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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 hypote...

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Detalles Bibliográficos
Autores principales: Khalid, Karniza, Ahmad, Raja Elina, Tong, Alwin Y.H., Lui, Sze Yee, Abidin, Ida Zaliza Zainol
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8117078/
https://www.ncbi.nlm.nih.gov/pubmed/34027217
http://dx.doi.org/10.5114/amsad.2021.105410
Descripción
Sumario: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.