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<p>Cardiac hypertrophy is a critical concern in pharmacological research, necessitating accurate monitoring methods. The standard 14-day isoprenaline protocol using ECG often yields false cases and premature developments, compromising group homogeneity. Relying solely on ECG lead II overlooks cardiac wall involvement beyond the inferior wall. This study highlights the importance of multiple ECG leads for comprehensive cardiac hypertrophy assessment. Male albino Wistar rats underwent nine-lead ECG localization on days 1, 5, and 10, revealing TP and ST segment depression, T wave inversion, and peaked QRS complexes in the lead I, ST elevation in the lead V3, while lead II appeared almost normal in many subjects. Elevated heart weight, biomarkers, and histopathological findings confirmed cardiac stress and damage. Relying solely on lead II risks missing cardiac hypertrophy in many subjects, emphasizing the necessity of multi-lead ECG monitoring. Moreover, this study implements clinical ECG lead localization techniques to identify wall involvement and map ischemic sites, facilitating accurate histology and other molecular estimations post-sacrifice.</p>

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Multi-lead ECG Monitoring for Accurate Detection of Cardiac Hypertrophy in Rodent Models: Overcoming Limitations of Lead II for Enhanced Pre-clinical Evaluation

  • 期刊论文

  • 发表日期：

    2025年9月5日

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  • Satyajit Mohanty,
  • Tuhin Mukherjee,
  • José Carlos Tatmatsu-Rocha,
  • Ashok Pattnaik

摘要

Cardiac hypertrophy is a critical concern in pharmacological research, necessitating accurate monitoring methods. The standard 14-day isoprenaline protocol using ECG often yields false cases and premature developments, compromising group homogeneity. Relying solely on ECG lead II overlooks cardiac wall involvement beyond the inferior wall. This study highlights the importance of multiple ECG leads for comprehensive cardiac hypertrophy assessment. Male albino Wistar rats underwent nine-lead ECG localization on days 1, 5, and 10, revealing TP and ST segment depression, T wave inversion, and peaked QRS complexes in the lead I, ST elevation in the lead V3, while lead II appeared almost normal in many subjects. Elevated heart weight, biomarkers, and histopathological findings confirmed cardiac stress and damage. Relying solely on lead II risks missing cardiac hypertrophy in many subjects, emphasizing the necessity of multi-lead ECG monitoring. Moreover, this study implements clinical ECG lead localization techniques to identify wall involvement and map ischemic sites, facilitating accurate histology and other molecular estimations post-sacrifice.