Department of Pharmacotherapy, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose, Tokyo 204-0004, Japan.
Clin Pharmacokinet. 2013 Mar;52(3):169-85. doi: 10.1007/s40262-012-0029-2.
Heart failure is one of the leading causes of death in developed countries, and its prevalence is expected to increase further in the coming years. While the pharmacokinetic changes observed in patients with heart failure have been reviewed twice in Clinical Pharmacokinetics, approximately a quarter century has passed since the latest article was published in 1988. Since then, many important classes of agents (e.g. ACE inhibitors, angiotensin receptor antagonists and inotropes) have been introduced for the treatment of heart failure. The aim of the present article is to update the information regarding the pharmacokinetics of these drugs. For this purpose we have made a systematic survey of literature using MEDLINE, EMBASE and Japan Centra Revuo Medicina (in Japanese) and found a total of 111 relevant publications for 58 drugs. Heart failure is a pathophysiological state where the damaged heart, from whatever causes, no longer pumps enough blood for the needs of body tissues at rest or during the normal daily activities. The spectrum of heart failure ranges from acute decompensated heart failure (including circulatory shock) to chronic compensated or decompensated heart failure. Because hypoperfusion of organs may influence drug absorption from the gastrointestinal tract, distribution into tissues and elimination either by the liver or kidneys, it is conceivable that the pharmacokinetics of many drugs may be altered in patients with heart failure. The pharmacokinetic changes of drugs in these patients in the light of a physiologically based pharmacokinetic model are discussed, since this model can interpret altered pharmacokinetics in terms of changes in the binding of drugs in plasma and tissue, blood flow to drug-eliminating organs and intrinsic activity of drug elimination. Pharmacokinetic changes of drugs after intravenous administration are described here in Part 1 and those after oral administration will be discussed in Part 2 in a later issue of the Clinical Pharmacokinetics. Reviewing the retrieved data, it was considered that patients with asymptomatic or compensated chronic heart failure seem to have no or minimal alterations in the pharmacokinetics of parenterally administered drugs as long as there was no concurrent liver and/or kidney dysfunction. In contrast, it was found that the systemic clearance of at least six drugs (i.e. milrinone, carperitide, molsidomine, theophylline, ciclosporin and hydralazine) was reduced after intravenous administration by 50 % or more in patients with acute decompensated heart failure or chronic severe heart failure (New York Heart Association class III or IV) as compared with healthy subjects. Because there is a paucity of information regarding the pharmacokinetics of drugs in patients with severe heart failure, close attention should be paid to monitoring the efficacy of these agents and their associated adverse effects.
心力衰竭是发达国家主要的死亡原因之一,预计在未来几年其发病率还将进一步上升。尽管临床药代动力学已经两次综述了心力衰竭患者的药代动力学变化,但自 1988 年发表的最新文章以来,已经过去了大约四分之一个世纪。自那时以来,许多重要的药物类别(例如 ACE 抑制剂、血管紧张素受体拮抗剂和正性肌力药)已被引入心力衰竭的治疗。本文的目的是更新这些药物药代动力学的信息。为此,我们使用 MEDLINE、EMBASE 和日本中央医学评论(日语)进行了系统的文献调查,共找到了 111 篇与 58 种药物相关的文献。心力衰竭是一种病理生理状态,受损的心脏由于任何原因,在休息或正常日常活动时不再能够泵出足够的血液满足身体组织的需要。心力衰竭的范围从急性失代偿性心力衰竭(包括循环休克)到慢性代偿或失代偿性心力衰竭。由于器官灌注不足可能影响胃肠道药物吸收、组织分布和通过肝脏或肾脏消除,因此可以想象许多药物的药代动力学在心力衰竭患者中可能会发生改变。根据基于生理的药代动力学模型讨论了这些患者中药物的药代动力学变化,因为该模型可以根据药物在血浆和组织中的结合、药物消除器官的血流和药物消除的内在活性的变化来解释改变的药代动力学。本文将首先描述静脉给药后药物的药代动力学变化,随后在以后的一期临床药代动力学中将讨论口服给药后的药代动力学变化。回顾检索到的数据,认为无症状或代偿性慢性心力衰竭患者只要没有同时存在肝和/或肾功能障碍,其静脉给药的药物药代动力学似乎没有或仅有最小的改变。相比之下,研究发现,与健康受试者相比,急性失代偿性心力衰竭或慢性严重心力衰竭(纽约心脏协会 III 或 IV 级)患者静脉注射至少六种药物(即米力农、卡培他滨、莫尔西多明、茶碱、环孢素和肼屈嗪)的全身清除率降低了 50%或更多。由于关于严重心力衰竭患者药物药代动力学的信息有限,应密切注意监测这些药物的疗效及其相关的不良反应。