急性心肌梗死中链激酶诱导的低血压的病理生理学:临床证据的系统回顾。

Karniza Khalid, Raja Elina Ahmad, Alwin Y H Tong, Sze Yee Lui, Ida Zaliza Zainol Abidin
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引用次数: 0

摘要

导读:尽管链激酶诱导的低血压在急性心肌梗死患者中很常见,但其潜在的病理生理机制仍然不清楚。我们的研究旨在通过对文献的系统回顾,收集关于链激酶诱导低血压的潜在机制的临床证据。材料和方法:检索Medline、Scopus和Web of Science中与链激酶诱导低血压相关的临床研究文献。结果:我们的搜索产生了972条引用。剔除重复后,878篇文章被筛选为合格,其中856篇因各种原因被排除。在剩余的22篇全文检索文章中,选择8篇相关文章进行最终分析。链激酶诱导的低血压的机制提出了三个主题,包括(i)降低总外周阻力,(ii)补体激活,(iii)排除涉及其他中介的假设。结论:我们的研究结果表明,链激酶诱导的低血压的潜在机制主要在于降低总外周抵抗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pathophysiology of streptokinase-induced hypotension in acute myocardial infarction: a systematic review of clinical evidence.

Pathophysiology of streptokinase-induced hypotension in acute myocardial infarction: a systematic review of clinical evidence.

Pathophysiology of streptokinase-induced hypotension in acute myocardial infarction: a systematic review of clinical evidence.

Introduction: Despite the common occurrence of streptokinase-induced hypotension among patients with acute myocardial infarction, the underlying pathophysiology remains obscure and poorly understood. Our study aimed to pool clinical evidence on the potential mechanism of streptokinase-induced hypotension through a systematic review of the literature.

Material and methods: We conducted literature search from Medline, Scopus and Web of Science on clinical studies related to streptokinase-induced hypotension.

Results: Our search yielded 972 citations. After removal of duplicates, 878 articles were screened for eligibility, of which 856 papers were excluded due to various reasons. Of the remaining 22 articles retrieved with full texts, eight relevant articles were selected for final analysis. Three themes emerged as the proposed mechanisms of streptokinase-induced hypotension, including (i) reduction in total peripheral resistance, (ii) complement activation, and (iii) dismissal of hypotheses involving other intermediaries.

Conclusions: Our findings suggest that the underlying mechanism of streptokinase-induced hypotension lies primarily in the reduction in total peripheral resistance.

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