Changes in global longitudinal strain and left ventricular ejection fraction during the first year after myocardial infarction: results from a large consecutive cohort

Changes in global longitudinal strain and left ventricular ejection fraction during the first... Abstract Aims To determine changes of global longitudinal strain (GLS) and their predictors in relation to classical echocardiographic parameters of left ventricular (LV) function, over 1 year, in consecutive patients with myocardial infarction (MI) and initially normal or impaired LV ejection fraction (EF). Methods and results A total of 285 patients with MI prospectively included in the REBUS (RElevance of Biomarkers for future risk of thromb-oembolic events in UnSelected post-myocardial infarction patients) study underwent echocardiography within 72 h from admission and after 1 year. At baseline, 213 (74.7%) of MI patients had a normal EF (≥52% in men or ≥54% in women), but in 70.4% of them, an impaired GLS ( ≥ −18.0%) was observed. During 1-year follow-up, in patients with normal EF at baseline, GLS improved from −15.8% to − 17.4% (10.1% relative change); EF decreased from 62.5% to 59.9% (4.0% relative change); indexed end-diastolic volume, indexed end-systolic volume, and indexed stroke volume increased with 15.6%, 24.8%, and 10.0% of relative change, respectively (P < 0.001 for all the comparisons). In the whole cohort, initial impairment of LV function [by EF, wall motion score index (WMSI), or GLS], male gender, non-smoking, and treatment with beta-blockers were the independent predictors of GLS improvement. In the group with initially impaired EF, over 1 year GLS improved from −11.9% to − 14.8% (24.4% relative change) and EF from 44.6% to 52.6% (18.2% relative change) (P < 0.001 for both). Improvement in GLS significantly correlated with EF increase in the group with impaired EF (r = −0.41, P = 0.001) but not in the patients with normal EF (r = −0.14, P = ns). Conclusions Despite diveregent evolution of GLS compared with EF and ventricular volumes, one year after MI GLS significantly improved in patients with initially both normal and impaired EF. Initial impairment of LV function (by EF, WMSI, or GLS), male gender, non-smoking, and treatment with beta-blockers were independent predictors of GLS improvement. LV remodelling was present even in patients with normal EF at baseline and during follow-up, confirming limited functional assessment by EF alone. left ventricular function, myocardial infarction, remodelling, global longitudinal strain Introduction For many decades, left ventricular (LV) ejection fraction (EF) has widely been used as the only determinant of LV systolic function in risk scores, registries, and therapeutical guidelines.1,2 Rapid and more effective treatments minimizing the extent of myocardial damage and the introduction of highly sensitive troponins have led to a search for novel sensitive imaging biomarkers with the ability to detect and follow-up minor myocardial impairment. About two-thirds of patients hospitalized today with acute myocardial infarction (MI) have normal LV EF,3,4 although the majority of them have at least one of the other markers of systolic function outside the normal range.5 Global longitudinal strain (GLS) obtained by speckle-tracking echocardiography has been introduced as the most promising marker of myocardial deformation impairment reflecting subclinical LV dysfunction in a wide range of cardiac disorders.6 Little is known about the changes in myocardial deformation after MI, in particular in patients with preserved or only mildly impaired EF, and thus post-infarction remodelling in this growing patient population. The aim of this study was to determine the changes of GLS in relation to classical echocardiographic measures of LV function and their predictors in a large unselected cohort of consecutive MI patients during a 12-month follow-up. Our patient cohort has a wide range of baseline EF but reflects the contemporary preponderance of normal baseline post-infarction EF, which sets it apart from earlier studies.7–9 Baseline echocardiographic characteristics of this cohort at the time of their hospitalization have been published previously.5 Methods Consecutive patients with MI hospitalized in the Department of Cardiology, Uppsala University Hospital, in the period from April 2010 to August 2012 were prospectively included in the REBUS (RElevance of Biomarkers for future risk of thromboembolic events in UnSelected post-myocardial infarction patients) study.5 Inclusion criteria were MI diagnosed by dynamic-raised cardiac troponin I (cTnI) with at least one value above the upper reference limit, together with at least one of the clinical or electrocardiographic criteria as well as the ability to attend the scheduled visits for evaluation procedures and signed informed consent. Patients who died within 5 days after MI were excluded. All patients enrolled in REBUS were treated according to clinical practice. Treatment and medical history data were collected before discharge and during follow-up visits. Echocardiography was performed per study protocol in the cardiac intensive care unit within 72 h and during follow-up at 12 months after hospital admission, and the prospectively collected echo data were retrospectively reviewed by experienced echocardiographers. After excluding patients lacking baseline or follow-up echo, and those during follow-up withdrew their consent or died, a total of 312 patients with echocardiographic studies recorded both at baseline and during follow-up completed study protocol. Furthermore, 27 (8.7%) patients were excluded due to non-satisfactory image quality. Figure 1 illustrates the inclusion process. Figure 1 View largeDownload slide Study population. CICU, cardiac intensive care unit, indicates echo studies during hospitalization (0); FU, follow-up, indicates follow-up studies after 12 months; LV EF, left ventricular ejection fraction; MI, myocardial infarction; *LV EF ≥ 54% in women, LV EF ≥ 52% in men. Figure 1 View largeDownload slide Study population. CICU, cardiac intensive care unit, indicates echo studies during hospitalization (0); FU, follow-up, indicates follow-up studies after 12 months; LV EF, left ventricular ejection fraction; MI, myocardial infarction; *LV EF ≥ 54% in women, LV EF ≥ 52% in men. Two-dimensional echocardiography was performed in the standard apical four-, three-, and two-chamber views. LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF were assessed using the biplane Simpson’s method. Left atrial volume was calculated using the monoplane area length method. Stenotic and regurgitant valve diseases were evaluated using semi-quantitative and quantitative methods as recommended by current guidelines.10,11 Since images were acquired with echo machines from two different vendors (Philips iE33 Ultrasound system at the cardiac intensive care unit and GE Vivid E9 Ultrasound system at follow-up), we used an external software, Image Arena V 4.6 Build 4.6.4.10 (TomTec Imaging system, Munich, Germany), for all speckle-tracking based analysis. In all apical views, the endocardial borders were manually traced in the end-systolic frame, while end-diastolic borders were provided automatically by the software allowing manual correction, if necessary. Global longitudinal strain (GLS) was then automatically calculated. According to recommendations from the American Society of Echocardiography and the European Association of Cardiovascular Imaging, we excluded images with suboptimal tracking of the endocardium in more than two segments in one single view or if frame rate was below 40 Hz.12 Normal values concerning systolic function and ventricular size were based on current echocardiographic recommendations (LV EF ≥ 54% in women and ≥52% in men, LV EDV ≤61 mL/m2 in women and ≤74 mL/m2 in men, and LV ESV ≤24 mL/m2 in women and ≤ 31 mL/m2 in men.13 cTnI was serially collected as part of clinical routine, and maximal values were obtained. The study was approved by the Regional Ethical Review Board at Uppsala University (reference number: 2009/210). Statistical methods Patients with normal and impaired LV EF were compared in terms of background factors, echocardiographic parameters, and biomarkers. Categorical variables were presented as the number of patients and frequencies. Continuous variables were presented as mean ± standard deviation or as median and interquartile range (IQR). The change in echocardiographic parameters between baseline and follow-up studies was presented as mean difference with a 95% confidence interval (CI). Categorical variables were compared with the χ2 test. Continuous variables were compared with paired and independent samples t-test where appropriate in cases of normally distributed data and with Mann–Whitney test in cases of non-normally distributed data. Associations between echocardiographic parameters, baseline patient characteristics, and cTnI were tested using linear regression or one-way analysis of variance. To identify independent predictors of GLS changes over time among background demographics (gender and age), clinical data (risk factors, co-morbidities, and medical history), coronary artery territory treated with percutaneous coronary intervention (PCI), medical treatments, and baseline echocardiographic characteristics including baseline LV function measures [EF, wall motion score index (WMSI), and GLS], univariate and multivariate logistic regression analyses were performed in the whole study population, as well as separately in patients with initially normal and impaired LV EF. All variables with P-value <0.05 in univariate analysis were introduced to the multivariate regression models. LV EF, GLS, and WMSI at baseline were used in multivariate models separately to avoid co-linearity. For all analyses, two-sided P-values <0.05 were defined as significant. As previously reported, the intraobserver variability for repeated measurements of all LV function parameters was excellent [intra-class correlation coefficient (ICC) >0.75 for all LV function parameters].5 In this analysis, to study inter-observer variability, a random sample of 70 studies was analysed by two experienced echocardiographers independently and ICC was calculated. Statistical analyses were performed using IBM SPSS V.24.0 (SPSS, IBM Corporation, Armonk, NY, USA). Results Baseline characteristics After excluding patients who withdrew their consent during follow-up (n = 18, 4.3%) or died (n = 7, 1.7%), a total of 312 patients with echocardiographic studies recorded both at baseline and during follow-up completed the study protocol. Further, 27 of them (8.7%) were excluded due to non-satisfactory image quality (Figure 1). A total of 285 patients were included to the final analysis. The mean age of the study population was 65.8 ± 10.1 years, and 80.0% (n = 228) of the patients were men. Clinical data are presented in Table 1. Since only patients who survived to 1 year after infarction were included, there was no mortality in the study group. Table 1 Demographics, medical history, clinical status, and treatments Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 a Including clopidogrel, ticagrelor, or prasugrel. b Including aldosterone receptor blockers. LV EF, left ventricular ejection fraction; BP, blood pressure; cTnI, cardiac troponin I; STEMI, ST-elevation myocardial infarction; MI, myocardial infarction; CHF, congestive heart failure; LV EF, left ventricular ejection fraction; ACEI, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; PCI, percutaneous coronary intervention; LAD, left anterior descending artery; LCx, left circumflex artery; RCA, right coronary artery; ECG, electrocardiography. Table 1 Demographics, medical history, clinical status, and treatments Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 a Including clopidogrel, ticagrelor, or prasugrel. b Including aldosterone receptor blockers. LV EF, left ventricular ejection fraction; BP, blood pressure; cTnI, cardiac troponin I; STEMI, ST-elevation myocardial infarction; MI, myocardial infarction; CHF, congestive heart failure; LV EF, left ventricular ejection fraction; ACEI, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; PCI, percutaneous coronary intervention; LAD, left anterior descending artery; LCx, left circumflex artery; RCA, right coronary artery; ECG, electrocardiography. The MI diagnosis was ST-elevation myocardial infarction (STEMI) in 51.2% (n = 146) of patients. The majority of the patients (89.5%, n = 255) were treated with PCI. In patients with STEMI, median time from both onset of symptoms and first ECG registration to recanalization was significantly shorter when compared with non-ST-elevation myocardial infarction (NSTEMI) patients, 177 (IQR 105–399) vs. 1421 (IQR 729–2173) min and 57 (IQR 44–83) vs. 1155 (IQR 405–1550) min, respectively (P < 0.001 for both), but did not differ between patients with normal and impaired LV EF, comprising all the MI types. LV systolic dysfunction defined according to the present criteria as EF below 52% in men and below 54% in women13 was observed in 25.3% (n = 72) of the patients <72 h after MI. History of previous MI was reported in 17.5% (n = 50) of all included patients and did not differ between the studied groups. Patients with impaired EF presented with higher peak cTnI concentrations, lower systolic blood pressure, and higher heart rate, compared with those with normal EF. No significant differences in demographics, cardiovascular risk factors, or co-morbidities were observed, except that history of congestive heart failure was more common in patients with impaired EF. There were no differences in invasive treatment and in prescribed medication, with the exception that patients with impaired EF more often received diuretics on discharge (Table 1). After 1 year, in the whole study group, systolic blood pressure was significantly higher, while diastolic blood pressure remained unchanged (132 ± 17 vs. 125 ± 16 mmHg, P < 0.001 and 74 ± 10 vs. 73 ± 10 mmHg, P = 0.084). Echocardiographic parameters at baseline and their change during follow-up Patients with impaired EF at baseline had significantly higher LV WMSI, LV mass, and left atrial volume and lower tricuspid annular plane systolic excursion, reflecting right ventricular longitudinal function, when compared with those with normal EF. Moderate or severe mitral regurgitation was also more frequent in patients with impaired EF (Table 2). Table 2 Echocardiographic study at baseline Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 LV EF, left ventricular ejection fraction; WMSI, wall motion score index; LVMi, left venricular mass index; LAVi, left atrial volume index; TAPSE, tricuspid annular plane systolic excursion; MV DT, mitral valve inflow deceleration time. Table 2 Echocardiographic study at baseline Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 LV EF, left ventricular ejection fraction; WMSI, wall motion score index; LVMi, left venricular mass index; LAVi, left atrial volume index; TAPSE, tricuspid annular plane systolic excursion; MV DT, mitral valve inflow deceleration time. Mean values of EF, GLS, and indexed to the body surface area EDV, ESV, and stroke volume at admission and at 12-month follow-up and their changes over time, described as absolute delta (12-month minus baseline value) in variable units and relative change in % are presented in Table 3. Among patients with normal EF, as many as 70.4% (n = 150) presented with abnormal GLS, defined as ≥ −18.0%.6 Table 3 Echocardiographic parameters, comparison between groups with normal and impaired LV EF at inclusion Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). EF, ejection fraction; GLS, global longitudinal strain; EDVi, end-diastolic volume index; ESVi, end systolic volume index; SVi, stroke volume index. Table 3 Echocardiographic parameters, comparison between groups with normal and impaired LV EF at inclusion Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). EF, ejection fraction; GLS, global longitudinal strain; EDVi, end-diastolic volume index; ESVi, end systolic volume index; SVi, stroke volume index. Among patients with initially normal EF during follow-up mean EF decreased by 2.5% (CI −3.6 to −1.5), corresponding to a 4.0% relative decrease, while mean GLS improved by 1.6% (CI −2.0 to −1.1, a 10.1% relative improvement). Mean indexed EDV (EDVi) increased by 6.5 mL/m2 (CI 5.0–7.9, relative increase 15.6%), mean indexed ESV (ESVi) increased by 3.9 mL/m2 (CI 3.0–4.7), and mean SV increased by 2.6 mL/m2 (CI 1.6–3.6, relative increase 10%). P-values were <0.001 for all the changes. In patients with impaired systolic function, after 12 months, mean EF had increased by 8.1% (CI 5.3–10.8), corresponding to a 18.2% relative increase, mean GLS improved by 2.9% (CI −3.7 to −2.2, relative increase 18.2%), and mean indexed SV increased by 4.9 mL/m2 (CI 3.1–6.7, relative increase 20.9%) No significant changes in EDVi and ESVi were noticed (Table 3 and Figure 2). Figure 2 View largeDownload slide Changes in different parameters of left ventricular function during 12-month follow-up in patients with normal and impaired LV EF. GLS, global longitudinal strain; EF, ejection fraction; EDVi, end-diastolic volume index, ESVi, end-systolic volume index; SVi, stroke volume index; Δ indicates a change in respective parameters; mean values and standard deviations are shown. %U indicates GLS and EF % units, not relative percent. Figure 2 View largeDownload slide Changes in different parameters of left ventricular function during 12-month follow-up in patients with normal and impaired LV EF. GLS, global longitudinal strain; EF, ejection fraction; EDVi, end-diastolic volume index, ESVi, end-systolic volume index; SVi, stroke volume index; Δ indicates a change in respective parameters; mean values and standard deviations are shown. %U indicates GLS and EF % units, not relative percent. Predictors of GLS improvement Improvement in GLS was significantly greater in the subgroup with impaired EFcompared with the subgroup with normal EF at baseline [delta GLS −2.9% (CI −3.7 to −2.2) vs. −1.6% (CI −2.0 to 1.2); P = 0.003], as well as in patients with pathologic WMSI compared with normal WMSI at baseline [delta GLS −2.2% (CI −2.6 to −1.7) vs. −0.9% (CI −1.8 to −0.1), P = 0.015]. GLS improvement correlated significantly with EF increase in a group with impaired EF (r = −0.41, P = 0.001) but not in those with initially normal EF (r = −0.14, P = 0.06; Figure 2). Men presented significantly higher improvement of GLS during follow-up than women in the whole studied group [−2.1% (CI −2.6 to −1.7) vs. −1.1% (CI −2.0 to −0.1), P = 0.03]. Patients with MI treated with PCI in the left anterior descending (LAD) coronary artery territory had significantly higher improvement in GLS when compared with those with PCI in the non-LAD infarction territory [−2.5% (CI −3.2 to −1.8) vs. –1.6% (CI −2.1 to −1.1); P = 0.032]. No significant differences were observed between type of MI (STEMI or NSTEMI) or other baseline clinical characteristics and change in GLS. Patients who were prescribed beta-blockers at discharge had a significantly greater improvement in GLS, compared to those not treated with beta-blockers [delta GLS −2.0% (CI −2.4 to −1.6) vs. −0.4% (CI −1.8 to 1.0); P = 0.037; Figure 3]. No other significant differences were observed between medications at discharge and change in GLS. Figure 3 View largeDownload slide Impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. Box plots showing significant impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. The box represents an interval between first and third quartile, the band inside the box indicates median value and the whiskers indicate 10th and 90th percentiles. Figure 3 View largeDownload slide Impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. Box plots showing significant impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. The box represents an interval between first and third quartile, the band inside the box indicates median value and the whiskers indicate 10th and 90th percentiles. No significant relationship between other LV measures or peak cTnI at baseline and change in GLS was found. Significant univariate predictors of GLS improvement during 1-year follow-up for the whole studied group and separately for patients with initially normal and impaired EF are presented in Table 4. Table 4 Prediction of LV GLS improvement Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). a Baseline EF, WMSI and GLS used in the multivariate analysis separately to avoid colinearity. LAD, left anterior descending artery; EF, ejection fraction; WMSI, wall motion score index; BP, blood pressure. Table 4 Prediction of LV GLS improvement Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). a Baseline EF, WMSI and GLS used in the multivariate analysis separately to avoid colinearity. LAD, left anterior descending artery; EF, ejection fraction; WMSI, wall motion score index; BP, blood pressure. To avoid co-linearity, separate multivariate regression models were constructed where baseline measures of LV function, such as EF, WMSI, and GLS were used separately. In multiple regression analysis, male gender, non-smoking, treatment with beta-blockers and in respective models more impaired EF, WMSI, and GLS at baseline were independent predictors of GLS improvement in the whole studied group. In patients with initially normal EF, more impaired GLS at baseline was the only measure of LV function that could predict GLS improvement over the time. In subgroup with impaired EF, no independent predictors of GLS improvement could be identified (Table 4). A difference in systolic and diastolic blood pressures between 1 year and baseline measurements, known as a potential confounder, did not show an independent predictive impact on GLS behaviour in any analysed models. In the whole group, correlation between EF and GLS was r = −0.53 (P < 0.001) at baseline and r = −0.42 after 12 months (P < 0.001). Intra- and interobserver variability The excellent intraobserver variability for repeated measurements of all LV function parameters (ICC > 0.75) was reported previously.5 Reproducibility of GLS measurements between two experienced echocardiographers in a random sample of 70 studies was also excellent [ICC 0.91 (95% CI 0.86–0.95); P < 0.001, for average measures). Discussion In this large contemporary ‘all-comers’ cohort of patients with both NSTEMI and STEMI, a divergent evolution of GLS compared with EF and ventricular volumes was observed. In the cohort as a whole, GLS significantly improved during the following 12 months. Initial impairment of LV function (by EF, WMSI, or GLS) was independently predictive for GLS improvement in the whole cohort. Further, male gender, non-smoking, and treatment with beta-blockers were independent predictors of GLS improvement. In the subgroup with normal EF at baseline, which in our study was considerably larger (75% of patients) than in earlier studies, GLS was impaired at baseline, improved significantly during follow-up, but still remained slightly impaired at 1 year. Only initial impairment of GLS remained significant as predictive parameter of later GLS improvement in a multivariate analysis. LV volumes, however, increased and EF decreased in this group, possibly reflecting at least in part initial remote hyperkinesia abating during follow-up. This discrepancy in the time course of EF and GLS (Figure 4) indicates that these parameters reflect different aspects of LV systolic function. Figure 4 View largeDownload slide Correlation between changes of GLS and EF (delta GLS and delta EF) in patients with initially normal and impaired LV EF. Figure 4 View largeDownload slide Correlation between changes of GLS and EF (delta GLS and delta EF) in patients with initially normal and impaired LV EF. In the subgroup with initially impaired EF (25% of patients), ESVs did not change significantly, but EDVs increased, leading to higher SVs and higher EF. Thus, there was more improvement in systolic function as measured by volumes in the initially impaired group than in the group with initially normal EF, perhaps because there was more ‘room for improvement’ in the former. This larger improvement is also reflected in the delta GLS, which was more than double as high (24.4 vs. 10.1% relative change) in the group with initially impaired EF compared with the group with initially normal EF. However, GLS on average remained below normal both initially and at follow-up. No independent predictors of GLS improvement were identified considering this group exclusively, likely related to lack of statistical power. Post-infarction remodelling is known as a morphological and functional process recruiting preload reserve by ventricular dilatation. Whether remodelling occurs in patients with normal early post-infarction EF has not been elucidated but is important, given its well-known adverse prognostic effect.14 Such patients, as demonstrated in our study, are increasingly common due to better acute therapy.4 Interestingly, in our patient group with initially normal EF, we observed a significant reduction of EF (albeit remaining in the normal range) parallel to an increase of both EDV and ESV, reflecting post-infarction remodelling in these apparently functionally intact patients. This indicates a shortcoming of using exclusively EF in post-infarction assessment, which is still the most widely used echocardiographic measure of LV systolic function with a prominent position in guidelines, registries, and predictive models. A few studies addressing evolution of GLS in post-infarction patients have been published.7–9 However, the study population, predominantly or exclusively with STEMI, had substantially lower EF when compared with our cohort. More commonly preserved LV function reflects the contemporary transition in patient characteristics towards smaller infarcts presumably due to more sensitive biomarker diagnostics, more effective therapy, and other factors. Antoni et al. used GLS as the only measure of LV function changes one year after MI. The study population was comparable with our impaired EF subgroup in terms of similar baseline EF (mean 45%) and slightly bigger volumes (EDVi, ESVi). The authors have found a gradual improvement of GLS (23% relative change), however not addressing changes in other functional parameters. Similarly to our results, Antoni et al.7 found GLS to be an independent predictor of LV function recovery 1 year after MI. Furthermore, they found the infarct size, LAD culprit vessel, and diastolic dysfunction as predictors of LV function recovery after MI. Hoogslag et al.8 reported parallel improvement of GLS (13 and 15% relative change, respectively) and EF (9 and 11% relative change, respectively) in diabetic and non-diabetic patients with initially mildly impaired EF (mean EF 47 and 48%, respectively) during 6 months after STEMI. Similar to our observations, EF improvement was associated with significant increase of EDV, while ESV remained unchanged. Diabetes, but also infarct size, and overt heart failure at baseline were the independent predictors of GLS improvement.8 In a further study,9 a large group of 1041 STEMI patients with mean EF 47% and mean GLS of − 15% and those with GLS poorer than −15% experienced more significant EDV increase. Baseline GLS, but also infarct size, HR, and LAD culprit lesion were independent predictors of post-MI remodelling. Changes in other parameters as EF or ESV were not reported.9 The reason for discrepancy in EF and GLS course in our study may lie in the presence of initial local hyperkinesia of remote left ventricular segments, which may affect EF more than GLS. In the whole population, we found a relationship between LV impairment at inclusion and subsequent change in GLS, meaning that more impaired EF is related to more significant improvement in GLS. Once hyperkinesia subsides, EF decreases, but GLS improves. Interestingly, in the subgroup of patients with normal EF at baseline, neither initially impaired EF nor WMSI, but only impaired GLS at baseline could predict GLS improvement over the time. This observation may reflect probably lower reliability of ‘higher normal’ values of EF in prediction of cardiac remodelling. Our study was observational and not designed to identify predictors of clinical outcome, but several studies have shown higher prognostic impact of GLS than EF in a wide range of cardiac disorders,15 including patients with MI.16,17 Ersboll et al.18 found that in patients with MI and normal or mildly impaired EF, those with GLS < 14% (absolute value) had an increased risk for the combined endpoint of all-cause mortality and heart failure admissions. Other areas where discrepancies between EF and GLS have been described are in the surveillance of patients undergoing cardiotoxic chemotherapy,19,20 valvular heart disease,21,22 cardiomyopathies,23 and heart failure with preserved EF.24,25 In our study, we were not able to show any impact of initial peak cTnI on GLS improvement during follow-up. This is in contrast to previous studies showing that an elevated level of cTnI is a prognostic factor not only for infarct size and LV EF but also on cardiac remodelling.26–28 The likely explanation is that the maximal possible value of detection for the cTnI assay we have used was 50 μg/L, which was present in a substantial number of patients and may have distorted relations with functional parameters. Limitations Several limitations of this study need to be acknowledged. One-fourth of the patients needed to be excluded due to missing one of two echo studies. Secondly, based on non-satisfactory image quality of baseline and/or follow-up study, 27 (8.7%) patients were excluded from the analysis, including those studies in which more than 2 segments could not be analysed. Thirdly, by study design, the patients who did not survive to follow-up were excluded, which introduces a selection. Fourthly, given the recently disputed accuracy and intervendor reproducibility of segmental longitudinal strain in ischaemic heart disease,29,30 we address only GLS measurements. Conclusion In the vast majority of consecutive contemporary patients with acute MI, the EF remains normal; however, GLS is impaired in 70% of them, and morphological LV remodelling occurs. During the 1-year follow-up, opposite changes in LV EF and GLS evolution were observed, suggesting that EF decrease might reflect subsiding compensatory hyperkinesia seen in the acute MI phase, while GLS improvement may more sensitively track ‘true’ systolic function improvement. Male gender, more impaired LV function at baseline, non-smoking, and treatment with beta-blockers were the independent predictors of GLS improvement in the whole studied group. The prognostic role of GLS changes after MI needs to be determined in future studies. Acknowledgements The author would like to thank Nermin Hadziosmanovic, biostatistician at Uppsala Clinical Research Center for his contribution to this article. Funding This work was supported by grants from Erik, Karin och Gösta Selanders Foundation. Conflict of interest: None declared. References 1 Steg PG , James SK , Atar D , Badano LP , Lundqvist CB , Borger MA. et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation . Eur Heart J 2012 ; 33 : 2569 – 619 . Google Scholar Crossref Search ADS PubMed 2 Hamm CW , Bassand JP , Agewall S , Bax J , Boersma E , Bueno H. et al. ; ESC Committee for Practice Guidelines . ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC) . Eur Heart J 2011 ; 32 : 2999 – 3054 . Google Scholar Crossref Search ADS PubMed 3 Choo EH , Chang K , Ahn Y , Jeon DS , Lee JM , Kim DB. et al. Benefit of β-blocker treatment for patients with acute myocardial infarction and preserved systolic function after percutaneous coronary intervention . Heart 2014 ; 100 : 492 – 9 . Google Scholar Crossref Search ADS PubMed 4 Hambraeus K , Held C , Johansson P , Svennberg L , Cider Å , James S. et al. SWEDEHEART Annual Report 2012 . Scand Cardiovasc J 2014 ; 48 : 2 – 133 . Google Scholar Crossref Search ADS 5 Baron T , Flachskampf FA , Johansson K , Hedin EM , Christersson C. Usefulness of traditional echocardiographic parameters in assessment of left ventricular function in patients with normal ejection fraction early after acute myocardial infarction: results from a large consecutive cohort . Eur Heart J Cardiovasc Imaging 2016 ; 17 : 413 – 20 . Google Scholar Crossref Search ADS PubMed 6 Smiseth OA , Torp H , Opdahl A , Haugaa KH , Urheim S. Myocardial strain imaging: how useful is it in clinical decision making? Eur Heart J 2016 ; 37 : 1196 – 207 . Google Scholar Crossref Search ADS PubMed 7 Antoni ML , Mollema SA , Atary JZ , Borleffs CJ , Boersma E , van de Veire NR. et al. Time course of global left ventricular strain after acute myocardial infarction . Eur Heart J 2010 ; 31 : 2006 – 13 . Google Scholar Crossref Search ADS PubMed 8 Hoogslag GE , Abou R , Joyce E , Boden H , Kamperidis V , Regeer MV. et al. Comparison of changes in global longitudinal peak systolic strain after ST-segment elevation myocardial infarction in patients with versus without diabetes mellitus . Am J Cardiol 2015 ; 116 : 1334 – 9 . Google Scholar Crossref Search ADS PubMed 9 Joyce E , Hoogslag GE , Leong DP , Debonnaire P , Katsanos S , Boden H. et al. Association between left ventricular global longitudinal strain and adverse left ventricular dilatation after ST-segment-elevation myocardial infarction . Circ Cardiovasc Imaging 2014 ; 7 : 74 – 81 . Google Scholar Crossref Search ADS PubMed 10 Vahanian A , Alfieri O , Andreotti F , Antunes MJ , Barón-Esquivias G , Baumgartner H. et al. Guidelines on the management of valvular heart disease (version 2012) . Eur Heart J 2012 ; 33 : 2451 – 96 . Google Scholar Crossref Search ADS PubMed 11 Lancellotti P , Tribouilloy C , Hagendorff A , Popescu BA , Edvardsen T , Pierard LA. et al. Recommendations for the echocardiographic assessment of native valvular regurgitation: an executive summary from the European Association of Cardiovascular Imaging . Eur Heart J Cardiovasc Imaging 2013 ; 14 : 611 – 44 . Google Scholar Crossref Search ADS PubMed 12 Voigt JU , Pedrizzetti G , Lysyansky P , Marwick TH , Houle H , Baumann R. et al. Definitions for a common standard for 2D speckle tracking echocardiography: consensus document of the EACVI/ASE/Industry Task Force to standardize deformation imaging . Eur Heart J Cardiovasc Imaging 2015 ; 16 : 1 – 11 . Google Scholar Crossref Search ADS PubMed 13 Lang RM , Badano LP , Mor-Avi V , Afilalo J , Armstrong A , Ernande L. et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging . Eur Heart J Cardiovasc Imaging 2015 ; 16 : 233 – 71 . Google Scholar Crossref Search ADS PubMed 14 White HD , Norris RM , Brown MA , Brandt PW , Whitlock RM , Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction . Circulation 1987 ; 76 : 44 – 51 . Google Scholar Crossref Search ADS PubMed 15 Kalam K , Otahal P , Marwick TH. Prognostic implications of global LV dysfunction: a systematic review and meta-analysis of global longitudinal strain and ejection fraction . Heart 2014 ; 100 : 1673 – 80 . Google Scholar Crossref Search ADS PubMed 16 Antoni ML , Mollema SA , Delgado V , Atary JZ , Borleffs CJW , Boersma E. et al. Prognostic importance of strain and strain rate after acute myocardial infarction . Eur Heart J 2010 ; 31 : 1640 – 7 . Google Scholar Crossref Search ADS PubMed 17 Munk K , Andersen NH , Terkelsen CJ , Bibby BM , Johnsen SP , Bøtker HE. et al. Global left ventricular longitudinal systolic strain for early risk assessment in patients with acute myocardial infarction treated with primary percutaneous intervention . J Am Soc Echocardiogr 2012 ; 25 : 644 – 51 . Google Scholar Crossref Search ADS PubMed 18 Ersbøll M , Valeur N , Mogensen UM , Andersen MJ , Møller JE , Velazquez EJ. et al. Prediction of all-cause mortality and heart failure admissions from global left ventricular longitudinal strain in patients with acute myocardial infarction and preserved left ventricular ejection fraction . J Am Coll Cardiol 2013 ; 61 : 2365 – 73 . Google Scholar Crossref Search ADS PubMed 19 Negishi K , Negishi T , Haluska BA , Hare JL , Plana JC , Marwick TH. Use of speckle strain to assess left ventricular responses to cardiotoxic chemotherapy and cardioprotection . Eur Heart J Cardiovasc Imaging 2014 ; 15 : 324 – 31 . Google Scholar Crossref Search ADS PubMed 20 Plana JC , Galderisi M , Barac A , Ewer MS , Ky B , Scherrer-Crosbie M. et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging . Eur Heart J Cardiovasc Imaging 2014 ; 15 : 1063 – 93 . Google Scholar Crossref Search ADS PubMed 21 Kearney LG , Lu K , Ord M , Patel SK , Profitis K , Matalanis G. et al. Global longitudinal strain is a strong independent predictor of all-cause mortality in patients with aortic stenosis . Eur Heart J Cardiovasc Imaging 2012 ; 13 : 827 – 33 . Google Scholar Crossref Search ADS PubMed 22 Kamperidis V , Marsan NA , Delgado V , Bax JJ. Left ventricular systolic function assessment in secondary mitral regurgitation: left ventricular ejection fraction vs. speckle tracking global longitudinal strain . Eur Heart J 2016 ; 37 : 811 – 6 . Google Scholar Crossref Search ADS PubMed 23 Urbano-Moral JA , Rowin EJ , Maron MS , Crean A , Pandian NG. Investigation of global and regional myocardial mechanics with 3-dimensional speckle tracking echocardiography and relations to hypertrophy and fibrosis in hypertrophic cardiomyopathy . Circ Cardiovasc Imaging 2014 ; 7 : 11 – 9 . Google Scholar Crossref Search ADS PubMed 24 DeVore AD , McNulty S , Alenezi F , Ersboll M , Vader JM , Oh JK. et al. Impaired left ventricular global longitudinal strain in patients with heart failure with preserved ejection fraction: insights from the RELAX trial . Eur J Heart Fail 2017 ; 19 : 893 – 900 . Google Scholar Crossref Search ADS PubMed 25 Kraigher-Krainer E , Shah AM , Gupta DK , Santos A , Claggett B , Pieske B. et al. Impaired systolic function by strain imaging in heart failure with preserved ejection fraction . J Am Coll Cardiol 2014 ; 63 : 447 – 56 . Google Scholar Crossref Search ADS PubMed 26 Hall TS , Hallén J , Krucoff MW , Roe MT , Brennan DM , Agewall S. et al. Cardiac troponin I for prediction of clinical outcomes and cardiac function through 3-month follow-up after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction . Am Heart J 2015 ; 169 : 257 – 65 . Google Scholar Crossref Search ADS PubMed 27 Chia S , Senatore F , Raffel OC , Lee H , Wackers FJT , Jang I-K. Utility of cardiac biomarkers in predicting infarct size, left ventricular function, and clinical outcome after primary percutaneous coronary intervention for st-segment elevation myocardial infarction . JACC Cardiovasc Interv 2008 ; 1 : 415 – 23 . Google Scholar Crossref Search ADS PubMed 28 Hallén J , Jensen JK , Fagerland MW , Jaffe AS , Atar D. Cardiac troponin I for the prediction of functional recovery and left ventricular remodelling following primary percutaneous coronary intervention for ST-elevation myocardial infarction . Heart 2010 ; 96 : 1892 – 7 . Google Scholar Crossref Search ADS PubMed 29 Mirea O , Pagourelias ED , Duchenne J , Bogaert J , Thomas JD , Badano LP. et al. Intervendor differences in the accuracy of detecting regional functional abnormalities: a report from the EACVI-ASE Strain Standardization Task Force . JACC Cardiovasc Imaging 2017 ;pii: S1936-878X(17)30363-7, 10.1016/j.jcmg.2017.02.014. 30 Mirea O , Pagourelias ED , Duchenne J , Bogaert J , Thomas JD , Badano LP. et al. Variability and reproducibility of segmental longitudinal strain measurement: a report from the EACVI-ASE Strain Standardization Task Force . JACC Cardiovasc Imaging 2017 ;pii: S1936-878X(17)30360-1, 10.1016/j.jcmg.2017.01.027. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Heart Journal – Cardiovascular Imaging Oxford University Press

Changes in global longitudinal strain and left ventricular ejection fraction during the first year after myocardial infarction: results from a large consecutive cohort

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Abstract

Abstract Aims To determine changes of global longitudinal strain (GLS) and their predictors in relation to classical echocardiographic parameters of left ventricular (LV) function, over 1 year, in consecutive patients with myocardial infarction (MI) and initially normal or impaired LV ejection fraction (EF). Methods and results A total of 285 patients with MI prospectively included in the REBUS (RElevance of Biomarkers for future risk of thromb-oembolic events in UnSelected post-myocardial infarction patients) study underwent echocardiography within 72 h from admission and after 1 year. At baseline, 213 (74.7%) of MI patients had a normal EF (≥52% in men or ≥54% in women), but in 70.4% of them, an impaired GLS ( ≥ −18.0%) was observed. During 1-year follow-up, in patients with normal EF at baseline, GLS improved from −15.8% to − 17.4% (10.1% relative change); EF decreased from 62.5% to 59.9% (4.0% relative change); indexed end-diastolic volume, indexed end-systolic volume, and indexed stroke volume increased with 15.6%, 24.8%, and 10.0% of relative change, respectively (P < 0.001 for all the comparisons). In the whole cohort, initial impairment of LV function [by EF, wall motion score index (WMSI), or GLS], male gender, non-smoking, and treatment with beta-blockers were the independent predictors of GLS improvement. In the group with initially impaired EF, over 1 year GLS improved from −11.9% to − 14.8% (24.4% relative change) and EF from 44.6% to 52.6% (18.2% relative change) (P < 0.001 for both). Improvement in GLS significantly correlated with EF increase in the group with impaired EF (r = −0.41, P = 0.001) but not in the patients with normal EF (r = −0.14, P = ns). Conclusions Despite diveregent evolution of GLS compared with EF and ventricular volumes, one year after MI GLS significantly improved in patients with initially both normal and impaired EF. Initial impairment of LV function (by EF, WMSI, or GLS), male gender, non-smoking, and treatment with beta-blockers were independent predictors of GLS improvement. LV remodelling was present even in patients with normal EF at baseline and during follow-up, confirming limited functional assessment by EF alone. left ventricular function, myocardial infarction, remodelling, global longitudinal strain Introduction For many decades, left ventricular (LV) ejection fraction (EF) has widely been used as the only determinant of LV systolic function in risk scores, registries, and therapeutical guidelines.1,2 Rapid and more effective treatments minimizing the extent of myocardial damage and the introduction of highly sensitive troponins have led to a search for novel sensitive imaging biomarkers with the ability to detect and follow-up minor myocardial impairment. About two-thirds of patients hospitalized today with acute myocardial infarction (MI) have normal LV EF,3,4 although the majority of them have at least one of the other markers of systolic function outside the normal range.5 Global longitudinal strain (GLS) obtained by speckle-tracking echocardiography has been introduced as the most promising marker of myocardial deformation impairment reflecting subclinical LV dysfunction in a wide range of cardiac disorders.6 Little is known about the changes in myocardial deformation after MI, in particular in patients with preserved or only mildly impaired EF, and thus post-infarction remodelling in this growing patient population. The aim of this study was to determine the changes of GLS in relation to classical echocardiographic measures of LV function and their predictors in a large unselected cohort of consecutive MI patients during a 12-month follow-up. Our patient cohort has a wide range of baseline EF but reflects the contemporary preponderance of normal baseline post-infarction EF, which sets it apart from earlier studies.7–9 Baseline echocardiographic characteristics of this cohort at the time of their hospitalization have been published previously.5 Methods Consecutive patients with MI hospitalized in the Department of Cardiology, Uppsala University Hospital, in the period from April 2010 to August 2012 were prospectively included in the REBUS (RElevance of Biomarkers for future risk of thromboembolic events in UnSelected post-myocardial infarction patients) study.5 Inclusion criteria were MI diagnosed by dynamic-raised cardiac troponin I (cTnI) with at least one value above the upper reference limit, together with at least one of the clinical or electrocardiographic criteria as well as the ability to attend the scheduled visits for evaluation procedures and signed informed consent. Patients who died within 5 days after MI were excluded. All patients enrolled in REBUS were treated according to clinical practice. Treatment and medical history data were collected before discharge and during follow-up visits. Echocardiography was performed per study protocol in the cardiac intensive care unit within 72 h and during follow-up at 12 months after hospital admission, and the prospectively collected echo data were retrospectively reviewed by experienced echocardiographers. After excluding patients lacking baseline or follow-up echo, and those during follow-up withdrew their consent or died, a total of 312 patients with echocardiographic studies recorded both at baseline and during follow-up completed study protocol. Furthermore, 27 (8.7%) patients were excluded due to non-satisfactory image quality. Figure 1 illustrates the inclusion process. Figure 1 View largeDownload slide Study population. CICU, cardiac intensive care unit, indicates echo studies during hospitalization (0); FU, follow-up, indicates follow-up studies after 12 months; LV EF, left ventricular ejection fraction; MI, myocardial infarction; *LV EF ≥ 54% in women, LV EF ≥ 52% in men. Figure 1 View largeDownload slide Study population. CICU, cardiac intensive care unit, indicates echo studies during hospitalization (0); FU, follow-up, indicates follow-up studies after 12 months; LV EF, left ventricular ejection fraction; MI, myocardial infarction; *LV EF ≥ 54% in women, LV EF ≥ 52% in men. Two-dimensional echocardiography was performed in the standard apical four-, three-, and two-chamber views. LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF were assessed using the biplane Simpson’s method. Left atrial volume was calculated using the monoplane area length method. Stenotic and regurgitant valve diseases were evaluated using semi-quantitative and quantitative methods as recommended by current guidelines.10,11 Since images were acquired with echo machines from two different vendors (Philips iE33 Ultrasound system at the cardiac intensive care unit and GE Vivid E9 Ultrasound system at follow-up), we used an external software, Image Arena V 4.6 Build 4.6.4.10 (TomTec Imaging system, Munich, Germany), for all speckle-tracking based analysis. In all apical views, the endocardial borders were manually traced in the end-systolic frame, while end-diastolic borders were provided automatically by the software allowing manual correction, if necessary. Global longitudinal strain (GLS) was then automatically calculated. According to recommendations from the American Society of Echocardiography and the European Association of Cardiovascular Imaging, we excluded images with suboptimal tracking of the endocardium in more than two segments in one single view or if frame rate was below 40 Hz.12 Normal values concerning systolic function and ventricular size were based on current echocardiographic recommendations (LV EF ≥ 54% in women and ≥52% in men, LV EDV ≤61 mL/m2 in women and ≤74 mL/m2 in men, and LV ESV ≤24 mL/m2 in women and ≤ 31 mL/m2 in men.13 cTnI was serially collected as part of clinical routine, and maximal values were obtained. The study was approved by the Regional Ethical Review Board at Uppsala University (reference number: 2009/210). Statistical methods Patients with normal and impaired LV EF were compared in terms of background factors, echocardiographic parameters, and biomarkers. Categorical variables were presented as the number of patients and frequencies. Continuous variables were presented as mean ± standard deviation or as median and interquartile range (IQR). The change in echocardiographic parameters between baseline and follow-up studies was presented as mean difference with a 95% confidence interval (CI). Categorical variables were compared with the χ2 test. Continuous variables were compared with paired and independent samples t-test where appropriate in cases of normally distributed data and with Mann–Whitney test in cases of non-normally distributed data. Associations between echocardiographic parameters, baseline patient characteristics, and cTnI were tested using linear regression or one-way analysis of variance. To identify independent predictors of GLS changes over time among background demographics (gender and age), clinical data (risk factors, co-morbidities, and medical history), coronary artery territory treated with percutaneous coronary intervention (PCI), medical treatments, and baseline echocardiographic characteristics including baseline LV function measures [EF, wall motion score index (WMSI), and GLS], univariate and multivariate logistic regression analyses were performed in the whole study population, as well as separately in patients with initially normal and impaired LV EF. All variables with P-value <0.05 in univariate analysis were introduced to the multivariate regression models. LV EF, GLS, and WMSI at baseline were used in multivariate models separately to avoid co-linearity. For all analyses, two-sided P-values <0.05 were defined as significant. As previously reported, the intraobserver variability for repeated measurements of all LV function parameters was excellent [intra-class correlation coefficient (ICC) >0.75 for all LV function parameters].5 In this analysis, to study inter-observer variability, a random sample of 70 studies was analysed by two experienced echocardiographers independently and ICC was calculated. Statistical analyses were performed using IBM SPSS V.24.0 (SPSS, IBM Corporation, Armonk, NY, USA). Results Baseline characteristics After excluding patients who withdrew their consent during follow-up (n = 18, 4.3%) or died (n = 7, 1.7%), a total of 312 patients with echocardiographic studies recorded both at baseline and during follow-up completed the study protocol. Further, 27 of them (8.7%) were excluded due to non-satisfactory image quality (Figure 1). A total of 285 patients were included to the final analysis. The mean age of the study population was 65.8 ± 10.1 years, and 80.0% (n = 228) of the patients were men. Clinical data are presented in Table 1. Since only patients who survived to 1 year after infarction were included, there was no mortality in the study group. Table 1 Demographics, medical history, clinical status, and treatments Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 a Including clopidogrel, ticagrelor, or prasugrel. b Including aldosterone receptor blockers. LV EF, left ventricular ejection fraction; BP, blood pressure; cTnI, cardiac troponin I; STEMI, ST-elevation myocardial infarction; MI, myocardial infarction; CHF, congestive heart failure; LV EF, left ventricular ejection fraction; ACEI, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; PCI, percutaneous coronary intervention; LAD, left anterior descending artery; LCx, left circumflex artery; RCA, right coronary artery; ECG, electrocardiography. Table 1 Demographics, medical history, clinical status, and treatments Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 Normal LV EF Impaired LV EF P-value (n = 213) (n = 72) Demographics, clinical findings at baseline, troponin and MI type  Age (years), mean ± SD 65.7 ± 9.8 66.2 ± 11.1 0.705  Male gender, % (n) 81.2 (173) 76.4 (55) 0.396  Heart rate (bpm), mean ± SD 75 ± 18 81 ± 19 0.026  Systolic BP (mmHg), mean ± SD 127 ± 17 120 ± 13 0.001  Diastolic BP (mmHg), mean ± SD 73 ± 9 72 ± 10 0.251  cTnI (μg/L), median (IQR) 6.88 (1.74–30.88) 18.54 (3.49–49.00) 0.009  STEMI, % (n) 47.9 (102) 61.1 (44) 0.057 Co-morbidities and past medical history  Hypertension, % (n) 50.2 (107) 48.6 (36) 0.892  Diabetes, % (n) 13.1 (28) 18.1 (13) 0.333  History of MI, % (n) 16.9 (36) 19.4 (14) 0.596  History of CHF, % (n) 2.3 (5) 11.1 (8) 0.005  History of atrial fibrillation, % (n) 7.0 (15) 13.9 (10) 0.827  History of stroke, % (n) 1.4 (3) 4.2 (3) 0.172 Invasive treatment and coronary artery territory treated during hospitalization  PCI at index MI, % (n) 89.7 (191) 88.9 (64) 0.827  LAD, % (n) 46.6 (89) 56.3 (36) 0.196  LCx, % (n) 25.1 (48) 21.9 (14) 0.737  RCA, % (n) 44.5 (85) 34.4 (22) 0.188  Time from symptom onset to recanalization (min), median (IQR) 405 (135–1381) 252 (132–1208) 0.490  Time from ECG registration to recanalization, median (IQR) 90 (47–902) 69 (53–211) 0.490 Medical treatment at discharge  Aspirin, % (n) 99.1 (211) 100.0 (72) 1.00  P2Y12 inhibitors,a % (n) 99.5 (212) 97.2 (70) 0.473  Statins, % (n) 93.4 (199) 98.6 (71) 0.126  ACEI/ARB, % (n) 78.4 (167) 88.9 (64) 0.062  Beta-blockers, % (n) 92.5 (197) 95.8 (69) 0.420  Diuretics,b % (n) 12.7 (27) 27.8 (20) 0.005 a Including clopidogrel, ticagrelor, or prasugrel. b Including aldosterone receptor blockers. LV EF, left ventricular ejection fraction; BP, blood pressure; cTnI, cardiac troponin I; STEMI, ST-elevation myocardial infarction; MI, myocardial infarction; CHF, congestive heart failure; LV EF, left ventricular ejection fraction; ACEI, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; PCI, percutaneous coronary intervention; LAD, left anterior descending artery; LCx, left circumflex artery; RCA, right coronary artery; ECG, electrocardiography. The MI diagnosis was ST-elevation myocardial infarction (STEMI) in 51.2% (n = 146) of patients. The majority of the patients (89.5%, n = 255) were treated with PCI. In patients with STEMI, median time from both onset of symptoms and first ECG registration to recanalization was significantly shorter when compared with non-ST-elevation myocardial infarction (NSTEMI) patients, 177 (IQR 105–399) vs. 1421 (IQR 729–2173) min and 57 (IQR 44–83) vs. 1155 (IQR 405–1550) min, respectively (P < 0.001 for both), but did not differ between patients with normal and impaired LV EF, comprising all the MI types. LV systolic dysfunction defined according to the present criteria as EF below 52% in men and below 54% in women13 was observed in 25.3% (n = 72) of the patients <72 h after MI. History of previous MI was reported in 17.5% (n = 50) of all included patients and did not differ between the studied groups. Patients with impaired EF presented with higher peak cTnI concentrations, lower systolic blood pressure, and higher heart rate, compared with those with normal EF. No significant differences in demographics, cardiovascular risk factors, or co-morbidities were observed, except that history of congestive heart failure was more common in patients with impaired EF. There were no differences in invasive treatment and in prescribed medication, with the exception that patients with impaired EF more often received diuretics on discharge (Table 1). After 1 year, in the whole study group, systolic blood pressure was significantly higher, while diastolic blood pressure remained unchanged (132 ± 17 vs. 125 ± 16 mmHg, P < 0.001 and 74 ± 10 vs. 73 ± 10 mmHg, P = 0.084). Echocardiographic parameters at baseline and their change during follow-up Patients with impaired EF at baseline had significantly higher LV WMSI, LV mass, and left atrial volume and lower tricuspid annular plane systolic excursion, reflecting right ventricular longitudinal function, when compared with those with normal EF. Moderate or severe mitral regurgitation was also more frequent in patients with impaired EF (Table 2). Table 2 Echocardiographic study at baseline Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 LV EF, left ventricular ejection fraction; WMSI, wall motion score index; LVMi, left venricular mass index; LAVi, left atrial volume index; TAPSE, tricuspid annular plane systolic excursion; MV DT, mitral valve inflow deceleration time. Table 2 Echocardiographic study at baseline Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 Normal LV EF Impaired LV EF P-value (n = 262) (n = 93) WMSI 1.19 ± 0.20 1.64 ± 0.34 <0.001 LVMi (g/m2) 104 ± 23 114 ± 30 <0.001 LAVi (mL/m2) 31.5 ± 10.3 37.1 ± 11.7 <0.001 TAPSE (cm) 2.18 ± 0.37 2.02 ± 0.36 0.002 E/A ratio 1.03 ± 0.38 (n=97) 1.14 ± 0.53 (n = 26) 0.207 MV DT (ms) 252 ± 63 (n=99) 229 ± 56 (n = 31) 0.069 eʹ (cm/s) 6.9 ± 2.3 (n=27) 5.8 ± 2.3 (n = 10) 0.200 Mitral regurgitation moderate/severe (%) 18.4 28.5 0.165 Tricuspid regurgitation Vmax (m/s) 2.50 ± 0.31 (n=34) 2.59 ± 0.29 (n = 16) 0.296 Aortic regurgitation moderate/severe (%) 11.7 7.9 0.804 LV EF, left ventricular ejection fraction; WMSI, wall motion score index; LVMi, left venricular mass index; LAVi, left atrial volume index; TAPSE, tricuspid annular plane systolic excursion; MV DT, mitral valve inflow deceleration time. Mean values of EF, GLS, and indexed to the body surface area EDV, ESV, and stroke volume at admission and at 12-month follow-up and their changes over time, described as absolute delta (12-month minus baseline value) in variable units and relative change in % are presented in Table 3. Among patients with normal EF, as many as 70.4% (n = 150) presented with abnormal GLS, defined as ≥ −18.0%.6 Table 3 Echocardiographic parameters, comparison between groups with normal and impaired LV EF at inclusion Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). EF, ejection fraction; GLS, global longitudinal strain; EDVi, end-diastolic volume index; ESVi, end systolic volume index; SVi, stroke volume index. Table 3 Echocardiographic parameters, comparison between groups with normal and impaired LV EF at inclusion Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Normal LV EF Impaired LV EF (n = 213) (n = 72) Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value Baseline, mean ± SD Follow-up, mean ± SD Absolute Δ mean (95% CI) Relative change P-value EF (%) 62.5 ± 6.4 59.9 ± 7.5 −2.5 (−3.6 to − 1.5) −4.0% <0.001 44.6 ± 5.5 52.6 ± 12.0 8.1 (5.3–10.8) +18.2% <0.001 GLS (%) −15.8 ± 3.6 −17.4 ± 3.7 −1.6 (−2.0 to − 1.1) −10.1% <0.001 −11.9 ± 4.1 −14.8 ± 4.5 −2.9 (−3.7 to − 2.2) −24.4% <0.001 EDVi (mL/m2) 41.7 ± 10.1 48.2 ± 11.0 6.5 (5.0–7.9) +15.6% <0.001 53.3 ± 18.1 56.3 ± 17.2 3.0 (−0.9 to 7.0) +5.6% 0.131 ESVi (mL/m2) 15.7 ± 4.8 19.6 ± 6.9 3.9 (3.00–4.7) +24.8% <0.001 29.9 ± 11.9 28.0 ± 14.9 −1.9 (−5.2 to 1.4) −6.4% 0.259 SVi (mL/m2) 26.0 ± 6.7 28.8 ± 6.4 2.6 (1.6–3.6) +10.0% <0.001 23.4 ± 7.2 28.3 ± 7.3 4.9 (3.1–6.7) +20.9% <0.001 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). EF, ejection fraction; GLS, global longitudinal strain; EDVi, end-diastolic volume index; ESVi, end systolic volume index; SVi, stroke volume index. Among patients with initially normal EF during follow-up mean EF decreased by 2.5% (CI −3.6 to −1.5), corresponding to a 4.0% relative decrease, while mean GLS improved by 1.6% (CI −2.0 to −1.1, a 10.1% relative improvement). Mean indexed EDV (EDVi) increased by 6.5 mL/m2 (CI 5.0–7.9, relative increase 15.6%), mean indexed ESV (ESVi) increased by 3.9 mL/m2 (CI 3.0–4.7), and mean SV increased by 2.6 mL/m2 (CI 1.6–3.6, relative increase 10%). P-values were <0.001 for all the changes. In patients with impaired systolic function, after 12 months, mean EF had increased by 8.1% (CI 5.3–10.8), corresponding to a 18.2% relative increase, mean GLS improved by 2.9% (CI −3.7 to −2.2, relative increase 18.2%), and mean indexed SV increased by 4.9 mL/m2 (CI 3.1–6.7, relative increase 20.9%) No significant changes in EDVi and ESVi were noticed (Table 3 and Figure 2). Figure 2 View largeDownload slide Changes in different parameters of left ventricular function during 12-month follow-up in patients with normal and impaired LV EF. GLS, global longitudinal strain; EF, ejection fraction; EDVi, end-diastolic volume index, ESVi, end-systolic volume index; SVi, stroke volume index; Δ indicates a change in respective parameters; mean values and standard deviations are shown. %U indicates GLS and EF % units, not relative percent. Figure 2 View largeDownload slide Changes in different parameters of left ventricular function during 12-month follow-up in patients with normal and impaired LV EF. GLS, global longitudinal strain; EF, ejection fraction; EDVi, end-diastolic volume index, ESVi, end-systolic volume index; SVi, stroke volume index; Δ indicates a change in respective parameters; mean values and standard deviations are shown. %U indicates GLS and EF % units, not relative percent. Predictors of GLS improvement Improvement in GLS was significantly greater in the subgroup with impaired EFcompared with the subgroup with normal EF at baseline [delta GLS −2.9% (CI −3.7 to −2.2) vs. −1.6% (CI −2.0 to 1.2); P = 0.003], as well as in patients with pathologic WMSI compared with normal WMSI at baseline [delta GLS −2.2% (CI −2.6 to −1.7) vs. −0.9% (CI −1.8 to −0.1), P = 0.015]. GLS improvement correlated significantly with EF increase in a group with impaired EF (r = −0.41, P = 0.001) but not in those with initially normal EF (r = −0.14, P = 0.06; Figure 2). Men presented significantly higher improvement of GLS during follow-up than women in the whole studied group [−2.1% (CI −2.6 to −1.7) vs. −1.1% (CI −2.0 to −0.1), P = 0.03]. Patients with MI treated with PCI in the left anterior descending (LAD) coronary artery territory had significantly higher improvement in GLS when compared with those with PCI in the non-LAD infarction territory [−2.5% (CI −3.2 to −1.8) vs. –1.6% (CI −2.1 to −1.1); P = 0.032]. No significant differences were observed between type of MI (STEMI or NSTEMI) or other baseline clinical characteristics and change in GLS. Patients who were prescribed beta-blockers at discharge had a significantly greater improvement in GLS, compared to those not treated with beta-blockers [delta GLS −2.0% (CI −2.4 to −1.6) vs. −0.4% (CI −1.8 to 1.0); P = 0.037; Figure 3]. No other significant differences were observed between medications at discharge and change in GLS. Figure 3 View largeDownload slide Impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. Box plots showing significant impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. The box represents an interval between first and third quartile, the band inside the box indicates median value and the whiskers indicate 10th and 90th percentiles. Figure 3 View largeDownload slide Impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. Box plots showing significant impact of gender and treatment with beta-blockers at discharge on change in GLS (Δ) during a 12-month follow-up. The box represents an interval between first and third quartile, the band inside the box indicates median value and the whiskers indicate 10th and 90th percentiles. No significant relationship between other LV measures or peak cTnI at baseline and change in GLS was found. Significant univariate predictors of GLS improvement during 1-year follow-up for the whole studied group and separately for patients with initially normal and impaired EF are presented in Table 4. Table 4 Prediction of LV GLS improvement Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). a Baseline EF, WMSI and GLS used in the multivariate analysis separately to avoid colinearity. LAD, left anterior descending artery; EF, ejection fraction; WMSI, wall motion score index; BP, blood pressure. Table 4 Prediction of LV GLS improvement Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Univariate analysis Multivariate analysisa B 95% CI P-value B 95% CI P-value Total cohort (n = 285)  Gender −1.07 −2.04 to − 0.11 0.03 −1.09 −2.05 to − 0.13 0.026 (WMSI)  Current smoking 1.11 0.23–1.98 0.013 1.18 0.32–2.04 0.007 (EF) 1.10 0.23–1.97 0.014 (WMSI) 0.99 0.19–1.79 0.016 (GLS)  Beta-blockers −1.65 −3.20 to − 0.10 0.037 −1.66 −3.20 to − 0.12 0.034 (EF) −1.65 −3.23 to − 0.07 0.040 (WMSI)  LAD territory −0.89 −1.70 to − 0.08 0.032  Baseline EF 0.06 0.02–0.10 0.003 0.05a 0.01–0.09 0.008 (EF)  Baseline WMSI −2.03 −3.28 to − 0.77 0.002 −1.70a −2.95 to − 0.46 0.008 (WMSI)  Baseline GLS −0.34 −0.43 to − 0.25 <0.001 −0.31a −0.40 to − 0.23 <0.001 (GLS) Normal LV EF at baseline (n=213)  Gender −1.33 −2.46 to − 0.20 0.022 −1.22 −2.35 to − 0.08 0.036 (WMSI) −1.06 −2.08 to − 0.05 0.041 (GLS)  Current smoking 1.33 0.34–2.31 0.009 1.31 0.28–2.34 0.013 (WMSI) 1.07 0.14–1.99 0.024 (GLS)  Beta-blockers −1.83 −3.51 to − 0.15 0.033 −2.10 −3.85 to − 0.36 0.018 (WMSI)  Δ diastolic BP 0.04 0.002–0.08 0.040  Baseline WMSI −2.39 −4.71 to − 0.07 0.044  Baseline GLS −0.39 −0.50 to − 0.28 <0.001 −0.36 −0.47 to − 0.24 <0.001 (GLS) Impaired LV EF at baseline (n=72)  LAD territory −1.67 −3.21;-0.13 0.034  Baseline GLS −0.22 −0.40;-0.04 0.019 Δ indicates difference between echoes performed at follow-up (12 months after inclusion) and at intensive care unit (at baseline). a Baseline EF, WMSI and GLS used in the multivariate analysis separately to avoid colinearity. LAD, left anterior descending artery; EF, ejection fraction; WMSI, wall motion score index; BP, blood pressure. To avoid co-linearity, separate multivariate regression models were constructed where baseline measures of LV function, such as EF, WMSI, and GLS were used separately. In multiple regression analysis, male gender, non-smoking, treatment with beta-blockers and in respective models more impaired EF, WMSI, and GLS at baseline were independent predictors of GLS improvement in the whole studied group. In patients with initially normal EF, more impaired GLS at baseline was the only measure of LV function that could predict GLS improvement over the time. In subgroup with impaired EF, no independent predictors of GLS improvement could be identified (Table 4). A difference in systolic and diastolic blood pressures between 1 year and baseline measurements, known as a potential confounder, did not show an independent predictive impact on GLS behaviour in any analysed models. In the whole group, correlation between EF and GLS was r = −0.53 (P < 0.001) at baseline and r = −0.42 after 12 months (P < 0.001). Intra- and interobserver variability The excellent intraobserver variability for repeated measurements of all LV function parameters (ICC > 0.75) was reported previously.5 Reproducibility of GLS measurements between two experienced echocardiographers in a random sample of 70 studies was also excellent [ICC 0.91 (95% CI 0.86–0.95); P < 0.001, for average measures). Discussion In this large contemporary ‘all-comers’ cohort of patients with both NSTEMI and STEMI, a divergent evolution of GLS compared with EF and ventricular volumes was observed. In the cohort as a whole, GLS significantly improved during the following 12 months. Initial impairment of LV function (by EF, WMSI, or GLS) was independently predictive for GLS improvement in the whole cohort. Further, male gender, non-smoking, and treatment with beta-blockers were independent predictors of GLS improvement. In the subgroup with normal EF at baseline, which in our study was considerably larger (75% of patients) than in earlier studies, GLS was impaired at baseline, improved significantly during follow-up, but still remained slightly impaired at 1 year. Only initial impairment of GLS remained significant as predictive parameter of later GLS improvement in a multivariate analysis. LV volumes, however, increased and EF decreased in this group, possibly reflecting at least in part initial remote hyperkinesia abating during follow-up. This discrepancy in the time course of EF and GLS (Figure 4) indicates that these parameters reflect different aspects of LV systolic function. Figure 4 View largeDownload slide Correlation between changes of GLS and EF (delta GLS and delta EF) in patients with initially normal and impaired LV EF. Figure 4 View largeDownload slide Correlation between changes of GLS and EF (delta GLS and delta EF) in patients with initially normal and impaired LV EF. In the subgroup with initially impaired EF (25% of patients), ESVs did not change significantly, but EDVs increased, leading to higher SVs and higher EF. Thus, there was more improvement in systolic function as measured by volumes in the initially impaired group than in the group with initially normal EF, perhaps because there was more ‘room for improvement’ in the former. This larger improvement is also reflected in the delta GLS, which was more than double as high (24.4 vs. 10.1% relative change) in the group with initially impaired EF compared with the group with initially normal EF. However, GLS on average remained below normal both initially and at follow-up. No independent predictors of GLS improvement were identified considering this group exclusively, likely related to lack of statistical power. Post-infarction remodelling is known as a morphological and functional process recruiting preload reserve by ventricular dilatation. Whether remodelling occurs in patients with normal early post-infarction EF has not been elucidated but is important, given its well-known adverse prognostic effect.14 Such patients, as demonstrated in our study, are increasingly common due to better acute therapy.4 Interestingly, in our patient group with initially normal EF, we observed a significant reduction of EF (albeit remaining in the normal range) parallel to an increase of both EDV and ESV, reflecting post-infarction remodelling in these apparently functionally intact patients. This indicates a shortcoming of using exclusively EF in post-infarction assessment, which is still the most widely used echocardiographic measure of LV systolic function with a prominent position in guidelines, registries, and predictive models. A few studies addressing evolution of GLS in post-infarction patients have been published.7–9 However, the study population, predominantly or exclusively with STEMI, had substantially lower EF when compared with our cohort. More commonly preserved LV function reflects the contemporary transition in patient characteristics towards smaller infarcts presumably due to more sensitive biomarker diagnostics, more effective therapy, and other factors. Antoni et al. used GLS as the only measure of LV function changes one year after MI. The study population was comparable with our impaired EF subgroup in terms of similar baseline EF (mean 45%) and slightly bigger volumes (EDVi, ESVi). The authors have found a gradual improvement of GLS (23% relative change), however not addressing changes in other functional parameters. Similarly to our results, Antoni et al.7 found GLS to be an independent predictor of LV function recovery 1 year after MI. Furthermore, they found the infarct size, LAD culprit vessel, and diastolic dysfunction as predictors of LV function recovery after MI. Hoogslag et al.8 reported parallel improvement of GLS (13 and 15% relative change, respectively) and EF (9 and 11% relative change, respectively) in diabetic and non-diabetic patients with initially mildly impaired EF (mean EF 47 and 48%, respectively) during 6 months after STEMI. Similar to our observations, EF improvement was associated with significant increase of EDV, while ESV remained unchanged. Diabetes, but also infarct size, and overt heart failure at baseline were the independent predictors of GLS improvement.8 In a further study,9 a large group of 1041 STEMI patients with mean EF 47% and mean GLS of − 15% and those with GLS poorer than −15% experienced more significant EDV increase. Baseline GLS, but also infarct size, HR, and LAD culprit lesion were independent predictors of post-MI remodelling. Changes in other parameters as EF or ESV were not reported.9 The reason for discrepancy in EF and GLS course in our study may lie in the presence of initial local hyperkinesia of remote left ventricular segments, which may affect EF more than GLS. In the whole population, we found a relationship between LV impairment at inclusion and subsequent change in GLS, meaning that more impaired EF is related to more significant improvement in GLS. Once hyperkinesia subsides, EF decreases, but GLS improves. Interestingly, in the subgroup of patients with normal EF at baseline, neither initially impaired EF nor WMSI, but only impaired GLS at baseline could predict GLS improvement over the time. This observation may reflect probably lower reliability of ‘higher normal’ values of EF in prediction of cardiac remodelling. Our study was observational and not designed to identify predictors of clinical outcome, but several studies have shown higher prognostic impact of GLS than EF in a wide range of cardiac disorders,15 including patients with MI.16,17 Ersboll et al.18 found that in patients with MI and normal or mildly impaired EF, those with GLS < 14% (absolute value) had an increased risk for the combined endpoint of all-cause mortality and heart failure admissions. Other areas where discrepancies between EF and GLS have been described are in the surveillance of patients undergoing cardiotoxic chemotherapy,19,20 valvular heart disease,21,22 cardiomyopathies,23 and heart failure with preserved EF.24,25 In our study, we were not able to show any impact of initial peak cTnI on GLS improvement during follow-up. This is in contrast to previous studies showing that an elevated level of cTnI is a prognostic factor not only for infarct size and LV EF but also on cardiac remodelling.26–28 The likely explanation is that the maximal possible value of detection for the cTnI assay we have used was 50 μg/L, which was present in a substantial number of patients and may have distorted relations with functional parameters. Limitations Several limitations of this study need to be acknowledged. One-fourth of the patients needed to be excluded due to missing one of two echo studies. Secondly, based on non-satisfactory image quality of baseline and/or follow-up study, 27 (8.7%) patients were excluded from the analysis, including those studies in which more than 2 segments could not be analysed. Thirdly, by study design, the patients who did not survive to follow-up were excluded, which introduces a selection. Fourthly, given the recently disputed accuracy and intervendor reproducibility of segmental longitudinal strain in ischaemic heart disease,29,30 we address only GLS measurements. Conclusion In the vast majority of consecutive contemporary patients with acute MI, the EF remains normal; however, GLS is impaired in 70% of them, and morphological LV remodelling occurs. During the 1-year follow-up, opposite changes in LV EF and GLS evolution were observed, suggesting that EF decrease might reflect subsiding compensatory hyperkinesia seen in the acute MI phase, while GLS improvement may more sensitively track ‘true’ systolic function improvement. Male gender, more impaired LV function at baseline, non-smoking, and treatment with beta-blockers were the independent predictors of GLS improvement in the whole studied group. The prognostic role of GLS changes after MI needs to be determined in future studies. Acknowledgements The author would like to thank Nermin Hadziosmanovic, biostatistician at Uppsala Clinical Research Center for his contribution to this article. Funding This work was supported by grants from Erik, Karin och Gösta Selanders Foundation. Conflict of interest: None declared. References 1 Steg PG , James SK , Atar D , Badano LP , Lundqvist CB , Borger MA. et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation . Eur Heart J 2012 ; 33 : 2569 – 619 . Google Scholar Crossref Search ADS PubMed 2 Hamm CW , Bassand JP , Agewall S , Bax J , Boersma E , Bueno H. et al. ; ESC Committee for Practice Guidelines . ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC) . 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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Journal

European Heart Journal – Cardiovascular ImagingOxford University Press

Published: Oct 1, 2018

References

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