2026/07/09 by José Luis Martín-Barrasa, Rafael Alayón-Afonso, Raquel Rodríguez‐González +6 · 1 voice
Medicine · #Sepsis Diagnosis and Treatment #Cardiac Fibrosis and Remodeling #Takotsubo Cardiomyopathy and Associated Phenomena
paper · pdf · doi:10.1080/09712119.2026.2697440
openalex publication_date 2026/07/09 · openalex created_date 2026/07/11 · openalex updated_date 2026/07/22
Sepsis-induced cardiomyopathy (SIC) is a major contributor to organ failure and poor clinical outcomes. Mechanisms underlying cardiac dysfunction during sepsis remain poorly understood. This study aims to establish a translational experimental model of SIC that integrates clinical, diagnostic imaging, histological and microbiological approaches to characterize SIC in early sepsis. Two experimental groups were assessed: sham group (n = 8) and sepsis-induced group (n = 10). Cardiac alterations were evaluated through electrocardiographic and echocardiographic assessments at the beginning and experimental endpoints (24 h after surgery). Samples were collected for histopathological, microbiological and biomarker analyses. Results showed histological heart injury with severe myocardial congestion, haemorrhage, interstitial oedema, inflammatory infiltrates and bacterial spread in septic animals. Although non-pathognomonic electrocardiographic changes were detected. Increase in QRS complex duration (p = 0.012) and elevation in ST segment (p = 0.009) were observed in septic group. Only C-reactive protein (CRP) present a significant increase in the septic group (p < 0.0001), providing limited information in early sepsis. Echocardiographic study showed increased left ventricular fraction shortening (p = 0.0001), not indicating improved cardiac contractility, but rather a pathological condition resulting from cardiac remodelling. CLP-induced sepsis in rats triggers early myocardial involvement, characterized by electrical alterations, echocardiographic changes under septic loading conditions, inflammatory histopathological lesions and an increased inflammatory response.