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Journal of
Clinical Medicine
Article
Assessment of Selected Baseline and Post-PCI
Electrocardiographic Parameters as Predictors of Left
Ventricular Systolic Dysfunction after a First ST-Segment
Elevation Myocardial Infarction
Tomasz Fabiszak 1, * , Michał Kasprzak 1, Marek Kozi ´nski 2and Jacek Kubica 1
Citation: Fabiszak, T.; Kasprzak, M.;
Kozi´nski, M.; Kubica, J. Assessment
of Selected Baseline and Post-PCI
Electrocardiographic Parameters as
Predictors of Left Ventricular Systolic
Dysfunction after a First ST-Segment
Elevation Myocardial Infarction. J.
Clin. Med. 2021,10, 5445. https://
doi.org/10.3390/jcm10225445
Academic Editors: Michał Ciurzy ´nski
and Justyna Domienik-Karłowicz
Received: 22 October 2021
Accepted: 18 November 2021
Published: 22 November 2021
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4.0/).
1Department of Cardiology and Internal Medicine, Collegium Medicum, Nicolaus Copernicus University,
ul. Skłodowskiej-Curie 9, 85-094 Bydgoszcz, Poland; medkas@o2.pl (M.K.); jwkubica@gmail.com (J.K.)
2Department of Cardiology and Internal Medicine, Medical University of Gda´nsk,
ul. Powstania Styczniowego 9B, 81-519 Gdynia, Poland; marek.kozinski@gumed.edu.pl
*Correspondence: tfabiszak@wp.pl; Tel.: +48-52-585-40-23; Fax: +48-52-585-40-24
Abstract:
Objective: To assess the performance of ten electrocardiographic (ECG) parameters regard-
ing the prediction of left ventricular systolic dysfunction (LVSD) after a first ST-segment-elevation
myocardial infarction (STEMI). Methods: We analyzed 249 patients (74.7% males) treated with pri-
mary percutaneous coronary intervention (PCI) included into a single-center cohort study. We sought
associations between baseline and post-PCI ECG parameters and the presence of LVSD (defined as
left ventricular ejection fraction [LVEF]
≤
40% on echocardiography) 6 months after STEMI. Results:
Patients presenting with LVSD (n= 52) had significantly higher values of heart rate, number of
leads with ST-segment elevation and pathological Q-waves, as well as total and maximal ST-segment
elevation at baseline and directly after PCI compared with patients without LVSD. They also showed
a significantly higher prevalence of anterior STEMI and considerably wider QRS complex after PCI,
while QRS duration measurement at baseline showed no significant difference. Additionally, patients
presenting with LVSD after 6 months showed markedly more severe ischemia on admission, as
assessed with the Sclarovsky-Birnbaum ischemia score, smaller reciprocal ST-segment depression
at baseline and less profound ST-segment resolution post PCI. In multivariate regression analysis
adjusted for demographic, clinical, biochemical and angiographic variables, anterior location of
STEMI (OR 17.78; 95% CI 6.45–48.96; p< 0.001), post-PCI QRS duration (OR 1.56; 95% CI 1.22–2.00;
p< 0.001) expressed per increments of 10 ms and impaired post-PCI flow in the infarct-related artery
(IRA; TIMI 3 vs. <3; OR 0.14; 95% CI 0.04–0.46; p= 0.001) were identified as independent predictors
of LVSD (Nagelkerke’s pseudo R
2
for the logistic regression model = 0.462). Similarly, in multiple
regression analysis, anterior location of STEMI, wider post-PCI QRS, higher baseline number of
pathological Q-waves and a higher baseline Sclarovsky-Birnbaum ischemia score, together with
impaired post-PCI flow in the IRA, higher values of body mass index and glucose concentration
on admission were independently associated with lower values of LVEF at 6 months (corrected
R
2
= 0.448; p< 0.00001). Conclusions: According to our study, baseline and post-PCI ECG parameters
are of modest value for the prediction of LVSD occurrence 6 months after a first STEMI.
Keywords:
myocardial infarction; ECG; risk stratification; left ventricular systolic dysfunction;
primary PCI
1. Introduction
Electrocardiography (ECG), invented by Willem Einthoven nearly 120 years ago,
remains one of the essential diagnostic modalities in cardiology [
1
], shaping the elementary
division of acute coronary syndromes into those with and without persistent ST-segment
depression, affecting the timing and mode of management and adding to short- and
long-term risk stratification [2–4].
J. Clin. Med. 2021,10, 5445. https://doi.org/10.3390/jcm10225445 https://www.mdpi.com/journal/jcm
J. Clin. Med. 2021,10, 5445 2 of 18
It is estimated that left ventricular systolic dysfunction (LVSD), recognized as a long-
term consequence of myocardial infarction (MI), may affect up to 60% of post-MI pa-
tients [
5
]. Its occurrence mainly depends on the presence of frozen myocardium, size of
post-MI necrosis, and occurrence of left ventricular remodeling [6,7].
Left ventricular ejection fraction (LVEF), measured with echocardiography, is by far
the most popular method for diagnosing LVSD in the clinical setting [8].
LVSD is a well-recognized marker of unfavorable prognosis in post-MI patients [
8
],
translating into a 3–4-fold increase in mortality and higher rates of cardiovascular adverse
outcomes, such as cardiac rupture, sudden cardiac arrest, recurrent myocardial infarction,
ventricular arrhythmias, stroke, prolonged hospitalization and rehospitalization [
7
,
9
–
11
].
The mortality rate among post-MI patients with asymptomatic LVSD after 12 months of MI
is as high as 12% and amounts to 36% in symptomatic patients [
12
]. LVSD independently
predicts short-, mid- and long-term mortality after MI [12–15].
There are many reports regarding the predictive value of ECG with respect to the
development of LVSD after STEMI [
4
,
16
,
17
]. A vast part of these reports however, comes
from the era of thrombolytic treatment of STEMI and was derived from non-uniform
cohorts of patients regarding forms of MI, reperfusion treatment and pharmacotherapy.
Nowadays, in consequence of current standards of STEMI management, incorporating
percutaneous coronary intervention (PCI) as a means of effective and safe reperfusion,
together with dual antiplatelet treatment, we have witnessed a spectacular reduction in the
rates of death, reinfarction, heart failure and strokes.
Our investigation aims to assess the relationship between selected baseline and post-
PCI ECG variables and the presence of LVSD 6 months after a first STEMI.
2. Methods
2.1. Study Design
The investigation was a prospective cohort trial including patients receiving primary
PCI with stent implantation for a first STEMI. Study design, including the inclusion and
exclusion criteria, was described in detail in our previous publication exploring associations
of ECG with post-MI left ventricular remodeling (LVR) [
18
]. Here, we provide only a
brief overview of the study design. Major exclusion criteria were as follows: any previous
myocardial infarction or coronary revascularization, presence of advanced acute or chronic
heart failure (defined as class IV according to the Killip classification or class
≥
III according
to the New York Heart Association), presence of ECG abnormalities that might become study
confounders (i.e., left bundle branch block, isolated posterior myocardial infarction, isolated
right ventricular myocardial infarction, permanent atrial fibrillation), severe valvular heart
disease, any cardiomyopathy, poorly controlled arterial hypertension (defined as blood
pressure
≥
180/110 mmHg on hospital admission) and significant kidney dysfunction on
hospital admission (defined as creatinine concentration exceeding 2 mg/dL).
The analyzed ECG parameters included:
1. heart rate,
2. location of STEMI,
3. number of leads with ST-segment elevation,
4. sum of ST-segment elevation in all leads,
5. maximal ST-segment elevation in a single lead,
6. ST-segment resolution,
7. presence of reciprocal ST-segment depression ≥0.1 mV on admission to hospital,
8. number of leads with pathological Q-waves [19],
9. Sclarovsky-Birnbaum ischemia score [2],
10.
QRS complex duration.
The primary study endpoint was the occurrence of LVSD 6 months after STEMI. LVSD
was defined as LVEF
≤
40% on transthoracic echocardiography. This cut-off value was
previously shown to be associated with unfavorable prognosis [
10
,
20
–
24
]. Additionally,
LVEF
≤
40% is used by the European Society of Cardiology guidelines for defining heart
J. Clin. Med. 2021,10, 5445 3 of 18
failure with reduced ejection fraction [
25
] and post-infarct patients who benefit from
therapy with a beta-blocker, angiotensin-converting enzyme inhibitor or mineralocorticoid
receptor antagonist [26].
First, we planned to compare the clinical, biochemical, angiographic and echocardio-
graphic characteristics. We also assessed differences in ECG parameters between patients
with and without LVSD 6 months after STEMI. Second, we prespecified uni- and multivari-
ate analyses aimed at identifying predictors of post-infarct LVSD. A particular focus was
placed on the investigated ECG parameters.
As a final step, we planned to check whether the variables predictive of the primary
study endpoint were associated with lower values of LVEF (expressed as a continuous
parameter) 6 months after STEMI.
Details of coronary angiography, PCI technique and ECG evaluation were also published
in our previous publication [
18
]. Importantly, we aimed to restore normal blood flow in the
infarct-related artery (IRA) during the primary PCI. Other non-culprit lesions of
≥
90% in major
coronary vessels were treated during the index hospitalization, while PCIs of the remaining
significant stenoses (70–90%) were done electively (within 1 month of STEMI occurrence).
Informed consent for participation in the study was obtained from each participant. The
study received approval from the local Bioethics Committee of Collegium Medicum, Nicolaus
Copernicus University in Toru´n (protocol code KB 440/2004). Throughout the entire course of
the study, the Declaration of Helsinki and the principles of good clinical practice were applied.
2.2. Echocardiographic Assessment
Two-dimensional transthoracic echocardiography was performed in order to evaluate
left ventricular systolic function using a Philips Sonos 7500 device (Philips, Andover, MA,
USA) at two time points: before hospital discharge and after 6 months. Image acquisitions
and measurements were performed according to the recommendations of the European
Association of Echocardiography and the American Society of Echocardiography [
27
,
28
].
The biplane method of discs (modified Simpson’s rule) based on apical 4-chamber and
2-chamber view was utilized for LVEF estimation. The echocardiographer was blinded to
the ECG analysis. The intra-observer coefficient of variation for LVEF estimation for the
first 50 patients was 2.5%.
2.3. Data Collection and Statistical Analysis
Relevant data were collected and initially analyzed using Microsoft Excel spreadsheet
software (Microsoft Corporation, Redmond, WA, USA). No missing data were present.
Descriptive analysis was used to summarize participant characteristics. Categorical
data are presented as frequencies and percentages. Continuous variables are reported as
medians and interquartile ranges. Correspondence with normal distribution was verified
with the Shapiro-Wilk test. Between-group differences were tested using the Mann-Whitney
U test for continuous variables and the Pearson Chi-square and Mantel-Haensztel tests for
categorical variables. In order to identify predictors of LVSD at 6 months, logistic regression
was used. The results are presented as odds ratios (OR) with 95% confidence intervals. Only
variables with univariate p-values of <0.1 were included in the multivariate models. Stepwise
backward selection was employed to select variables included in the best-fitting models. To
identify predictors of LVEF at 6 months, we used multiple linear regression. Variables showing
univariate p-values of <0.1 were considered eligible for multivariate analyses. The variables
were then removed via stepwise backward selection. p-values of <0.05 were considered
significant. Data analysis was conducted using Statistica version 13 (TIBCO Software Inc.,
Palo Alto, CA, USA) and SPSS version 23 (IBM, Armonk, NY, USA).
3. Results
3.1. The Course of the Study
The final analysis included 249 patients. A detailed description of the course of the
study can be found in our previous publication [18].
J. Clin. Med. 2021,10, 5445 4 of 18
3.2. Clinical, Demographic, Angiographic and Biochemical Parameters
The study cohort was primarily composed of middle-aged men. At baseline, patients
who presented with LVSD after 6 months of follow-up showed a higher prevalence of
diabetes mellitus, left anterior descending artery (LAD) as the IRA and TIMI 0 flow before
PCI, but less frequent TIMI 3 flow post PCI. Slightly worse kidney function (assessed based
on glomerular filtration rate), higher plasma glucose concentration on admission to hospital,
larger enzymatic infarct size (as assessed with maximal concentration of troponin I and
maximal activity of isoenzyme MB of creatinine kinase [CK-MB]), higher concentration of
B-type natriuretic peptide (BNP) and more common usage of GPIIb/IIIa inhibitors during
PCI could also be found in this group. Detailed characteristics of the study population are
presented in Table 1.
Table 1.
Clinical characteristics of the study population in relation to the occurrence of LVSD. Data are presented as median
(lower quartile-upper quartile) or number (percent) when appropriate.
Variable Overall Study
Population (n= 249)
Patients with LVSD
at 6 Months (n= 52)
Patients without LVSD
at 6 Months (n= 197) p*
Age [years] 57.0 (51.0–64.0) 61.0 (52.0–67.0) 56.0 (51.0–64.0) 0.090
Gender [male/female] 186 (74.7%)/63 (25.3%) 42 (80.8%)/10 (19.3%) 144 (73.1%)/53 (26.9%) 0.258
Time from symptom onset to PCI [min] 220.0 (150.0–331.5) 223.5 (148.5–346.0) 220.0 (150.0–321.5) 0.727
Risk factors for coronary artery disease
BMI [kg/m2]26.8 (24.2–29.4) 27.4 (25.0–30.2) 26.5 (24.1–29.1) 0.058
Hypertension 103 (41.4%) 24 (46.2%) 79 (40.1%) 0.431
Diabetes mellitus 50 (20.1%) 16 (30.8%) 34 (17.3%) 0.031
Current or ex-smoker 164 (65.9%) 29 (55.8%) 135 (68.5%) 0.084
Positive family history of IHD 61 (24.5%) 10 (19.2%) 51 (25.9%) 0.321
Angiographic characteristics
IRA: LAD/other 121 (48.6%)/128 (52.4) 47 (90.4%)/5 (9.6%) 74 (37.6%)/123 (62.4%) <0.001
IRA TIMI 0 flow prior to PCI 144 (57.8%) 39 (75.0%) 105 (53.3%) 0.005
IRA TIMI 3 flow post PCI 229 (92.0%) 41 (78.8%) 188 (95.4%) 0.001
Multivessel coronary artery disease 143 (57,4%) 34 (65.4%) 109 (55.3%) 0.192
Stent implantation 245 (98.4%) 51 (98.1%) 194 (98.5%) 0.678
GP IIb/IIIa inhibitor usage 66 (26.5%) 25 (48.1%) 41 (21.0%) <0.001
Biochemical characteristics
eGFR (CKD-EPI equation)
[mL/min/1.73 m2]84.4 (74.1–94.5) 80.3 (72.8–88.1) 86.5 (75.0–96.6) 0.036
Glucose on admission [mg/dL] 138.5 (122.0–169.0) 157.0 (133.0–193.0) 135 (118.0–168.0) 0.001
cTnImax [ng/mL] 41.2 (11.8–50.0) 50.0 (50.0–50.0) 29.1 (9.7–50.0) <0.001
CK-MBmax [U/L] 242.0 (116.5–414.0) 489.0 (361.5–747.0) 178.5 (95.0–347.5) <0.001
Total cholesterol [mg/dL] 223.0 (195.0–251.0) 223.0 (195.0–252.0) 223.0 (195.0–251.0) 0.688
LDL-C [mg/dL] 145.0 (125.0–173.0) 145.0 (131.5–170.0) 146.0 (124.0–174.0) 0.712
HDL-C [mg/dL] 52.0 (46.0–59.0) 51.0 (43.0–56.0) 52.0(46.0–59.0) 0.128
Triglycerides [mg/dL] 82.0 (59.0–128.0) 89.5 (62.5–130.5) 78.0(58.0–125.0) 0.103
BNP on admission [pg/mL] 53.9 (27.9–106.5) 74.8 (31.8–155.7) 50.6(27.3–101.9) 0.045
BNP at discharge [pg/mL] 139.8 (74.7–284.2) 436.7 (223.6–735.5) 111.9 (65.3–198.3) <0.001
BMI, body mass index; BNP, B-type natriuretic peptide; CKD-EPI, Chronic Kidney Disease Epidemiology Collaboration; CK-MB
max
,
maximal activity of isoenzyme MB of creatinine kinase; cTnI
max
, maximal activity of troponin I; eGFR, estimated glomerular filtration rate;
HDL-C, high-density-lipoprotein cholesterol; IHD, ischemic heart disease; IRA, infarct-related artery; LAD, left anterior descending artery;
LDL-C, low-density-lipoprotein cholesterol; LVSD, left ventricular systolic dysfunction; PCI, percutaneous coronary intervention; TIMI,
thrombolysis in myocardial infarction score. * for comparison between groups with and without LVSD at 6 months.
J. Clin. Med. 2021,10, 5445 5 of 18
3.3. Echocardiographic Characteristics
Table 2presents major echocardiographic parameters at the time of discharge from
hospital and after 6 months in the overall study population and in the subgroups with and
without LVSD. Within 6 months of STEMI, a significant increase in median values of LVEF
from 44% to 46% could be noted, leading to a decline in the percentage of patients with
LVEF ≤40% from a baseline value of 33.7% to 20.9% after 6 months (p< 0.001; Table 3).
Table 2.
Echocardiographic characteristics of the study population in relation to LVSD occurrence. Data are presented as
median (lower quartile-upper quartile).
Variable Overall Study
Population (n= 249)
Patients with LVSD
at 6 Months (n= 52)
Patients without LVSD
at 6 Months (n= 197) p*
At discharge
LA [mm] 40.0 (37.0–43.0) 41.0 (38.0–45.0) 39.0 (37.0–42.0) 0.007
LVEDd [mm] 49.0 (45.0–53.0) 53.0 (49.0–56.0) 47.0 (45.0–52.0) <0.001
LVESd [mm] 34.0 (30.0–37.0) 38.0 (35.0–40.5) 33.0 (30.0–36.0) <0.001
LVEDV [mL] 99.4 (84.0–121.0) 121.5 (102.5–132.5) 93.0 (81.0–111.0) <0.001
LVESV [mL] 55.0 (45.0–69.0) 75.0 (66.0–84.5) 51.0 (42.5–62.0) <0.001
LVEF [%] 44.0 (39.0–48.4) 36.0 (33.5–38.5) 45.9 (42.0–50.0) <0.001
LVSD (LVEF ≤40%) 84.0 (33.7%) 45 (86.5%) 39 (19.8%) <0.001
WMSI [points] 1.56 (1.38–1.75) 1.88 (1.78–1.94) 1.44 (1.38–1.69) <0.001
6 months after discharge
LA [mm] 40.0 (38.0–44.0) 44.0 (40.0–46.0) 40.0 (37.0–42.0) <0.001
LVEDd [mm] 50.0 (46.0–54.0) 55.0 (52.0–57.0) 48.0 (45.0–53.0) <0.001
LVESd [mm] 34.0 (31.0–37.0) 40.0 (36.0–44.0) 33.0 (31.0–36.0) <0.001
LVEDV [mL] 110.0 (94.0–134.0) 145.0 (129.5–163.0) 105.0 (91.0–125.0) <0.001
LVESV [mL] 57.0 (48.0–76.0) 92.0 (79.0–103.0) 53.0 (45.0–65.0) <0.001
LVEF [%] 46.0 (42.0–51.5) 36.0 (33.7–38.5) 48.0 (44.8–52.5) <0.001
WMSI [points] 1.44 (1.31–1.69) 1.88 (1.75–1.94) 1.38 (1.31–1.50) <0.001
LA, left atrium end-systolic diameter; LVEDd, left ventricular end-diastolic diameter; LVEDV, left ventricular end-diastolic volume; LVEF,
left ventricular ejection fraction; LVESd, left ventricular end-systolic diameter; LVESV, left ventricular end-systolic volume; LVSD, left
ventricular systolic dysfunction; WMSI, wall motion score index. * for comparison between groups with and without LVSD at 6 months.
Table 3.
Occurrence of LVEF
≤
40 % on transthoracic echocardiography at hospital discharge and at
6 months.
LVEF ≤40 % (LVSD) at 6 Months
Absent (n= 197) Present (n= 52)
LVEF ≤40 %at
hospital discharge
Absent (n= 165) 158 (63.5%) 7 (2.8%)
Present (n= 84) 39 (15.7%) 45 (18.1%)
LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction.
Interestingly, patients with LVEF
≤
40% at the time of discharge from hospital, but not
6 months after STEMI (n= 39), when compared with those presenting with LVEF
≤
40%
both at hospital discharge and LVSD 6 months after STEMI (n= 45), had a lower pro-
portion of the LAD as the IRA (31 [79.5%] vs. 42 [93.3%]; p= 0.058), more frequent
TIMI 3 flow in the IRA following PCI (38 [97.4%] vs. 34 [75.6%]; p= 0.002) and lower
values of cardiac biomarkers, including maximal concentration of cardiac troponin I
(50.0 [
27.7–50.0
] vs. 50.0 [
50.0–50.0
] ng/mL; p= 0.039), maximal activity of CK-MB (354
[159–404] vs. 555 [
378–761
] U/L; p< 0.001) and BNP concentration on hospital discharge
(177.3 [113.5–282.0] vs. 439.3 [233.0–751.5] pg/mL; p< 0.001).
J. Clin. Med. 2021,10, 5445 6 of 18
3.4. Electrocardiographic Characteristics
Detailed baseline and post-PCI electrocardiographic data are reported in Table 4.
Table 4.
Electrocardiographic characteristics of the study population in relation to LVSD occurrence. Data are presented as
median (lower quartile-upper quartile) or number (percent) when appropriate.
Variable Overall Study
Population (n= 249)
Patients with LVSD
at 6 Months (n= 52)
Patients without LVSD
at 6 Months (n= 197) p*
Baseline
Heart rate [BPM] 75.0 (62.0–88.0) 81.0 (68.5–97.0) 74.0 (60.0–85.0) <0.001
Anterior location of STEMI 116 (47.0%) 47 (90.4%) 69 (35.0%) <0.001
Number of leads with ST-segment
elevation [n]4.0 (3.0–6.0) 6.0 (5.0–7.0) 3.0 (3.0–5.0) <0.001
Sum of ST-segment elevation [mm] 8.5 (4.0–14.0) 13.8 (9.8–18.0) 7.0 (4.0–12.0) <0.001
Maximal ST-segment elevation [mm] 3.0 (2.0–4.0) 3.5 (3.0–5.0) 2.5 (1.5–4.0) <0.001
Number of leads with pathologic Q
waves [n]2.0 (1.0–4.0) 4.0 (3.0–5.0) 2.0 (1.0–3.0) <0.001
Presence of reciprocal ST-segment
depression ≥1mm 193 (77.5%) 34 (65.4%) 159 (80.7%) 0.019
QRS duration [ms] 95.0 (85.0–100.0) 95.0 (86.0–110.0) 95.0 (85.0–100.0) 0.399
Sclarovsky-Birnbaum ischemia score grade 2: 198 (79.5%);
grade 3: 51 (20.5%)
grade 2: 35 (67.3%)
grade 3: 17 (32.7%)
grade 2: 163 (82.7%);
grade 3: 34 (17.3%) 0.014
Post PCI
Heart rate [BPM] 77.0 (66.0–89.0) 83.0 (72.0–94.0) 75.0 (64.0–88.0) 0.003
ST-segment resolution [%] 60.6 (30.0–88.9) 39.4 (0.0–69.3) 70.0 (40.0–100.0) <0.001
ST-segment resolution (≥50%) 160 (64.3%) 22 (42.3%) 138 (70.1%) <0.001
ST-segment resolution after PCI
(trichotomised)
<30%–62 (24.9%)
≥30–69%–82 (32.9%)
≥70%–105 (42.2%)
<30%–22 (42.3%)
≥30–69%–24 (46.2%)
≥70%–6 (11.5%)
<30%–40 (20.3%)
≥30–69%–58 (29.4%)
≥70%–99 (50.3%)
<0.001
Number of leads with ST-segment
elevation [n]3.0 (1.0–5.0) 5.5 (4.0–7.0) 3.0 (0.0–4.0) <0.001
Sum of ST-segment elevation [mm] 3.0 (1.0–7.0) 8.3 (5.0–13.0) 2.0 (0.0–4.5) <0.001
Maximal ST-segment elevation [mm] 1.0 (0.5–2.0) 2.3 (1.5–4.0) 1.0 (0.5–1.5) <0.001
Number of leads with pathologic Q
waves [n]3.0 (2.0–5.0) 5.0 (4.0–7.0) 3.0 (1.0–4.0) <0.001
QRS duration [ms] 90.0 (84.0–100.0) 99.5 (87.5–111.0) 90.0 (83.0–100.0) 0.003
BPM, beats per minute; LVSD, left ventricular systolic dysfunction; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation
myocardial infarction. * for comparison between groups with and without LVSD at 6 months.
3.5. Characteristics Comparison of Patients with and without LVSD
As reported in Table 1, both groups showed no significant demographic nor clinical
differences, except for a higher prevalence of diabetes in the LVSD (+) group. LVSD (+)
patients also presented a less favorable angiographic profile, including more frequent
involvement of LAD as the IRA, more widespread usage of GP IIb/IIIa inhibitor, a higher
incidence of TIMI 0 and less frequent occurrence of TIMI 3 flow before and after PCI,
respectively. Patients who presented with LVSD after 6 months were also characterized
at baseline by worse renal function as assessed with glomerular filtration rate, higher
blood glucose concentration on admission, more extensive release of myocardial necrosis
markers and higher concentrations of B-type natriuretic peptide both on admission and at
discharge. At discharge, both groups were receiving similar pharmacological treatment
regarding aspirin, clopidogrel, statin, beta-blocker and ACEI/ARB (all used in
≥
98.5%
of patients); however, LVSD (+) patients were receiving aldosterone antagonist (28.8% vs.
5.1%; p< 0.001) and diuretic (28.8% vs. 4.6%; p< 0.001) more frequently than their LVSD
(–) counterparts.
J. Clin. Med. 2021,10, 5445 7 of 18
3.6. Electrocardiographic Characteristics of Patients with LVSD
The analyzed ECG parameters, both at baseline and post PCI, point to more severe
ischemia and a more extensive MI in the LVSD (+) group. These include faster heart
rate, more widespread ST-segment elevation and Q-wave development and higher total
and maximal ST-segment elevation. More pronounced ischemia in LVSD (+) patients
was also evidenced by a higher incidence of anterior wall location, reciprocal ST-segment
depression
≥
1 mm and grade 3 according to Sclarovsky-Birnbaum ischemia grading
system at baseline. In post-PCI ECG assessment, lower incidence and degree of ST-segment
resolution and longer duration of the QRS complex were associated with the presence of
LVSD after 6 months. A detailed comparison of ECG parameters is reported in
Table 4
.
As shown in Figure 1, we also found visual variability and a linear trend toward an
increasing rate of LVSD at 6 months with an increasing duration of the QRS complex on
admission (OR for the upper vs. combined lower and middle terciles 1.59; 95% CI 0.80–3.17;
p= 0.180) and after PCI (OR for the upper vs. combined lower and middle terciles 3.42;
95% CI
1.76–6.66
;p< 0.001). We also noticed significantly lower values of LVEF in the
highest tercile of baseline and post-PCI QRS duration, compared with the lowest and
middle terciles (see Figure 1).
J. Clin. Med. 2021, 10, x FOR PEER REVIEW 8 of 19
Figure 1. LVSD prevalence 6 months after STEMI according to terciles of QRS duration (a) on admission and (b) post PCI.
Median LVEF 6 months after STEMI according to increasing terciles of QRS duration (c) on admission and (d) post PCI.
LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction; ms, milliseconds; PCI, percutaneous
coronary intervention; STEMI, ST-segment elevation myocardial infarction.
3.7. Predictors of the Presence of LVSD 6 Months after Discharge from Hospital
Initially, we performed a univariate regression analysis, including electrocardio-
graphic parameters and the variables from Table 1, to identify possible predictors of
LVSD after 6 months. Unadjusted models are summarized in Figure 2. Our results indi-
cate strong association of LVSD after 6 months with the majority of electrocardiographic
parameters assessed at the time of presentation to hospital and post PCI. Only baseline
QRS duration did not show statistical significance. Of note, reciprocal ST-segment de-
pression ≥ 1mm at baseline pointed to a lower likelihood of LVSD after 6 months.
Among the analyzed angiographic variables, LAD as the IRA and usage of GP
IIb/IIIa inhibitor were identified as predictors of LVSD occurrence, while TIMI 0 flow
before PCI and TIMI 3 flow post PCI were associated with a lower incidence of LVSD
after 6 months. The biochemical variables predicting LVSD occurrence included glucose
concentration on admission, maximal cardiac troponin I concentration and CK-MB ac-
tivity, as well as BNP concentration at discharge from hospital. The only clinical variable
predictive of LVSD was the presence of diabetes mellitus.
Figure 1.
LVSD prevalence 6 months after STEMI according to terciles of QRS duration (
a
) on admission and (
b
) post PCI.
Median LVEF 6 months after STEMI according to increasing terciles of QRS duration (
c
) on admission and (
d
) post PCI.
LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction; ms, milliseconds; PCI, percutaneous
coronary intervention; STEMI, ST-segment elevation myocardial infarction.
3.7. Predictors of the Presence of LVSD 6 Months after Discharge from Hospital
Initially, we performed a univariate regression analysis, including electrocardiographic
parameters and the variables from Table 1, to identify possible predictors of LVSD after
6 months. Unadjusted models are summarized in Figure 2. Our results indicate strong
association of LVSD after 6 months with the majority of electrocardiographic parameters
assessed at the time of presentation to hospital and post PCI. Only baseline QRS duration
did not show statistical significance. Of note, reciprocal ST-segment depression
≥
1mm at
baseline pointed to a lower likelihood of LVSD after 6 months.
J. Clin. Med. 2021,10, 5445 8 of 18
J. Clin. Med. 2021, 10, x FOR PEER REVIEW 9 of 19
Figure 2. Predictors of LVSD occurrence after 6 months of follow-up according to the univariate
logistic regression analysis: (a) demographic, clinical, angiographic and biochemical variables; (b)
baseline electrocardiographic variables; (c) post-PCI electrocardiographic variables. BNP, B-type
natriuretic peptide; CK-MBmax, maximal activity of isoenzyme MB of creatinine kinase; cTnImax,
maximal concentration of troponin I; CI, confidence interval; IRA, infarct-related artery; LAD, left
anterior descending artery; LVSD, left ventricular systolic dysfunction; ms, milliseconds; OR, odds
ratio; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarc-
tion; TIMI, thrombolysis in myocardial infarction score.
Next, in order to determine possible independent predictors of LVSD after 6 months,
a multivariate logistic regression analysis was performed. We identified anterior location
of STEMI, longer post-PCI QRS duration and impaired post-PCI flow in the IRA as the
independent predictors of LVSD 6 months after STEMI (Figure 3).
Figure 2.
Predictors of LVSD occurrence after 6 months of follow-up according to the univariate
logistic regression analysis: (
a
) demographic, clinical, angiographic and biochemical variables;
(
b
) baseline electrocardiographic variables; (
c
) post-PCI electrocardiographic variables. BNP, B-type
natriuretic peptide; CK-MBmax, maximal activity of isoenzyme MB of creatinine kinase; cTnImax,
maximal concentration of troponin I; CI, confidence interval; IRA, infarct-related artery; LAD, left
anterior descending artery; LVSD, left ventricular systolic dysfunction; ms, milliseconds; OR, odds
ratio; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction;
TIMI, thrombolysis in myocardial infarction score.
Among the analyzed angiographic variables, LAD as the IRA and usage of GP IIb/IIIa
inhibitor were identified as predictors of LVSD occurrence, while TIMI 0 flow before PCI
and TIMI 3 flow post PCI were associated with a lower incidence of LVSD after 6 months.
The biochemical variables predicting LVSD occurrence included glucose concentration on
admission, maximal cardiac troponin I concentration and CK-MB activity, as well as BNP
concentration at discharge from hospital. The only clinical variable predictive of LVSD was
the presence of diabetes mellitus.
Next, in order to determine possible independent predictors of LVSD after 6 months,
a multivariate logistic regression analysis was performed. We identified anterior location
J. Clin. Med. 2021,10, 5445 9 of 18
of STEMI, longer post-PCI QRS duration and impaired post-PCI flow in the IRA as the
independent predictors of LVSD 6 months after STEMI (Figure 3).
J. Clin. Med. 2021, 10, x FOR PEER REVIEW 10 of 19
Figure 3. Predictors of LVSD presence after 6 months of follow-up. The model was created using multivariate logistic
regression analysis by adding all electrocardiographic variables to the demographic, clinical, angiographic and bio-
chemical data. CI, confidence interval; IRA, infarct-related artery; LVSD, left ventricular systolic dysfunction; ms, milli-
seconds; OR, odds ratio; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction,
TIMI, thrombolysis in myocardial infarction score.
3.8. Determinants of LVEF Deterioration
In an attempt to more thoroughly explore the relationship between ECG parameters
and LVEF, multiple linear regression analysis with a backward elimination was applied
(Table 5). We found that anterior location of STEMI, longer post-PCI QRS duration,
higher baseline number of pathological Q-waves and higher baseline Sclarov-
sky-Birnbaum ischemia score, together with impaired post-PCI flow in the IRA, higher
values of body mass index and glucose concentration on admission, were independently
associated with lower values of LVEF at 6 months.
Table 5. Impact of demographic, clinical, angiographic, biochemical and electrocardiographic variables on left ventricular
ejection fraction (LVEF) 6 months after STEMI. The model was obtained using multiple regression by adding all electro-
cardiographic variables to the demographic, clinical and angiographic data.
Variable Beta Coefficient
Beta Coefficient
Standard Error
Direction
Component
Beta
Direction
Component
Beta Standard
Error
p
Model characteristics: R = 0.682; R
2
=
0.464; corrected R
2
=
0.448; p < 0.00001
Intercept 70.49 3.71 <0.0001
BMI [kg/m
2
] −0.10 0.05 −0.20 0.10 0.0461
Glucose on admission [per
increments of 10 mg/dL] −0.16 0.05 −0.21 0.07 0.0021
IRA TIMI 3 flow after PCI 0.12 0.05 −3.20 1.36 0.0196
Anterior location of STEMI −0.36 0.05 −5.45 0.83 <0.0001
QRS duration on admission [per
increments of 10 ms] −0.28 0.05 −1.36 0.25 <0.0001
Number of leads with pathologic Q
waves on admission −0.24 0.05 −0.82 0.18 <0.0001
Sclarovsky-Birnbaum ischemia score
[grade 3 vs. grade 2] −0.12 0.05 −2.33 0.94 0.0137
BMI, body mass index; IRA, infarct-related artery; PCI, percutaneous coronary intervention; STEMI, ST-segment eleva-
tion myocardial infarction; TIMI, thrombolysis in myocardial infarction score.
Figure 3.
Predictors of LVSD presence after 6 months of follow-up. The model was created using multivariate logistic
regression analysis by adding all electrocardiographic variables to the demographic, clinical, angiographic and biochemical
data. CI, confidence interval; IRA, infarct-related artery; LVSD, left ventricular systolic dysfunction; ms, milliseconds;
OR, odds ratio; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction, TIMI,
thrombolysis in myocardial infarction score.
3.8. Determinants of LVEF Deterioration
In an attempt to more thoroughly explore the relationship between ECG parameters
and LVEF, multiple linear regression analysis with a backward elimination was applied
(Table 5). We found that anterior location of STEMI, longer post-PCI QRS duration, higher
baseline number of pathological Q-waves and higher baseline Sclarovsky-Birnbaum is-
chemia score, together with impaired post-PCI flow in the IRA, higher values of body mass
index and glucose concentration on admission, were independently associated with lower
values of LVEF at 6 months.
Table 5.
Impact of demographic, clinical, angiographic, biochemical and electrocardiographic variables on left ventric-
ular ejection fraction (LVEF) 6 months after STEMI. The model was obtained using multiple regression by adding all
electrocardiographic variables to the demographic, clinical and angiographic data.
Variable Beta
Coefficient
Beta Coefficient
Standard Error
Direction
Component Beta
Direction Component
Beta Standard Error p
Model characteristics: R = 0.682; R2= 0.464; corrected R2= 0.448; p< 0.00001
Intercept 70.49 3.71 <0.0001
BMI [kg/m2]−0.10 0.05 −0.20 0.10 0.0461
Glucose on admission [per
increments of 10 mg/dL] −0.16 0.05 −0.21 0.07 0.0021
IRA TIMI 3 flow after PCI 0.12 0.05 −3.20 1.36 0.0196
Anterior location of STEMI −0.36 0.05 −5.45 0.83 <0.0001
QRS duration on admission [per
increments of 10 ms] −0.28 0.05 −1.36 0.25 <0.0001
Number of leads with pathologic
Q waves on admission −0.24 0.05 −0.82 0.18 <0.0001
Sclarovsky-Birnbaum ischemia
score [grade 3 vs. grade 2] −0.12 0.05 −2.33 0.94 0.0137
BMI, body mass index; IRA, infarct-related artery; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial
infarction; TIMI, thrombolysis in myocardial infarction score.
J. Clin. Med. 2021,10, 5445 10 of 18
4. Discussion
4.1. General Findings and Study Strengths
According to our results, the majority of the analyzed electrocardiographic param-
eters measured at baseline and directly after PCI were associated with LVSD 6 months
after STEMI. However, when we considered demographic, clinical, angiographic and
biochemical characteristics of our study participants, among all assessed ECG parameters,
only anterior location of STEMI and longer post-PCI QRS duration remained indepen-
dent predictors of post-MI LVSD. Additionally, in our study, anterior location of STEMI,
longer post-PCI QRS duration, higher baseline number of pathological Q-waves and higher
baseline Sclarovsky-Birnbaum ischemia score, together with impaired post-PCI flow in
the IRA, higher values of body mass index and glucose concentration on admission, were
independently associated with lower LVEF at 6 months.
All electrocardiographic parameters selected for our analysis have been described
in the literature to have some predictive value towards LVEF and LVSD. However, many
of these reports come from the thrombolysis era and from inhomogeneous cohorts of
patients. Our study cohort is characterized by homogeneity concerning the form of acute
coronary syndrome presentation (exclusively patients with a first STEMI), reperfusion
therapy (exclusively primary PCI) and subsequent pharmacotherapy [
18
]. This uniformity
in study cohort profile, in conjunction with appropriate inclusion and exclusion criteria,
allowed us to avoid many potential confounders and enables the extrapolation of these
results to the majority of contemporary patients with a first STEMI. Importantly, besides
multiple ECG parameters, we examined the impact of numerous demographic, clinical,
angiographic and biochemical variables on LVSD occurrence.
4.2. Heart Rate
Increased heart rate is a well-recognized risk factor for all-cause and cardiovascular
mortality in the general population [
29
–
35
], as well as in patients with stable coronary
disease [
36
–
40
], heart failure [
41
–
45
] and MI [
46
–
48
]. In STEMI patients, heart rate > 70 bpm
recorded at hospital discharge was associated with 2-fold higher 1 year and 4 year mortality
rates, while a 5 bpm increment of heart rate was considered to enhance 1 year and 4 year
mortality by 29% and 24%, respectively [
49
]. As reflected by a U-shaped curve, extreme
heart rate values (both high and low) are associated with increased mortality [50].
However, we have not found any relevant reports in the literature on the relation of
heart rate in the early phase of STEMI with LVEF and the development of post-MI LVSD.
4.3. STEMI Location
Anterior wall location of STEMI is a strong independent predictor of bad prognosis,
including death [
51
] and the occurrence of cardiogenic shock in the course of STEMI [
52
,
53
],
even in the era of primary PCI for STEMI. Associations between anterior location of STEMI
and more common development of LVSD [
10
,
11
] and left ventricular remodeling [
54
] have
also been reported; however, they were not seen in all studies [55].
4.4. ST-Segment-Elevation-Related Parameters
We also evaluated three parameters related to ST-segment elevation (number of leads
with ST-segment elevation, sum of ST-segment elevations in all leads, maximal ST-segment
elevation in a single lead). According to Rodríguez-Palomares et al., the first two of the
three parameters measured in pre-PCI ECG correlated with the size of myocardium at
risk [
56
]. In research by Manes et al., the sum of ST-segment elevation, maximal ST-segment
elevation and the number of leads with ST-segment elevation
≥
1 mm in predischarge ECG
in patients with anterior STEMI predicted a lower probability of recovery of left ventricular
function after 90 days [
17
]. The 3 ST-segment-related parameters have been shown to
predict post-STEMI mortality [
50
,
57
]. The amplitude of ST-segment elevation was found
to be an independent predictor of post-MI 30-day mortality, particularly for total ampli-
tudes
≥
15 mm [
58
], and a marker of coronary microcirculation obstruction, performing
J. Clin. Med. 2021,10, 5445 11 of 18
even superior to ST-segment resolution [
59
]. It also predicted lack of improvement in left
ventricular systolic function after STEMI in 6-month follow-up [60].
4.5. ST-Segment Resolution
Resolution of ST-segment elevation of
≥
50% is considered a reliable indicator of
patency of the IRA. However, restoration of myocardial tissue perfusion occurs only when
complete (
≥
70%) ST-elevation resolution is achieved. Complete (
≥
70%) resolution of
ST-segment elevation predicts lower 1–3 year mortality and lower rates of cardiovascular
adverse events [
61
–
63
] and was associated with better preservation of left ventricular
function in comparison with partial (30–70%) or no (<30%) ST-segment resolution. The
beneficial outcome of early complete resolution of ST-segment elevation can be seen
even after successful primary PCI, with early (i.e., directly after PCI) assessment being
more precise in terms of predicting cardiovascular adverse events than assessment after
90 min [
64
–
67
]. Additionally, patients with such early ST-segment resolution also had
higher LVEF in comparison to those who achieved ST-segment resolution after 90 min [
64
].
Failure to achieve complete ST-segment resolution also determined higher peak creatine
kinase levels and more common prevalence of significant LVSD [68].
4.6. Reciprocal ST-Segment Depression
Besides ECG changes recorded in leads overlying the area of STEMI, the presence of
reciprocal ST-segment depressions at baseline may also hold prognostic value. In literature
reports it reflected larger infarct area and multivessel coronary artery disease and was
associated with increased mortality and higher rates of heart failure, cardiogenic shock
and second- and third-degree heart block in a manner proportional to their extent and
amplitude [
69
,
70
]. Additionally, sustained ST-segment depressions after PCI are predictive
of increased mortality after STEMI [
71
]. We have found no literature reports concerning
associations of reciprocal ST-segment depressions with LVSD.
4.7. Pathological Q-Waves
The number of leads with pathological Q-waves is another well-recognized predictor
of post-MI mortality. It successfully predicted lack of recovery of left ventricular sys-
tolic function (defined as absolute LVEF improvement by <10%) within 6 months after
STEMI [
60
]. The presence of pathological Q-waves on the admission ECG is predictive
of increased mortality, heart failure and cardiogenic shock after STEMI [
3
,
4
,
72
]. Accord-
ing to Lopez-Castillo et al., the sum of Q-wave depth at discharge performs better than
the number of leads with pathological Q-waves as an independent predictor of LVSD
development [73].
4.8. Sclarovsky-Birnbaum Ischemia Score
Based on the morphology of the terminal portion of the QRS complex and the rel-
ative magnitude of ST-segment elevation, the score identifies three grades of ischemia,
with grade 3 reflecting most severe ischemia [
74
] and being an independent predictor of
no-reflow phenomenon [
67
] and mortality [
75
,
76
]. Compared with grade 2, it indicates
a more extensive infarction area and a higher rate of mortality, heart failure and rein-
farction
[67,76–84]
. In terms of left ventricular systolic function, grade 3 of ischemia was
associated with lower LVEF [82,85] and a higher incidence of LVSD [67].
4.9. QRS Duration
Prolonged QRS duration is another well-established predictor of increased mortality
in STEMI patients [
86
–
88
]. The detrimental effects can already be seen with QRS duration
of
≥
100 ms [
89
]. An increase in 30-day mortality was even found for prolongation of
QRS duration still within normal ranges (100 ms vs. 80 ms) [
50
]. Literature reports
documenting the relation between QRS duration and LVSD are much scarcer; however,
J. Clin. Med. 2021,10, 5445 12 of 18
they point to prolonged QRS duration, and even QRS duration of
≥
100 ms, as a predictor
of LVSD [16,90].
4.10. Detailed Analysis of the Study Results
As one can surmise from the above review of the prognostic value of the electrocardio-
graphic parameters, the majority of the literature concerns their association with mortality,
while there is a scarcity of data concerning associations with LVSD or LVEF. This fact pre-
cludes direct comparison of our results with the cited investigations. However, recognizing
LVSD as a surrogate for cardiovascular mortality, the results of our investigation support
the prognostic value of ECG regarding prognosis assessment following STEMI.
The results of our investigation basically support the data from the literature. Our
study participants who presented with LVSD 6 months after STEMI, in comparison to
those without LVSD, had significantly higher values of heart rate, number of leads with ST-
segment elevation and pathological Q-waves, sum of ST-segment elevation and maximal
ST-segment elevation on admission to hospital and directly after PCI. They also showed
a higher prevalence of anterior STEMI and considerably wider QRS after PCI, while
QRS duration measurement at baseline showed no significant difference. Additionally,
patients presenting with LVSD after 6 months showed more severe ischemia on admission,
as assessed with Sclarovsky-Birnbaum ischemia score, smaller reciprocal ST-segment
depression at baseline and less profound ST-segment resolution post PCI.
In univariate analysis, all but one of the ECG parameters predicted LVSD occurrence
6 months after STEMI, the most powerful being anterior location of STEMI (OR 17.44;
95% CI 6.63–45.88). Our analysis also indicates good predictive value of ST-segment
resolution and grade 3 according to the Sclarovsky-Birnbaum ischemia score, which came
in as the second and third most powerful LVSD predictors. However, it is important to
remember that some of the remaining parameters were reported per increments, which
means that their actual final impact potentiates when the increments are multiplied in
measurements. The only exception was QRS duration at baseline, which did not show
statistical significance. In contrast to literature data, in our investigation, the presence of
reciprocal ST-segment depressions diminished the likelihood of LVSD occurrence 6 months
after STEMI. Whether this could be a consequence of shorter time-to-balloon delay in
this group, compared with patients without reciprocal ST-segment depressions, remains
a matter of speculation and requires verification in a larger group since the difference in
time-to-balloon between patients with and without LVSD was not statistically significant.
In the model adjusted for demographic, clinical, biochemical and angiographic vari-
ables, however, the majority of the ECG parameters did not maintain statistical significance.
The only two parameters contributing to the multivariate regression model and thus recog-
nized as independent predictors of LVSD in 6-month follow-up were anterior location of
STEMI (OR 17.78; 95% CI 6.45–48.96; p< 0.001) and post-PCI QRS duration (OR 1.56; 95%
CI 1.22–2.00; p< 0.001) expressed per increment of 10 ms. The highest tercile of post-PCI
QRS duration (i.e.,
≥
100 ms) was associated with the highest prevalence of LVSD after
6 months and therefore appears to have the best discriminative value. The highest terciles
of baseline and post-PCI QRS duration were also associated with significantly lower values
of LVEF, compared with lower terciles.
4.11. Study Limitations
There are some limitations of this study to be mentioned. First, the study population
is a fraction of the original cohort of patients recruited between 2005 and 2008. The time
that had elapsed from patient recruitment to the onset of the project and clinical practice
modifications implemented over that time could possibly impact the results. Second, LVSD,
used as the endpoint in our investigation, is a well-documented prognostic factor in post-
STEMI patients; however, it is still a surrogate of clinical endpoints. The choice of LVSD as
an endpoint was dictated by lack of power of this study to evaluate clinical endpoints. Third,
the duration of follow-up in our research was restricted to 6 months. It seems likely that
J. Clin. Med. 2021,10, 5445 13 of 18
extending this period might render more favorable results in terms of predictive capabilities
of ECG. Forth, the relatively moderate left ventricular systolic function impairment and
the applied exclusion criteria noticeably blunting the risk of death and the rate of adverse
cardiovascular outcomes in our study group, together with the relatively short time to
reperfusion, limit the applicability of our results to all STEMI patients. This warrants further
research in non-uniform STEMI cohorts before unrestricted extrapolation of our findings to
the general population is feasible. Fifth, enhanced precision of evaluation of left ventricular
systolic function, size of myocardial necrosis and patency of the coronary microcirculation
could possibly be achieved by employing magnetic resonance imaging. Sixth, we routinely
used neither fractional flow reserve measurement nor intravascular ultrasound for the
assessment of non-culprit lesions. Seventh, non-critical, non-culprit coronary lesions
(stenoses 70–90%) were revascularized electively (within 1 month of the index hospital
admission). This fact might have some impact on the study findings. Eighth, in a substantial
number of our study participants, maximal concentration of cardiac troponin I exceeded
50 ng/mL. These serum samples were not further diluted, preventing precise estimation of
the biochemical infarct size. Ninth, patients with left bundle branch block, isolated posterior
myocardial infarction, isolated right ventricular myocardial infarction or permanent atrial
fibrillation were excluded from the study. Therefore, the study findings may not to be
attributable to such patients. Finally, post-reperfusion ECG parameters in time points other
than directly after PCI were not assessed.
5. Conclusions
According to our study, baseline and post-PCI ECG parameters possess a modest
predictive value for LVSD occurrence within 6 months of a first STEMI.
Author Contributions:
Conceptualization, M.K. (Marek Kozi ´nski) and J.K.; data curation, T.F.;
formal analysis, M.K. (Michał Kasprzak); investigation, T.F.; methodology, T.F. and M.K. (Marek
Kozi´nski); project administration, J.K.; supervision, M.K. (Marek Kozi ´nski) and J.K.; visualization,
M.K. (Michał Kasprzak); writing—original draft, T.F. and M.K. (Michał Kasprzak); writing—review
and editing, M.K. All authors have read and agreed to the published version of the manuscript.
Funding:
This study was supported by the financial resources of the Polish Ministry of Science and
Higher Education for Science, 2008–2011 (Research Project No. N402179534).
Institutional Review Board Statement:
The study was conducted according to the guidelines of the
Declaration of Helsinki and approved by the Ethics Committee of Collegium Medicum, Nicolaus
Copernicus University (protocol code KB 440/2004, date of approval 5 August 2004).
Informed Consent Statement:
Informed consent was obtained from all subjects involved in the study.
Data Availability Statement: Data sharing is not applicable to this article.
Acknowledgments:
We are grateful to the staff of the Echocardiography Laboratory, particularly
Iwona ´
Swi ˛atkiewicz, for performing echocardiographic examinations. We would also like to thank
the residents and nurses for their important contribution in participant enrolment, blood sampling
and data collection.
Conflicts of Interest:
The authors declare that there is no conflict of interest. The funders had no role
in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the
manuscript, or in the decision to publish the results.
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