Structural and functional remodelling of left atrium in various localizations of myocardial infarction

• Main Authors: K. G. Adamyan, A. L. Chilingaryan, L. R. Tumasyan
• Format: Article
• Language: Russian
• Published: «SILICEA-POLIGRAF» LLC 2010-02-01
• Series: Кардиоваскулярная терапия и профилактика
• Subjects: remodelling; myocardial infarction; transoesophageal parameters; left atrium
• Online Access: https://cardiovascular.elpub.ru/jour/article/view/2013
• ISSN: 1728-8800; 2619-0125

Aim. To study the dynamics of structural and functional parameters of left atrium (LA) in various localizations of myocardial infarction (MI), as a response to structural and functional remodelling of left ventriculum (LV). Material and methods. In total, 180 patients with primary acute LV MI and ST segment elevation were randomised into three groups: Group I – anterior MI (AIM); Group II – inferior MI (IMI); and Group III – posterior/lateral MI (PLMI). At Days 7, 90, and one year later, transoesophageal, transthoracic two-dimensional, flow and tissue Doppler ultrasound was performed, with the assessment of LV, LA body, and LA appendage (LAA) structure and function. Results. At baseline, LF structure and function were significantly lower, and end-systolic volume index was significantly higher in AIM than in IMI and PLMI, due to reduced LV contractility and increased LV rigidity. The maximal changes in baseline volume and functional LA characteristics were registered in PLMI, due to direct myocardial damage, the minimal changes – in IMI, with no negative dynamics in one year. The follow-up demonstrated progressing structural and functional LV and LA changes in AMI, with relatively stable LAA function. In PLMI, LAA function was reduced during the entire follow-up period. Conclusion. Structural and functional post-MI changes were observed for LV and LA, with the magnitude of these changes depending on MI localization. The most severe LV and LA dysfunction were registered in AMI. In PLMI, LA dysfunction was explained by the direct myocardial damage.