The number of patients included in the current study was 50 (55.6 ± 10 years). Patients were admitted by anterior STEMI, in King Fahad hospital of the university, Saudi Arabia in the period between January 2017 and December 2017. Acute STEMI was diagnosed by rise and fall of cardiac enzymes together with at least one of signs of myocardial ischaemia (chest pain, new ST-elevation at the J-point in 2 contiguous leads with the cut-point ≥1 mm in leads other than leads V2 - V3 where the following cut points apply: ≥2 mm in men ≥40 years; ≥2.5 mm in men <40 years, or ≥1.5 mm in women regardless of age, and development of pathological Q waves) [9] .

Post-operative MI, preexisting cardiomyopathies, significant valvular heart disease, chronic renal and liver conditions were all set as exclusion criteria. 20 sex- and age-matched persons who had history of stable angina and normal LVEF were assigned as controls. The study was approved by local ethics committee, and informed consent was obtained from all patients before participation in the study.

A twelve lead ECG was done for all patients using MAC 3500 resting ECG analysis system (GE healthcare, Milwaukee, WI, USA) with a 25 mm/s paper speed and standardization adjusted to 1 mm/mv. An anterior STEMI was diagnosed by the presence of an elevated ST segment in leads representing the anterior wall (V1 - V6).

A 2D transthoracic echocardiography was carried out (VIVID E9 machine; GE Healthcare, Chicago, IL, USA). The standard parasternal and apical imaging views were used, and the average of three consecutive heartbeats was then studied. The standard 2D and M-mode measurements were recorded. The left ventricle ejection fraction (LVEF) was evaluated by the method of biplane disks (the modified Simpson’s rule). The recommendations of the American Society of Echocardiography were applied when registering all of the 2D and conventional Doppler variables [10] . Tissue Doppler Imaging (TDI), Pulsed Doppler Echocardiography, and Left Atrial Volume Index (LAVI), and tricuspid regurgitation (TR) velocity were employed to assess the diastolic function the left ventricle. Recommendations of the American Society of Echocardiography were followed in this regard [11] .

All of the data were stored digitally in a cine loop arrangement, and the speckle-tracking imaging of the LV was done offline using an EchoPAC workstation (GE Healthcare, Chicago, IL, USA). The frame rate was adjusted from 60 to 100 frames per second to display grayscale 2D images. The time of the aortic valve closure was estimated at the beginning of the study through the apical long axis view. This was then followed by views of the apical four and the apical two chambers. Automated functional imaging (AFI) [12] was used to record the LV GLS. The software allows automated tracing of the regions of interest to identify the whole myocardial wall. To achieve a better tracking score, the endocardial trace line was adopted in those segments with poor traceability. Each LV wall was subdivided into six segments, and the intra-segmental peak systolic strains were then calculated by computer software. GLS-Average represents the summative peak systolic longitudinal strains of the entire LV segments.

Protein concentration was estimated in serum samples that were collected at 24 hours of chest pain onset using the BCA protein estimation kit (ThermoFisher Scientific, USA). Appropriate sample dilution was done prior to enzyme-linked immunosorbent assay (ELISA) of pentraxin-3. Standard stock was serially diluted and all samples were loaded into the pre-coated ELISA plate. The procedure was followed according to the instructions in the datasheet of human pentraxin 3 ELISA kit (#SEK411Hu, Cloud-Clone Corp., Katy, Texas, USA). The concentration of pentraxin-3 in control and patient samples was derived from the standard curve equation. Other laboratory investigations were done including creatine Kinase-MB (CK-MB), troponin-I, lipid profile, complete blood count and serum creatinine.

Data analysis was done using the IBM SPSS software package version 20.0 (IBM Corp, Armonk, NY, USA). Normal distribution of data was investigated using the Kolmogorov-Smirnov, Shapiro-Wilk, and D’agostino tests. Group statistical comparisons were done using chi-squared test (Fisher or Monte Carlo) for the categorical variables. The Student’s t-test was used to compare the statistical difference between quantitative variables that follow the Gaussian distribution. The Mann-Whitney U test was used to compare the statistical differences between quantitative variables that do not meet the criteria of Gaussian distribution. Spearman’s and Pearson’s coefficient tests were used to study correlation between the variables. P values ≤ 0.05 indicate statistically significant difference.

The current study cohort consists of 50 anterior STEMI patients. Male patients represent 62% (31 M) of the study population, whereas female subjects constitute 38% of the study population (19 F) (55.6 ± 10 years). Amongst patients, sixteen (32%) of cases were hypertensive, and 25 (50%) were diabetic and 12 (24%) had family history of CAD. Twenty sex- and age-matched subjects with a history of stable coronary artery disease were assigned as controls (Table 1 and Table 2).

2D Doppler and TDI echocardiography showed that LVEF was significantly decreased in patient with STEMI when compared to the control. A significant reduction in the peak systolic velocity at mitral annulus (Sa) velocity was observed in STEMI patients than in control group. LV diastolic filling parameters varied significantly between both groups reflecting impaired LV diastolic filling in STEMI group. The mitral E velocity, E/A ratio and TDI mitral annulus Ea wave were significantly reduced (p < 0.001), while the A velocity, E/Ea ratio and LAVI were increased in STEMI group as compared to the control group; this increase was statistically significant, p < 0.001 for A velocity and E/Ea, and 0.002 for LAVI (Table 3).

BP: blood pressure, DM: diabetes mellitus, BSA: body surface area, BMI: body mass index, HDL-C: High density lipoprotein cholesterol, LDL-C: Low density lipoprotein cholesterol, CAD: Coronary artery disease.

PCI: Percutaneous coronary intervention, LAD: left anterior descending artery, ACEI: angiotensin Convertingenzyme inhibitors, CK-MB: creatine Kinase-MB.

LAVI: left atrial volume index, E: early peak pulsed Doppler velocity on mitral valve, A: late pulsed Doppler velocity on mitral valve, DT: deceleration time, TR: tricuspid regurgitation, Sa: peak systolic velocity atmitral annulus, Ea: early tissue velocity of the mitral annulus, Aa: late tissue velocity of the mitral annulus.

LV speckle tracking longitudinal strain results are demonstrated in Table 4. Average GLS was reduced in cases in comparison to control subjects (−11.2 ± 2.4 versus −20.2 ± 2.1, p < 0.001) (Table 4 and Figure 1).

Cases group revealed significant higher levels of pentraxin-3 in comparison to control group (8.3 ± 3.1 versus 3.4 ± 1.2 ng/ml, p ≤ 0.001) (Table 5 and Figure 2).

The association between serum pentraxin-3 level and LVEF was statistically significant as confirmed by correlation studies (r = −0.572, p < 0.001) and average LVGLS (r = −0.475, p < 0.001) (Figure 3). There was also a significant association between peak troponin-I level and LVEF (r = −0.557, p < 0.001) and LVGLS (r = −0.529, p < 0.001) (Table 6).

28 (56%) STEMI patients had LVEF less than 50%. Serum pentraxin-3 cutoff value > 8.3 ng/ml showed an estimated sensitivity of 81.8% and specificity of 86.4% to detect LVEF less than 50% (p < 0.001). While, peak cardiac troponin-I level > 34 ng/ml was 86% sensitive to detect LVEF less than 50% with specificity of 90.9% (Table 7 and Figure 4).

GLS: global longitudinal strain.

r: Pearson coefficient.