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药物性应激性心肌病

Drug-Induced Takotsubo Cardiomyopathy.

作者信息

Kido Kazuhiko, Guglin Maya

机构信息

1 Department of Pharmacy Practice, South Dakota State University, Sioux Falls, SD, USA.

2 Department of Pharmacy, Avera McKennan Hospital, Sioux Falls, SD, USA.

出版信息

J Cardiovasc Pharmacol Ther. 2017 Nov;22(6):552-563. doi: 10.1177/1074248417708618. Epub 2017 May 11.

DOI:10.1177/1074248417708618
PMID:28490198
Abstract

BACKGROUND

The most plausible hypothesis for takotsubo cardiomyopathy (TCM) is a catecholamine surge. Direct administration of catecholamines or medications causing catecholamine surge is frequently used in clinical practice.

METHODS

A Medline/PubMed database search was conducted for case reports or series of drug-induced TCM. All reported cases of drug-induced TCM were systemically identified and analyzed.

RESULTS

We identified 157 cases of drug-induced TCM. Fifty-seven (36.3%) cases were related to the administration of exogenous catecholamines. In 50 (31.9%) other cases, there was potential adrenergic effect. This included drugs with adrenergic vasoconstriction properties (3.2%), hyperadrenergic state due to alcohol or opioid withdrawal (7.7%), inhibitors of catecholamine reuptake (14.7%), anaphylactic reaction that is accompanied by catecholamine release (3.2%), and psychological or somatic stress coinciding with the administration of a drug that was thought to be the culprit (3.2%). Overall, 68.2% of these drug-induced TCM cases were catecholamine related. In 14 (8.9%) cases, the likely etiology of cardiomyopathy was chemotherapy-induced coronary vasospasm.

CONCLUSION

Our systematic review showed that over two-thirds of drug-induced TCM cases were due to direct or indirect catecholamine stimulation. The lowest effective dose and shortest duration of catecholamines should be utilized, and alternative therapies should be considered if feasible.

摘要

背景

对于应激性心肌病(TCM),最合理的假说是儿茶酚胺激增。在临床实践中,经常直接使用儿茶酚胺或导致儿茶酚胺激增的药物。

方法

对Medline/PubMed数据库进行检索,查找药物诱发TCM的病例报告或系列病例。对所有报告的药物诱发TCM病例进行系统识别和分析。

结果

我们识别出157例药物诱发的TCM病例。57例(36.3%)与外源性儿茶酚胺的使用有关。在其他50例(31.9%)病例中,存在潜在的肾上腺素能效应。这包括具有肾上腺素能血管收缩特性的药物(3.2%)、因酒精或阿片类药物戒断导致的高肾上腺素能状态(7.7%)、儿茶酚胺再摄取抑制剂(14.7%)、伴有儿茶酚胺释放的过敏反应(3.2%),以及在使用被认为是罪魁祸首的药物时同时出现的心理或躯体应激(3.2%)。总体而言,这些药物诱发的TCM病例中有68.2%与儿茶酚胺有关。在14例(8.9%)病例中,心肌病可能的病因是化疗诱发的冠状动脉痉挛。

结论

我们的系统评价表明,超过三分之二的药物诱发TCM病例是由于直接或间接的儿茶酚胺刺激。应使用最低有效剂量和最短疗程的儿茶酚胺,并且如果可行的话应考虑替代疗法。

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