Department of Medicine, University of Queensland, Brisbane, Australia.
Int J Cardiol. 2010 Mar 4;139(2):107-12. doi: 10.1016/j.ijcard.2009.08.007. Epub 2009 Oct 18.
Perhexiline improves functional capacity in heart failure, but the mechanisms are undefined. We sought its effects on myocardial deformation in patients with viable myocardium.
Thirty-six medically-treated patients, stable at least 6 months post-infarction with LV dysfunction and myocardial viability shown by dobutamine echo (DbE) were randomised to receive perhexiline or matching placebo for 1 year. Cardiopulmonary exercise testing and DbE were performed at baseline and follow-up. Peak-systolic strain (S) and strain rate (SR) were measured offline in 111 dysfunctional segments in the placebo and 88 in the treatment group at rest, low-dose (LDD) and peak-dose dobutamine (PDD).
The serum perhexiline level was 0.27+/-0.7 microg/l. There was no difference in the wall motion response to dobutamine at baseline and follow-up. Resting strain and SR were similar in the two groups at baseline and follow-up. However, SR at LDD and PDD increased in the placebo group and worsened during the same period in the perhexiline group. Patients on perhexiline and placebo had a similar rate-pressure product and exercise duration at baseline (7.9+/-2.7 vs 8.7+/-3.3 min, p=NS) and follow-up (9.6+/-4.6 vs 10.1+/-3.03 min, p=NS).
Perhexiline does not improve the deformation of abnormal myocardial segments in patients with ischaemic LV dysfunction.
哌克昔林可改善心力衰竭患者的功能能力,但作用机制尚不清楚。我们研究了它对存活心肌患者心肌变形的影响。
36 例经医学治疗的患者,在梗死后至少 6 个月病情稳定,左心室功能障碍和存活心肌通过多巴酚丁胺超声心动图(DbE)显示,随机分为哌克昔林组或匹配的安慰剂组,接受治疗 1 年。在基线和随访时进行心肺运动测试和 DbE。在静息、低剂量(LDD)和最大剂量多巴酚丁胺(PDD)时,对安慰剂组的 111 个功能障碍节段和治疗组的 88 个节段进行离线测量峰值收缩期应变(S)和应变率(SR)。
血清哌克昔林浓度为 0.27+/-0.7 microg/l。多巴酚丁胺的壁运动反应在基线和随访时没有差异。两组在基线和随访时的静息应变和 SR 相似。然而,LDD 和 PDD 时的 SR 在安慰剂组中增加,而在哌克昔林组中同一时期恶化。在基线(7.9+/-2.7 与 8.7+/-3.3 min,p=NS)和随访(9.6+/-4.6 与 10.1+/-3.03 min,p=NS)时,服用哌克昔林和安慰剂的患者的心率-血压乘积和运动时间相似。
哌克昔林不能改善缺血性左心室功能障碍患者异常心肌节段的变形。