a b s t r a c t

Objectives: To investigate the clinical characteristics of patients with the fragmented QRS complexes (fQRS) and the predictive value of fQRS in patients undergoing primary percutaneous coronary intervention (p-PCI).

Methods: The study enrolled 227 consecutive patients with ST-elevation myocardial infarction who underwent p-PCI. Baseline clinical characteristics, the percentage of ST-segment resolution, and parameters of electrocardiography and coronary angiography were investigated. The relationship between fQRS on pre-PCI and post-PCI electrocardiogram and the percentage of ST-segment resolution after PCI were studied.

Results: Patients with fQRS have higher troponin I, creatine kinase-MB levels, prolonged QRS duration, higher Gensini score, lower percentage of total ST-segment resolution, and left ventricular ejection fraction compared with patients without fQRS. Gensini score (odds ratio [OR], 1.013; 95% confidence interval [CI], 1.002-1.024; P b .006) and percentage of total ST-segment resolution (OR, 0.384; 95% CI, 0.186-0.795; P = .01) were indepen- dently associated with the presence of fQRS. A multivariate logistic regression analysis selected presence of fQRS pre-PCI (OR, 2.908; 95% CI, 1.095-7.723; P = .032) and the number of leads with fQRS before PCI (OR, 1.582; 95% CI, 1.250-2.002; P b .001) as independent predictors of imperfect ST-segment resolution.

Conclusions: The presence of fQRS is a predictor in ST-elevation myocardial infarction patients undergoing p-PCI. The occurrence of fQRS is beneficial to identify the patients with severe coronary lesion, left ventricular contraction dysfunction, and larger areas of Ischemic injury.

(C) 2015 The Authors. This is an open access article under the CC BY-NC-ND license

(http://creativecommons.org/licenses/by-nc-nd/4.0/).

1. Introduction

Fragmented QRS complexes (fQRS) on the routine 12-lead electro- cardiograms (ECGs) refer to various RSR? patterns (>= 1 R? or notching of S wave or R wave) with or without Q wave and QRS duration less than 120 milliseconds in 2 or more contiguous leads corresponding to a major coronary artery territory [1]. There are some other well- known myocardial ischemia markers such as ST-segment depression and elevation, T-wave flattening or inversion, and pathologic Q waves. Fragmented QRS is regarded as nonhomogeneous myocardial depolari- zation of the ventricles due to myocardial scar or fibrosis in patients with myocardial infarction (MI). Previous research demonstrated that the presence of fQRS in the 12-lead ECG was an ECG marker of prior

* Corresponding author. Tel.: +86 13702029695; fax: +86 22 88328119.

E-mail addresses: [email protected] (X. Ma), [email protected] (W. Duan), [email protected] (P. Poudel), [email protected] (J. Ma), [email protected] (D. Sharma), [email protected] (Y. Xu).

¹ Equal contribution of first author.

MI and left ventricular aneurysm [2,3]. Furthermore, fQRS was found to be a predictor of all-cause mortality and adverse cardiac arrhythmic events [4-6]. However, at present, the relationship between fQRS and myocardial reperfusion in patients with ST-elevation MI (STEMI) has received little attention [7]. The purpose of this study is to investigate whether fQRS has predictive value of imperfect ST-segment resolution in patients with STEMI undergoing primary percutaneous coronary intervention (p-PCI).

1. Methods
   1. Study population

A total of 227 consecutive patients who were diagnosed with acute STEMI and underwent p-PCI within 12 hours of the onset of chest pain in cardiology department were prospectively enrolled in this study. Patients with prior MI, bundle-branch block, cardiomyopathy, organic valvular heart disease, Wolff-Parkinson-White syndrome, and those with permanent pacemakers were excluded from this study.

http://dx.doi.org/10.1016/j.ajem.2015.11.010

0735-6757/(C) 2015 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

The study protocol was approved by our institutional ethics committee. Informed consent was obtained from all patients enrolled before the study.

Clinical data and Laboratory measurements

The baseline clinical characteristics and risk factors for coronary artery disease including age, sex, smoking history, hypertension, diabe- tes mellitus, and stroke were collected. Cardiac biomarkers levels in- cluding troponin I (cTnI), creatine kinase (CK), and creatine kinase-MB (CK-MB) were measured on admission and 8 hours after admission, and then their peak values were recorded for analysis. Routine blood chemistry, Uric acid (UA), creatinine (Cr), urea nitrogen, and D-dimer levels were determined by standard methods on admission. Fasting glucose, lipid profile, and liver function tests were performed and recorded after fasting for at least 8 hours.

Electrocardiography

The standard 12-lead ECGs were obtained at a paper speed of 25 mm/s, amplitude of 10 mm/mv, and a filter range 0.5 to 150 Hz. All the patients’ ECG records were reobtained on hospital admission and 2 hours after p-PCI, respectively. The percentage of total ST resolution, delta QRS time, the sum ST elevations, and QRS duration of pre-PCI and post-PCI ECG was analyzed by 2 independent readers who were blinded to study design and results. The diagnosis of acute STEMI was made according to an ECG obtained during admission with the presence of clinical symptoms and findings. Patients with chest pain that continued for longer than 30 minutes and with the presence of new or presumed new ST-segment elevation at the J point in greater than or equal to 2 contiguous leads of greater than or equal to 0.2 mV in leads V₁, V₂, or V₃ and greater than or equal to 0.1 mV in other leads. Marked ST depression, which was maximal in leads V₁ through V₃, without ST-segment elevation in other leads, was designated as posterior wall MI [8].

Diagnosis standard for fQRS defined as presence of RSR pattern with various morphologies of the QRS interval (QRS duration b 120 millisec- onds) with or without the Q wave. It was defined by the presence of an additional R wave (R?) or notching in the nadir of the S wave or the presence of greater than 1 R (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory [1].

The sum of ST-segment elevations (?STE) amount in millimeters on each ST elevation before and after p-PCI ECG was measured manually 20 milliseconds after the end of QRS complex (the J point) using a hand- held caliper. The difference between 2 measurements was regarded as resolution of the sum of ST elevations and expressed as percentage of total ST-segment resolution (?STR). Post-PCI ?STR was determined as following formula: ?STR = [(the sum of ST-segment elevation on pre-PCI ECG) - (the sum of ST-segment elevation on post-PCI ECG)]/ (the sum of ST-segment elevation on pre-PCI ECG) x 100%. ?STR less than 50% was considered as imperfect ST-segment resolution and was regarded as a predictor of No-reflow phenomenon. ?STR greater than or equal to 70% was considered as a ECG sign of successful myocardial perfusion [9-11]. Delta QRS time was calculated by formula: Delta QRS time = (QRS duration pre-PCI ECG) - (QRS duration post- PCI ECG).

Coronary angiography and p-PCI

All patients received an equivalent dose of 300 mg aspirin and 300 mg or 600 mg clopidogrel as a loading dose before the p-PCI proce- dure. After the operation, all patients were monitored in the coronary care unit until they were stabilized. They received aspirin (75 mg/d), clopidogrel (75 mg/d), and low-molecular-weight heparin sodium (0.8 mL/d) postoperatively. Glycoprotein IIb/IIIa receptor blocker (tirofiban) was administered at the decision of the operator. All the patients were

treated according to the recommendations of 2013 American College of Cardiology Foundation/American Heart Association Guideline for the Management of ST-Elevation Myocardial Infarction [12].

Percutaneous coronary intervention was performed using the stan- dard Judkins technique through the Radial artery. Quantitative analysis of computer systems was performed to assess coronary stenosis by the number of vessels involved (vessel score) and Gensini score. Signif- icant coronary stenosis, that is, greater than or equal to 50% reduction in lumen diameter compared with the nearest normal segment, was con- sidered as coronary angiography positive. Depending on the number of vessels involved, vessel score ranged from 0 to 3 (0: b 50% luminal narrowing; 1, 2, and 3: no. of luminal narrowed vessels of >= 50%). The angiographic characteristics, which included lesion location and severi- ty of stenosis, were determined by Gensini scores [13]. Thrombolysis in Myocardial Infarction grade flow classification system was used to scale coronary flow over the culprit lesion [14].

Statistical analysis

All statistical analyses were carried out using SPSS version 19.0 (SPSS, Chicago, IL). Normal distribution of continuous data was tested using the Kolmogorov-Smirnov test. Continuous and normally distrib- uted variables were expressed as mean +- SDs and compared the means by the Student t test. Nonnormally distributed data were expressed as median with interquartile range, and the Mann-Whitney U test was used to compare the differences between 2 groups. Categor- ical variables were expressed as percentage and compared using the ?² Correlation analyses. logistic regression model analysis was performed to identify the predictors of total ST resolution less than 50% by univar- iate and multivariate analyses. The following explanatory variables were used in the univariate analyses: Age 65 years or older, anterior wall MI, cTnI, pain to balloon time, delta QRS time, fQRS, number of leads with fQRS, post-PCI TIMI 3 grade, the number of stent, triple- vessel coronary disease, and Gensini score. On the univariate analyses, explanatory variables with a P value less than .1 were selected and en- tered into a multivariate analysis. All tests in respect to significance were 2 tailed. P b .05 was considered to be statistically significant.

1. Results
   1. Baseline clinical data and laboratory measurements

A total of 227 STEMI patients were enrolled in this study (Table 1). The ECG analysis of all the patients with STEMI demonstrated that fQRS was present in 62.6% of cases on post-PCI ECG. These patients were classified as fQRS group (n = 142). Eighty-five cases without fQRS served as a control group. The 2 groups were compared; 50.2% (n = 114) of cases have fQRS on pre-PCI ECG. Of all fQRS cases, 16.1% (n = 23) of cases developed fQRS after p-PCI procedure. There was no significant difference between non-fQRS and fQRS group with regard in baseline clinical characteristics such as age, sex, smoking, hyperten- sion, diabetes mellitus, cerebrovascular disease, Killip score, and pain to door time.

Patients with fQRS had higher cardiac biomarker level including cTnI (P = .019), CK (P = .001), and CK-MB level (P = .017). They also had even higher level of alanine transaminase (ALT) (P = .020), and aspar- tate aminotransferase (AST) (P = .029), Cr (P = .001), UA (P = .006), and lower left ventricular ejection fraction (LVEF) (P = .003) in compar- ison to patients without fQRS. The Incidence of arrhythmia, amiodarone used, and lidocaine used were significantly higher in the fQRS group, compared with the non-fQRS group (P b .05).

Electrocardiography and angiographic results

The patients with fQRS had prolonged QRS duration, higher the sum of ST-segment elevation, lower ?STR, more frequent Q waves, higher

Table 1

Baseline clinical characteristics of 2 groups Parameters Non-fQRS group

	(n = 85)	(n = 142)	and ?2
Age (y)	63 +- 11	64 +- 13	-1.016	.291
Sex (male), n (%)	53 (62.4)	89 (62.7)	0.002	.961
Smoking, n (%)	49 (57.6)	92 (64.8)	1.152	.283
Hypertension, n (%)	46 (54.1)	76 (53.7)	0.008	.930
Diabetes mellitus, n (%)	23 (27.1)	30 (21.1)	1.045	.307
Stroke, n (%)	12 (14.1)	16 (11.3)	0.399	.527
Pain to balloon time (h)	4 (2.71-5.50)	3.5 (2.19-5.33)	-0.843	.399
Killip score (3 and 4)	39 (3.5)	14 (9.9)	3.075	.080
cTnI (ug/L)	14 (1.53-28.7)	20.5 (7.0-31.8)	-2.338	.019
CK (U/L)	1052 (433.7-1600)	1600 (769.3-2073)	-3.277	.001
CK-MB (U/L)	117 (47.2-185.1)	141.7 (71-242.9)	-2.384	.017
ALT (g/L)	31.5 (21.0-41.4)	37.5 (23.2-56.7)	-2.322	.020
AST (g/L)	108 (49.2-185)	136 (77.3-208)	-2.188	.029
Triglyceride (mmol/L)	1.63 (0.96-2.08)	1.20 (0.81-1.69)	-2.725	.006
TC (mmol/L)	4.91 +- 1.00	4.69 +- 0.92	1.631	.104
HDL (mmol/L)	0.91 (0.75-1.05)	0.93 (0.81-1.08)	-1.456	.145
LDL (mmol/L)	3.26 +- 0.91	3.05 +- 0.77	-0.767	.444
Urea nitrogen (mmol/L)	5.7 (4.9-6.6)	6.2 (4.9-7.4)	-1.561	.119
Cr (umol/L)	70.8 (56.8-78.8)	76.9 (67.6-88.0)	-3.213	.001
UA (umol/L)	306 +- 67	336 +- 83	-2.755	.006
WBC (x109/L)	9.3 (8.0-10.8)	8.7 (7.2-11.3)	-0.818	.413
Glucose (mmol/L)	6.89 (5.81-8.25)	6.43 (5.51-7.57)	-1.596	.110
LVEF (%)	55.95 +- 9.47	51.3 +- 11.92	3.02	.003
Tirofiban	55 (64.7)	65 (46.4)	7.099	.008
Amiodarone	1 (1.2)	15 (10.7)	7.284	.007
Lidocaine	4 (4.7)	24 (17.1)	7.508	.006
Arrhythmia	5 (5.9)	32 (22.5)	10.808	.001

fQRS group

t, Z, P

fQRS; group 2, 2 to 3 leads with fQRS; and group 3, greater than 3 leads with fQRS. The presence and higher number of leads with fQRS on ECGs show statistically significant relation with cardiac marker. Sum of ST-segment elevation and ?STR have significance difference between group 1 when compared with that of groups 2 and 3. Gensini score, incidence of arrhythmia, and triple-vessel disease also have statistically significant when compared among these groups.

The relationship of fQRS with infarct-related parameters

The presence or absence of fQRS was significantly correlated with

?STR (r = -0.207; P = .002), Gensini score (r = -0.191; P = .04), LVEF (r = -0.188; P = .006), and cTnI (r = -0.172; P = .010) (Table 4).

Abbreviations: TC, total cholesterol; HDL, high-density lipoprotein; LDL, low-density lipoprotein.

Gensini score, and lower TIMI score post-PCI compared to patients with- out fQRS (Table 2). The incidence of triple-vessel disease was higher in fQRS group. However, the incidence of Single-vessel disease was lower in fQRS group than that of non-fQRS group.

The relationship of the number of leads with fQRS and infarct-related parameters

The patients enrolled were divided into 3 groups according to the number of lead with fQRS (Table 3): group 1, less than 2 leads with

Table 2

Comparison of ECG and coronary angiography results between the 2 groups

Parameters	Non-fQRS group	fQRS group (n = 142)	Z and ?2	P
	(n = 85)
QRS duration pre-PCI	98 (90-106)	104 (95-111)	-3.094		.002
(milliseconds) QRS duration post-PCI	103 (95-112)	107 (100-114)	-2.884	.004
(milliseconds) Delta QRS time	8 (4.0-14.8)	9 (2.0-20.1)	-0.535	.593
(milliseconds)
?STE pre-PCI (mv)	8 (4.0-14.4)	14 (7.0-18.1)	-2.874	.004
?STE post-PCI (mv)	1 (1-7)	5 (3-12)	-4.550	.000
?STR (%)	1 (0.75-1.00)	0.84 (0.56-1.00)	-3.276	.001
Q wave, n (%)	52 (61.2)	118 (81.3)	13.59	b.001
Single-vessel disease, n (%)	26 (30.6)	26 (18.3)	0.033	.015
2-vessel disease, n (%)	25 (29.4)	35 (24.6)	0.621	.431
3-vessel disease, n (%) Infarct-related artery, n (%) LAD	35 (41.2) 33 (38.8)	82 (57.7) 73 (51.4)	5.845 3.383	.016 .066
LCX	17 (20.0)	23 (16.2)	0.53	.467
RCA	38 (44.7)	58 (40.8)	0.325	.569
Gensini score	70 (48.0-83.4)	84 (60.0-96.6)	-2.948	.003
No. of stent	1 (1.0-1.5)	1 (1.0-2.0)	-0.023	.982

Independent predictors of fQRS

Multivariate logistic regression analysis demonstrated that Gensini score (odds ratio [OR], 1.013; 95% confidence interval [CI], 1.002- 1.024; P b .006) and ?STR (OR, 0.384; 95% CI, 0.186-0.795; P = .01)

were independently related to the presence of fQRS (Table 5).

Comparison of clinical characteristics between patients with different degree of ST resolution

According to the degree of ST-segment resolution, the patients en- rolled were divided into 4 groups: ?STR greater than or equal to 50% and ?STR less than 50%, ?STR greater than or equal to 70% and

?STR less than 70%. After p-PCI, the patients with ?STR less than 50% has higher Gensini score and increased incidence of fQRS than those with ?STR greater than or equal to 50% (P b .01 or .05). Similarly,

?STR less than 70% group also has higher incidence of fQRS and Gensini score than that of ?STR greater than or equal to 70% group. The appearance and the number of fQRS on admission or post-PCI were associated with the low ?STR.

The relationship between the presence of fQRS pre-PCI and imperfect ST-segment resolution

Univariate logistic regression analysis showed that cTnI, delta QRS, Gensini score, the presence of fQRS, and the number of leads with fQRS were significantly related with imperfect ST-segment resolution. Multivariate logistic regression analysis demonstrated that the presence of fQRS (OR, 2.908; 95% CI, 1.095-7.723; P = .032), the number of leads with fQRS (OR, 1.582; 95% CI, 1.250-2.002; P b .01), and delta QRS (OR,

0.955; 95% CI, 0.924-0.988; P = .008) were independent predictors of imperfect ST-segment resolution.

1. Discussion

There are some other well-known myocardial ischemia markers such as ST-segment depression and elevation, T-wave flattening or in- version, and Pathologic Q waves, but fragmented QRS may be the only convenient marker of myocardial scar and ischemia evaluated by 12- lead ECG. QRS wave is a comprehensive vector of ventricular depolariza- tion. Regional myocardial scar and ischemia may lead to nonhomoge- neous myocardial electrical activation, resulting in multiple spikes within the QRS complex, thus appearance of fQRS in the ECG record [15]. Recent studies demonstrated that fQRS represents not only prior occurrence and diagnosis of MI and silent MI [16] but also an indepen- dent predictor of cardiac events in patient with coronary artery disease [17,18]. However, the possible relation of fQRS and myocardial reperfu- sion has been still unclear until now.

Pre-PCI TIMI (0/1) (%)	56 (56.9)	97 (70.8)	0.593	.441	In this study, we found that fQRS was correlated with cTnI level and
Post-PCI TIMI 3 (%)	83 (97.4)	123 (89.8)	4.85	.032	Gensini score. The study demonstrated that patients with fQRS had se-

Abbreviations: LAD, left anterior descending; LCX, circumflex coronary artery; RCA, right coronary artery.

vere coronary lesion, larger areas of ischemic injury, and myocardium

infarction than those of without fQRS. There are 2 possible reasons to

Table 3

The relationship of the number of fQRS with infarct-related parameters

Parameters	No. of leads with fQRS			Z and ?2	P
	0-1 (n = 85)	2-3 (n = 74)	N 3 (n = 68)
cTnI (ug/L)	10.0 (1.5-25.0)	18.0 (8.6-33.3)	25.0 (7.0-32.7)	8.774	.012
CK (U/L)	943 (304-1600)	1600 (813-2076)	1600 (591-2241)	15.61	.000
CK-MB (U/L)	99 (37-181)	147 (97-242)	138 (71-241)	8.488	.014
ALT (g/L)	32 (20-45)	38 (27-53)	34 (19-59)	5.182	.075
AST (g/L)	112 (49-166)	136 (93-215)	131 (77-200)	4.063	.131
Triglyceride (mmol/L)	1.63 (0.96-2.08)	1.09 (0.80-1.47)	1.40 (0.96-2.04)	12.00	.002
Cr (umol/L)	70.8 (56.5-81.0)	77.2 (67.6-90.3)	76.8 (68.0-86.5)	9.610	.008
UA (umol/L)	305 (261-357)	329 (261-369)	355 (292-387)	7.517	.023
LVEF (%)	55 (51-63)	54 (47-60)	44 (54-58)	8.169	.017
QRS time pre-PCI (milliseconds)	98 (90-104)	102 (95-110)	105 (98-112)	9.210	.010
QRS time post-PCI (milliseconds)	95 (86-105)	100 (94-105)	100 (91-107)	4.111	.128
?STE pre-PCI (mv)	4.0 (2.5-8.0)	3.5 (5.0-11.5)	9.0 (4.0-16.0)	9.494	.009
?STE post-PCI (mv)	1.0 (0.0-3.0)	2.5 (0.5-4.5)	3.3 (2.0-5.0)	15.731	.000
?STR (%)	75 (50-100)	57 (23-88)	56 (29-81)	7.199	.027
Gensini score	48 (35-70)	60 (39-79)	68 (46-88)	7.736	.021
Arrhythmia	5 (5.9)	20 (27)	12 (17.6)	13.094	.001
3-vessel disease, n (%)	35 (41.2)	49 (66.2)	33 (48.5)	10.284	.006
Post-PCI TIMI 3 (%)	82 (96.5)	72 (98.6)	66 (97.1)	0.814	.666

explain this result: Patients with fQRS before MI may have severe fixed coronary stenotic lesion and slow coronary flow that could be beneficial in the development of collateral circulation. When coronary artery is oc- cluded, due to collateral circulation, myocardial infarct region may have viable myocardium. The ventricular depolarization delay caused by via- ble myocardium may lead to the presence of fQRS [19,20]. Then again, the changes in ECG are based upon the degree and size of multifocal MI. Patients with triple-vessel disease may produce multifocal MI, and even of single infarction larger than 2 to 3 mm may lead to heteroge- neous ventricular depolarization that leads to formation of fQRS on ECG. Our study suggested that the presence of fQRS correlated with LVEF. Patients with fQRS had a lower LVEF than those without fQRS. Hyrn et al

[21] revealed that scar size, location, and transmurality were indepen- dent predictors of LVEF and left ventricular volumes in patients with MI. Fragmented QRS is significantly related to myocardial fibrosis in pa- tients with ischemic or nonischemic left ventricular dysfunction [22]. The patients with fQRS have larger areas of necrotic myocardium, jeop- ardized ischemia, and severe myocardial fibrosis, which may lead to left ventricular systolic and diastolic dysfunction. The further progression of myocardial scar and ischemia can result in heart failure and ventricular arrhythmia, which is related to increase in mortality and morbidity [23]. This study indicated that QRS time before and after PCI had prolonged in fQRS group compared with non-fQRS group. We speculat- ed that the sequence of ventricular depolarization was altered due to myocardial conduction delay, owing to myocardial scar and ischemia. Brilakis et al [24] found that QRS duration greater than or equal to 100 milliseconds in the absence of bundle-branch block was an independent predictor of increased mortality in patients with non-STEMI. Recent studies demonstrated that prolonged QRS duration was associated with increased long-term mortality because of increased risk of arrhythmia, heart failure, and ischemia [25-28]. Therefore, clinicians should pay more attention on MI patients with fQRS on ECG to prevent

the occurrence of adverse events.

Table 4

The relationship of fQRS with infarct-related parameters Variables fQRS

Early reperfusion therapy, which could prevent necrosis of the ischemic myocardium and improve prognosis, is the preferred treat- ment option for STEMI. The ?STR and TIMI score are both the methods to evaluate the effect of reperfusion therapy. However, there were no correlations between the 2 parameters in our study. Ito et al [29] put for- ward “no reflow phenomenon,” that is, in spite of getting TIMI 3 grade after reperfusion therapy, there were still 16% of patients not reaching the level of myocardial reperfusion. No-reflow phenomenon can be ex- plained by inadequate perfusion of myocardial microcirculation caused by microcirculation embolism, microvascular spasm, microcirculation reperfusion injury, and microvascular stunning. Because of the change of ion distribution on both sides of cell membrane brought about by injuries of cell membrane, ECG expresses ST-segment elevation in patients with STEMI. When extracellular high concentration of potassi- um ions is removed after myocardial reperfusion, cell membranes re- turn to normal electrophysiological state with ST-segment resolution on ECG. Consequently, ST-segment resolution which is dependent on microcirculation reperfusion can be regarded as an indicator of myocar- dial reperfusion.

Multivariate logistic regression analysis demonstrated that the presence and number of fQRS were independent predictors of imperfect ST-segment resolution. The following 2 reasons may explain the relationship between them: First, recent studies showed that fQRS was related to increased C-reaction protein level, so the development of fQRS may be associated with systemic inflammation in patients with acute coronary syndromes and stable angina pectoris [30,31]. Inflammatory response mediated by oxygen free radical might lead to microVascular injury, which is a reason of early no-reflow phenomenon. Second, patients with fQRS had higher Gensini score and more frequent triple-vessel disease in our study. Severe coronary lesion may increase the risk of plaque chips falling down and embolizing microvas- culature to some extent. Imperfect ST-segment resolution post-PCI is independently associated with cardiac dysfunction, cardiac death, and short- and long-term Clinical prognosis in patients with STEMI [32]. The patients with fQRS may have higher risk of imperfect ST-segment resolution and inadequate myocardial reperfusion. Some adjuvant

Table 5

Independent predictors of fQRS

R P

cTnI	0.172	.010		Variables	?	SE	Wald	OR	95% CI	P
LVEF	-0.188	.006		?STR	-0.835	0.378	4.870	0.434	0.207-0.911	.027
Gensini score	0.191	.004		Gensini score	0.010	0.006	3.162	1.010	0.999-1.022	.075
?STR	-0.207	.002		cTnI	0.015	0.009	2.616	1.015	0.997-1.033	.106
Post-PCI TIMI 3	-0.128	.054		LVEF	-0.018	0.017	1.194	0.982	0.950-1.015	.275

treatment, such as the use of adenosine and glycoprotein IIb/IIIa receptor blockers, should be prescribed to improve endothelial function, to main- tain homeostasis of myocardial metabolism, and to reduce myocardial reperfusion injury.

1. Study limitations

There are a few limitation of this study. This is a single-center study that included a relatively small sample size. Therefore, the results of this study need to be confirmed by additional prospective studies with a large sample size. In this study, we just measured the percentage of ST-segment resolution, but we did not investigate myocardial Blush grade during coronary angiography, which can also objectively evaluate myocardial reperfusion.

1. Conclusions

The occurrence of fQRS is beneficial to identify the patients with severe coronary lesion, left ventricular contraction dysfunction, and larger areas of ischemic injury. In addition, fQRS is a potent predictor of imperfect ST-segment resolution in STEMI patients undergoing p-PCI.

Competing interest

The authors declare that they have no conflict of interest.

Author contributions

Xianghong Ma, Wenting Duan, and Yanmin Xu made substantial contributions to conception, design, acquisition of data, analysis, and interpretation of data.

Pradeep Poudel and Junwei Ma were involved in drafting the manuscript and revising it critically for important intellectual content.

Deepak Sharma has given final approval of the version to be published.

The authors have participated sufficiently in the work to take public responsibility for appropriate portions of the content.

Acknowledgments

The authors thank all staff of the Second Hospital of Tianjin Medical University, Tianjin, China.

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