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Left Atrial Function Assessed by Left Atrial Strain in Patients with Left Circumflex Branch Culprit Acute Myocardial Infarction
Author(s) -
Lee Dong Hyun,
Park TaeHo,
Lee Jung Eun,
Cho YoungRak,
Park Kyungil,
Park Jong Sung,
Kim MooHyun,
Kim YoungDae
Publication year - 2015
Publication title -
echocardiography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.404
H-Index - 62
eISSN - 1540-8175
pISSN - 0742-2822
DOI - 10.1111/echo.12828
Subject(s) - medicine , cardiology , culprit , myocardial infarction , percutaneous coronary intervention , circumflex , artery
Introduction Although left atrium ( LA ) has played an important role in diastole, ischemic insult of atrium in acute myocardial infarction ( AMI ) has not been clearly evaluated. Methods We hypothesized that LA function would be further decreased in AMI patients with a culprit lesion in the left circumflex branch ( LCX ). This was an observational cohort study in a single university hospital. Echocardiography was performed to evaluate left ventricular diastolic function, LA volume, and LA function. Systolic ( LA S ) and late diastolic ( LA A ) LA strain were measured using speckle tracking echocardiography. Results Sixty‐eight AMI patients treated with emergent or urgent percutaneous coronary intervention were enrolled. Global LA S strain was significantly lower in patients with a culprit lesion in the LCX than culprit lesions in other vessels (left anterior descending, 27.3 ± 6.8%; left circumflex, 20.1 ± 8.9%; right coronary artery, 23.3 ± 6.5%; P = 0.007). LA volume index did not differ significantly (P = 0.093). Other clinical and conventional echocardiographic parameters, including Doppler measurements, did not differ significantly. Conclusions Global LA S strain was lower in AMI patients with a culprit lesion in the LCX than those with culprit lesions in other vessels, without any significant difference in LA volume index. The lower global LA S strain might suggest decreased LA function resulting from ischemic insult by AMI with culprit lesions in the LCX .

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