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.
Left atrial (LA) dilatation after acute myocardial infarction (AMI) has been associated with adverse outcomes in several studies. Most studies have evaluated the presence of LA enlargement immediately after AMI. However, complex alterations in ventricular architecture and function after AMI can result in diastolic dysfunction and therefore dilatation of the left atrium during follow-up after AMI. Data about the occurrence of LA remodeling during the follow-up of patients after AMI are scarce. Some evidence is available that LA remodeling occurs during follow-up in patients after high-risk AMI. However, in the current population of patients with AMI treated with primary percutaneous coronary intervention, the prevalence of LA remodeling and the effects on LA function during follow-up are unknown.
Accordingly, the purpose of the current study was to evaluate changes in LA dimensions and function during 1-year follow-up in patients after AMI. LA function was assessed extensively using mechanical function derived from LA volumes and myocardial deformation using novel speckle-tracking imaging. Furthermore, clinical and echocardiographic predictors of LA remodeling were established, and the effect of LA remodeling on changes in LA function was assessed.
Methods
Patient Population and Protocol
The study population included 407 patients from an ongoing clinical registry (MISSION!) with ST-segment elevation AMI who were treated with primary percutaneous coronary intervention. Clinical and echocardiographic data were prospectively entered into the departmental cardiology information system (EPD-Vision; Leiden University Medical Center, Leiden, The Netherlands) and the echocardiography database, respectively, and retrospectively analyzed. All patients were treated according to the institutional protocol (MISSION!), which includes standardized medical care according to the most recent guidelines. Within 24 hours of admission, medication is initiated, and within 24 to 48 hours of admission, echocardiography is performed. Thereafter, patients are scheduled for visits at the outpatient clinic, and echocardiography is repeated at 12-month follow-up. LA dimensions and function using conventional and speckle-tracking echocardiography were evaluated at baseline and at 12-month follow-up. The purpose of the current study was to investigate the changes in LA dimensions and function during 1-year follow-up in patients after AMI. Furthermore, the patient population was divided according to the presence of LA remodeling during follow-up, and clinical and echocardiographic predictors of LA remodeling were established. Finally, the effect of LA remodeling on changes in LA function was assessed, and the occurrence of new-onset fibrillation during 1-year follow-up was noted. Atrial fibrillation was determined on the basis of electrocardiographic findings consistent with the diagnosis of atrial fibrillation on 12-lead electrocardiograms and Holter recordings during hospitalization and follow-up at the outpatient clinic.
Echocardiography
According to the protocol (MISSION!), within 24 to 48 hours of admission for the index infarction and after 12-month follow-up, extensive two-dimensional echocardiographic evaluation was performed. Patients were imaged in the left lateral decubitus position using a commercially available system (Vivid 7; GE Vingmed Ultrasound AS, Horten, Norway). Images were obtained, with a simultaneous electrocardiographic signal, using a 3.5-MHz transducer at a depth of 16 cm in the parasternal and apical views. Standard M-mode and two-dimensional images were acquired during breath hold, and analysis of echocardiographic images was performed randomly offline by experienced observers (EchoPAC version 108.1.5; GE Vingmed Ultrasound AS).
Left ventricular (LV) end-systolic volume, LV end-diastolic volume, and LV ejection fraction were calculated using the biplane Simpson’s technique from the apical four-chamber and two-chamber views. Thereafter, the left ventricle was divided into 16 segments to calculate wall motion score index. Each segment was analyzed individually and scored on the basis of its motion and systolic thickening (1 = normokinesis, 2 = hypokinesis, 3 = akinesis, 4 = dyskinesis). Wall motion score index was calculated as the sum of the segment scores divided by the number of segments scored.
Mitral regurgitation was characterized as mild (jet area/LA area < 20%, vena contracta width < 0.30 cm), moderate (jet area/LA area, 20%–40%; vena contracta width, 0.30–0.69 cm), or severe (jet area/LA area > 40%, vena contracta width ≥ 0.70 cm).
To assess diastolic function, pulsed-wave Doppler of the mitral valve was performed by placing the Doppler sample volume between the tips of the mitral leaflets. The early (E) and late (A) peak diastolic velocities and E-wave deceleration time were measured. The E/E’ ratio was obtained by dividing E by E’, which was measured using color-coded Doppler tissue imaging at the septal side of the mitral annulus in the apical four-chamber view.
Diastolic function was graded according to the most recent recommendations of the American Society of Echocardiography. Diastolic function was graded as normal when septal E’ was ≥8, the E/A ratio was ≥1 and <2, and the deceleration time of the E wave was between 160 and 200 msec. Diastolic dysfunction was graded as mild (grade I) when septal E’ was <8, the E/A ratio was <0.8, and deceleration time was >200 msec; as moderate (grade II) when septal E’ was <8, the E/A ratio was 0.8 to 1.5, and deceleration time was 160 to 200 msec; and severe (grade III) when septal E’ was <8, the E/A ratio was ≥2, and deceleration time was <160 msec.
All measurements were performed by two experienced observers, and any discordances were discussed to obtain accurate measurements.
Analysis of LA Dimensions and Function
The apical two-chamber and four-chamber views were used to measure LA volumes using the biplane Simpson’s method. LA volumes were measured at three time points during the cardiac cycle: (1) maximal volume (LA max) at end-systole, just before mitral valve opening; (2) minimal volume (LA min) at end-diastole, just before mitral valve closure; and (3) volume before atrial active contraction (LA preA), obtained from the last frame before mitral valve reopening or at the time of the P wave on the surface electrocardiogram. All LA volumes were indexed to body surface area, as recommended.
LA mechanical function was derived from LA volumes and expressed with the following formulas :
total atrial emptying fraction: LA total ejection fraction = [ ( LA max − LA min ) / LA max ] × 100 ;
active atrial emptying fraction: LA active ejection fraction = [ ( LA preA − LA min ) / LA preA ] × 100 , which is considered an index of LA active contraction;
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