BACKGROUND: Left atrial (LA) size has been associated with adverse outcome in patients after acute myocardial infarction. However, data about the occurrence of late LA enlargement and changes in LA function during follow-up are scarce. The purpose of the current study was to evaluate changes in LA size and function during 1-year follow-up. METHODS: The study population comprised 407 patients with acute myocardial infarction who were treated with primary percutaneous coronary intervention. At baseline and 12 months, two-dimensional echocardiography was performed to assess LA volumes and function using speckle-tracking strain and strain rate. RESULTS: The mean age was 60 ± 11 years, and most patients were men (78%). LA maximal volume increased from 25 ± 8 to 28 ± 8 mL/m(2) (P < .001) from baseline to 1 year. Echocardiographic assessment at 1-year follow-up showed that 92 patients (25%) had developed LA remodeling (defined as an increase of ≥8 mL/m(2) in LA maximal volume). On multivariate analysis, only LA maximal volume at baseline (odds ratio, 0.95; 95% confidence interval, 0.91-0.98; P = .003) and LA strain at baseline (odds ratio, 0.94; 95% confidence interval, 0.92-0.97; P < .001) were independent predictors of LA remodeling during follow-up. Interestingly in patients without LA remodeling, no changes were observed in LA function during follow-up. However, in patients with LA remodeling, LA function significantly worsened during follow-up. In line, LA strain and strain rate were significantly lower at 12 months compared with baseline (24 ± 7% vs 27 ± 6%, P < .001, and 1.8 ± 0.5 vs 2.4 ± 0.7 sec(-1), P < .001, respectively). CONCLUSIONS: LA remodeling occurred in 22% of patients after acute myocardial infarction. In patients without LA remodeling, no changes in LA function were observed, but in patients with LA remodeling, LA function deteriorated significantly.
BACKGROUND: Left atrial (LA) size has been associated with adverse outcome in patients after acute myocardial infarction. However, data about the occurrence of late LA enlargement and changes in LA function during follow-up are scarce. The purpose of the current study was to evaluate changes in LA size and function during 1-year follow-up. METHODS: The study population comprised 407 patients with acute myocardial infarction who were treated with primary percutaneous coronary intervention. At baseline and 12 months, two-dimensional echocardiography was performed to assess LA volumes and function using speckle-tracking strain and strain rate. RESULTS: The mean age was 60 ± 11 years, and most patients were men (78%). LA maximal volume increased from 25 ± 8 to 28 ± 8 mL/m(2) (P < .001) from baseline to 1 year. Echocardiographic assessment at 1-year follow-up showed that 92 patients (25%) had developed LA remodeling (defined as an increase of ≥8 mL/m(2) in LA maximal volume). On multivariate analysis, only LA maximal volume at baseline (odds ratio, 0.95; 95% confidence interval, 0.91-0.98; P = .003) and LA strain at baseline (odds ratio, 0.94; 95% confidence interval, 0.92-0.97; P < .001) were independent predictors of LA remodeling during follow-up. Interestingly in patients without LA remodeling, no changes were observed in LA function during follow-up. However, in patients with LA remodeling, LA function significantly worsened during follow-up. In line, LA strain and strain rate were significantly lower at 12 months compared with baseline (24 ± 7% vs 27 ± 6%, P < .001, and 1.8 ± 0.5 vs 2.4 ± 0.7 sec(-1), P < .001, respectively). CONCLUSIONS: LA remodeling occurred in 22% of patients after acute myocardial infarction. In patients without LA remodeling, no changes in LA function were observed, but in patients with LA remodeling, LA function deteriorated significantly.
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