺动脉高压患者(4名女性;年龄范围37 - 78岁)(1例原发性肺动脉高压,5例血栓栓塞性疾病)。
2例患者平均肺动脉压和肺血管阻力降低超过20%,1例患者平均肺动脉压降低超过20%,肺血管阻力降低19%。因此,6例患者中有2例对氨氯地平有反应,1例部分有反应。
全组平均(标准误)肺动脉压从47.7(4.2)毫米汞柱降至41.7(4.4)毫米汞柱,平均肺血管阻力从8.6(2.1)伍德单位降至7.1(1.8)伍德单位。心输出量平均(范围)增加4%(-20.8至 +20.8),心率增加8.8%(-10至 +33),全身收缩压降低12%(-29.2至 -5.8),舒张压降低6.8%(-28.2至 +20.0)。无全身低血压症状。
这些结果表明,口服氨氯地平可使肺动脉高压患者产生急性肺血管扩张。需要进一步研究,但氨氯地平可能被证明对原发性肺动脉高压的治疗有价值。